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The mechanisms of splenic control in the Antarctic fish, Pagothenia borchgrevinki, were investigated using isolated spleen and mesenteric artery strips in vitro and perfused spleen preparations in situ. Splenosomatic index (SSI) [100 x (spleen wt/body wt)] and hematocrit were determined in animals treated with atropine and phentolamine. Atropine injection increased the SSI from 0.60 +/- 0.06 to 0.89 +/- 0.04, whereas phentolamine decreased SSI to 0.45 +/- 0.03. In atropine-injected fish, hematocrit was 18.6 +/- 1.4 before and 6.6 +/- 0.8% 3 h after injection. Electrical stimulation of the splenic nerves produced biphasic flow responses. In 11 of 12 tested preparations, atropine (3 x 10(-7) to 10(-6) M) abolished the response, suggesting a major cholinergic component in the splenic innervation. Isolated spleen strip preparations contracted in response to carbachol, a response that was antagonized by atropine. The response to acetylcholine was markedly enhanced by the specific cholinesterase inhibitor BW-284c51. Catecholamine effects were somewhat irregular, and maximal contraction force with epinephrine and norepinephrine was 41 and 56%, respectively, of the carbachol response. The results suggest a mainly, if not solely, cholinergic autonomic control of the borch spleen, and a major function of the cholinergic innervation in the control of hematocrit in this species.

Tachykinin control of gut blood flow (measured by pulsed Doppler technique), dorsal aortic pressure, and heart rate were studied in unrestrained spiny dogfish Squalus acanthias injected with the elasmobranch tachykinins scyliorhinin I and II (SCY I and SCY II), the trout tachykinins substance P (SP), and neurokinin A (NKA). Effects on somatic vasculature were measured by in vitro perfusion of the isolated tail. SCY I and trout SP produced hypotension due to a general vasodilation. This caused a transient increase in mesenteric blood flow and a prolonged increase in celiac blood flow. SCY II caused an initial hypertension induced by a general vasoconstriction, followed eventually by an elevated flow in both gut arteries due to dilation of the vascular beds. Trout NKA evoked a short-lasting increase in celiac blood flow due to a decrease in vascular resistance, a late decrease in mesenteric flow due to vasoconstriction, and no effect on the somatic vasculature. None of the peptides affected heart rate. The study demonstrates a significant vasoactive function of fish tachykinins in the vascular system of an elasmobranch species and, in addition, the occurrence of tachykinin receptor subtypes. Immunohistochemistry revealed a NKA/SCY II-like peptide in nerve fibers innervating many vessels, including the celiac and the mesenteric arteries, the gastrointestinal canal, and the heart.

The effects of preload and afterload on the performance of the systemic heart of the hagfish Myxine glutinosa were investigated before and during sotalol treatment using an in situ perfusion technique. Elevation of input pressure (preload) increased flow by means of increased stroke volume and heart rate in accordance with Starling's law of the heart, while increased output pressure (afterload) decreased flow mainly because of decreased stroke volume. Treatment with the beta-adrenoceptor antagonist sotalol did not change the quality of the responses to increased preload or afterload, although power output decreased by 40 % and flow rate was reduced by 35 % mainly due to a decrease in heart rate. Isolated preparations of the systemic heart and the portal heart provided information on the chronotropic effects of different agonists and antagonists. Both the systemic heart and the portal heart were insensitive to adrenergic and cholinergic agonists, adrenocorticotropic hormone and the cholinoceptor antagonist atropine. Sotalol treatment lowered the rate of spontaneous contractions by 30 % in the systemic heart preparation and by 21 % in the portal heart preparation. This study has given further evidence for the existence of a tonic beta-adrenoceptor stimulation of the hagfish systemic heart and portal heart, and demonstrated the importance of that stimulation in maintaining systemic heart performance.

The portal heart of the New Zealand hagfish (Eptatretus cirrhatus) was perfused in situ. Stroke volume, cardiac output and power output increased in response to increased preload, in accordance with Starling's law of the heart. A positive chronotropic effect was found when the input pressure increased from 0.05 to 0.1 kPa. Increased afterload decreased stroke volume and cardiac output. Power output peaked at an output pressure of 0.22 kPa, after which it decreased. There was no change in heart rate in response to increased afterload. In unanaesthetized resting animals, the pressure in the supraintestinal vein, which supplies the portal heart, ranged from 0.025 to 0.07 kPa (mean 0.040±0.005 kPa). The beta-adrenoceptor antagonist sotalol did not affect the response to different input and output pressures. Sotalol produced a significant decrease in heart rate and abolished the pressure-sensitive increase in heart rate. Bolus injections of adrenaline produced a transient increase in portal heart rate. The negative chronotropic response to sotalol and the response to adrenaline indicate the presence of an endogenous beta-adrenergic tonus on the portal heart.

Prolonged submergence imposes special demands on the cardiovascular system. Unlike the situation in diving birds and mammals, crocodilians have the ability to shunt blood away from the lungs, despite having an anatomically divided ventricle. This remarkable cardiovascular flexibility is due in part to three anatomical peculiarities: (1) an 'extra' aorta (the left aorta) that leaves the right ventricle and allows the blood from the right ventricle to take an alternative route into the systemic circulation instead of going to the lungs; (2) the foramen of Panizza, an aperture that connects the right and left aortas at their base immediately outside the ventricle; and (3) a set of connective tissue outpushings in the pulmonary outflow tract in the right ventricle. Using high-resolution angioscopy, we have studied these structures in the beating crocodile heart and correlated their movements with in vivo pressure and flow recordings. The connective tissue outpushings in the pulmonary outflow tract represent an active mechanism used to restrict blood flow into the lungs, thus creating one of the conditions required for a right-to-left shunt. We observed that the foramen of Panizza was obstructed by the medial cusp of the right aortic valve during most of systole, effectively differentiating the left and right aortic blood pressure. During diastole, however, the foramen remained open, allowing pressure equilibration between the two aortas. Contrary to current theories, we found that the left aortic valves were unable to cover the foramen of Panizza during any part of the cardiac cycle, supporting the reversed foramen flow hypothesis. This would ensure a supply of blood to the coronary and cephalic circulation during a complete shut-down of the left side of the heart, such as might occur during prolonged submergence.

Previous studies have suggested that trout cardiac performance is highly dependent on coronary blood flow during periods of increased activity or hypoxia. To examine the relationship between coronary perfusion and cardiac performance in swimming trout, cardiac output (Q), coronary blood flow (qcor), and dorsal aortic blood pressure were measured in rainbow trout (Oncorhynchus mykiss) during normoxia and hypoxia (PO2 approximately 9 kPa). In normoxic trout, stepwise changes in cardiovascular variables were observed as the swimming speed was incrementally increased from 0.15 body lengths (bl)/s to 1.0 bl/s. At 1.0 bl/s, qcor and cardiac power output had both increased by approximately 110%, and coronary artery resistance (Rcor) had decreased by 40%. During hypoxia, resting qcor was 35% higher, and Rcor was 20% lower, compared with normoxic values. In hypoxic swimming trout, the maximum changes in qcor (155% increase) and Rcor (50% decrease) were recorded at 0.75 bl/s. In contrast, cardiac power output and Q increased by an additional 40 and 20%, respectively, as swimming speed was increased from 0.75 to 1.0 bl/s. The results indicate that 1) increases in qcor parallel changes in cardiac power output; 2) during hypoxia there are compensatory increases in cardiac performance and coronary perfusion; and 3) the scope for increasing qcor in swimming trout is approximately 150%. In addition, results from preliminary experiments suggest that beta-adrenergic, but not cholinergic, mechanisms are involved in the regulation of coronary blood flow during exercise.

All elasmobranchs and about one-third of the teleosts studied have a well-developed coronary system. In species with a coronary system, there is a large inter-species variation in the proportion of the myocardium that is supplied, with a correlation between activity level and dependence on a coronary system. In fish, most of the knowledge about the control of the coronary circulation stems from in situ or in vitro work with only a few recent in vivo studies. In salmonids, about one percent of cardiac output is returned to compact myocardium through the coronary circulation. It has been shown that, as in mammals, the coronary circulation is compromised by the mechanical work of the heart and peak coronary flow occurs during diastole. The control systems involved in the regulation of the coronary vascular resistance changes include both neuronal and humoral components. As in mammals, there are alpha- and beta-adrenoceptors located in the coronary circulation and a cholinergically mediated vasodilatation has been described. ATP, ADP and prostaglandins are probably also involved in the control of the vascular resistance, and there is evidence that local metabolites also have a strong influence on the blood flow through the coronary system.

The two aortas of the crocodile are in open connection at two sites, the foramen of Panizzae immediately outside the ventricles, and the arterial anastomosis at the level of the gut. The present study was performed to elucidate the innervation of the cardiovascular structures of the crocodile, in part to provide a further basis for the assumption that the apertures of the foramen and the anastomosis may be altered, possibly leading to changes in the flow profiles of the central vessels. The presence of smooth muscle arranged at the circumference of the foramen and in the walls of the anastomosis was demonstrated. The cardiovascular structures were innervated by nerves containing co-existing tyrosine hydroxylase, NPY and somatostatin immunoreactivities, which also occurred in neurons of the sympathetic ganglia. CGRP and substance P immunoreactive material co-existed in cardiovascular nerves, and in the nodose ganglion. In addition, bombesin, VIP and galanin immunoreactive nerves were found. Effects of neuropeptides on blood flows and blood pressures were studied in vivo. Substance P increased all blood flows measured, NPY increased the flow through the arterial anastomosis while neurotensin caused an initial decrease in the flow through the arterial anastomosis. In conclusion, there is a rich innervation of the heart and major vessels of the estuarine crocodile, including the foramen of Panizza and the arterial anastomosis. These nerves possibly regulate the distribution of blood in the cardiovascular system, which is further suggested by the results of the injection of neuropeptides.

Cannulated specimens of the benthic Antarctic teleost Trematomus bernacchii were subjected to a five min period of handling stress, following which blood pressures were measured and then blood samples taken for measurement of plasma catecholamine concentrations. There were two control groups of fish, one group of undisturbed fish at Scott Base, Antarctica and the other group of undisturbed fish measured in Christchurch.Plasma catecholamine concentrations were not changed following 5 min of acute handling stress. However, heart rate, ventral aortic blood pressure and haematocrit were elevated following handling, suggesting increased sumpathetic nerve activity. The low plasma catecholamine concentrations measured in all three groups of fish are similar to those found in other species of teleost at rest.The resting heart rates found in this series of experiments were approximately double those recorded in previous work on this species and this difference may be correlated with the length of time that the fish are held in captivity. The fish transported to Christchurch also had higher mean cell haemoglobin concentrations (MCHC) and lower plasma chloride concentrations.

An in situ perfused crocodile (Crocodylus porosus) heart preparation was used to examine the mechanical responses of the heart to increases in adrenaline concentration, to a decrease in oxygen tension and to opening of the pericardium. Starling and power curves were constructed before and after these experimental manipulations. Increasing adrenaline concentration in the perfusate from 5 nmol l-1 to 0.5 µmol l-1 produced a significant increase in heart rate and a decrease in stroke volume, leaving cardiac output unchanged. With maximal adrenergic stimulation, the left ventricle was able to generate greater power outputs at high right aortic output pressures; however, the right ventricle showed a decrease in performance with increasing output pressure. Decreasing the PO2 of the perfusate to 10 kPa resulted in a significant bradycardia. Both the flow and pressure-generating capabilities of the perfused heart preparation were reduced, although the heart was able to maintain low work levels at this PO2. Opening the pericardium permitted greater movement/expansion of the cardiac chambers and resulted in an increase in heart rate. Higher flows were generated at low filling pressures during the input pressure challenge as a result of an increase in the sensitivity of the Starling response.

Until recently, direct measurements of coronary blood flow in fishes had not been made. This review presents and compares in vivo measurements of coronary flow recorded from the school shark, Galeorhinus australis, and the coho salmon, Oncorhynchus kisutch. In both species, the coronary blood flow was phasic and strongly influenced by the cardiac cycle. Coronary blood flow in the school shark was more severely compromised by the cardiac cycle with a short retrograde flow occurring during systole. In the coho salmon, there was an anterograde coronary blood flow throughout the cardiac cycle. Differences in coronary hemodynamics are discussed in relation to differences in the myoarchitecture of the school shark and coho salmon hearts. The regulation of coronary blood flow through changes in vascular resistance (vasoactivity of the coronary vessels) is also discussed.

Changes in cardiac output, heart rate, dorsal aortic blood pressure and coeliac artery blood flow were measured in unrestrained rainbow trout, Oncorhynchus mykiss, following injections of the elasmobranch tachykinins scyliorhinin I and II. The resistance in the coeliac vascular bed and the total systemic vasculature were calculated from blood pressure and flow. In addition, isolated tails were perfused to investigate the effect of the peptides on the somatic vasculature. Scyliorhinin I (SCY I) produced a biphasic change in the coeliac vascular resistance: an initial decrease was followed by an increase. The decrease in coeliac vascular resistance was accompanied by a decrease in the total systemic vascular resistance, leading to an increased cardiac output. The ensuing increase in coeliac vascular resistance caused a slight increase in blood pressure. In the perfused tail, SCY I produced a marked increase in the somatic vascular resistance. Scyliorhinin II (SCY II) decreased the systemic vascular resistance, causing an increase in cardiac output. SCY II also caused a late increase in the coeliac vascular resistance, which led to hypertension and bradycardia. In vitro, SCY II produced a biphasic response in which an initial decrease in the somatic resistance was followed by a larger increase. The results demonstrate that exogenous SCY I and II are vasoactive peptides that act by different mechanisms in the rainbow trout cardiovascular system. Their actions also differ from the actions of substance P previously observed in the cod, Gadus morhua, and possibly involve a neural reflex.

The Australian lungfish Neoceratodus forsteri is one of the few extant species of a phylogenetically ancient group. Immunohistochemistry showed the presence of galanin-, vasoactive intestinal polypeptide (VIP)-, neurotensin-, substance P-, and calcitonin gene-related peptide (CGRP)-like immunoreactivities in nerve fibers in the heart, lung, and gut, with a coexistence of VIP-, galanin-, and somatostatin-like immunoreactivity in the lung and galanin- and somatostatin-like immunoreactivity in the gut. About 20% of the substance P-immunoreactive fibers in gut and lung contained CGRP-like material. Major vessels showed a sparse innervation. In free-swimming unanesthetized fish, neurotensin (1 nmol/kg), galanin (1 nmol/kg), and bombesin (10 nmol/kg) reduced the heart rate. In two specimens tested, the effect of neurotensin was partially antagonized by atropine. Galanin and bombesin reduced and cholecystokinin 8 (CCK-8-S) increased blood flow to the lung. Neurotensin decreased, CCK-8-S increased, and substance P had no effect on dorsal aortic pressure, and all three decreased flow to the gut. It can be concluded from the present study that the general vertebrate pattern of cardiovascular and visceral nervous control by several neuropeptides is present also in Neoceratodus.

Of the extant vertebrate animals, the hagfishes are generally considered to be the group which diverged first from the ancestral vertebrate lineage, although molecular sequence analysis has recently suggested that they form a monophyletic group with lampreys (Stock and Whitt, 1992). The circulatory system of hagfishes has features that have been described as 'primitive' (Burggren et al. 1985), but their gills are effective gas exchangers. The gills are contained within discrete muscular pouches, and the anatomy of the blood system and ventilatory ducts has an ideal countercurrent arrangement (Mallatt and Paulsen, 1986; Elger, 1987). Reite (1969) first reported effects of catecholamines and other drugs on the branchial vasculature of hagfish. Recent studies of both perfused gills in situ and of blood flow in vivo have suggested that blood flow through the gills of hagfish is under tonic control by catecholamines (Axelsson et al. 1990; Forster et al. 1992). In teleosts, several studies have shown that adrenergic control mechanisms are involved in the distribution of blood between the arterio-arterial and the arterio-venous pathways of the gill vasculature (see Nilsson, 1983). Anatomical and ultrastructural studies have demonstrated the existence of similar pathways in hagfish (Cole, 1925; Mallatt and Paulsen, 1986; Elger, 1987). The experiments reported here demonstrate that, in the hagfish gill pouch, both adrenaline and isoprenaline can increase the proportion of fluid leaving via the efferent arterial route, at the expense of the venous outflow. Hagfish (Eptatretus cirrhatus Forster) were collected off Motunau, North Canterbury, New Zealand, and held in seawater aquaria until used. The masses of the 11 animals used in these experiments ranged from 680 to 1720 g with a mean of 1140±110 g (s.e.m.). Animals were anaesthetized in a 0.4 % solution of benzocaine in sea water. The hagfish were opened ventrally to expose the gills and their blood supply. Individual gill pouches were prepared for perfusion studies.

The mechanisms of cardiovascular control in the Antarctic fish Pagothenia borchgrevinki were investigated during rest and swimming exercise using pharmacological tools to reveal the nature of the control systems involved. Simultaneous and continuous recordings of ventral and dorsal aortic blood pressure, heart rate and ventral aortic blood flow (cardiac output) were made using standard cannulation procedures and a single-crystal Doppler flowmeter. Exercise produced a clear and consistent decrease in dorsal aortic blood pressure caused by a decrease in systemic vascular resistance. At the same time, ventral aortic blood pressure increased owing to the combined effects of a markedly increased cardiac output (by about 80 %) and branchial vasoconstriction. Judged from the effects of the alpha-adrenoceptor antagonist prazosin, control of the branchial vasculature involves an alpha-adrenoceptor-mediated vasoconstriction, in addition to more traditional cholinergic vasoconstrictor and ss-adrenoceptor-mediated dilatory mechanisms. The range of heart rates is large, from 3-4 beats min-1 in individual fish during hypertensive bradycardia to about 28 beats min-1 after atropine treatment. Both chronotropic and inotropic effects are responsible for a marked increase in cardiac output during exercise. The increase in blood pressure caused by adrenaline injection was due largely to an increase in cardiac output, while direct effects on the systemic vasculature were small and transient. The increase in cardiac output, in turn, was due solely to an adrenergic stimulation of stroke volume. A barostatic bradycardia, often seen in other vertebrates in response to adrenaline injection, was absent and it is possible that a decrease in heart rate was offset by direct adrenergic stimulation of the heart. Angiotensin II (Ang II) produced consistent hypertension by systemic vasoconstriction. In contrast to the effects of adrenaline injection, the hypertension caused by Ang II was accompanied by a marked bradycardia. This could be abolished by atropine, suggesting a cholinergic vagal reflex of the type found in other vertebrates. Angiotensin I also caused an elevated blood pressure, and this effect was abolished by the angiotensin converting enzyme inhibitor enalapril, demonstrating elements of an angiotensin-related cardiovascular control system.

An in situ perfused crocodile (Crocodylus porosus) heart preparation was developed to investigate the effects of input and output pressure on cardiac dynamics and to determine the conditions that lead to a right-to-left cardiac shunt. The pericardium was kept intact, both the left and right atria were perfused and all three outflow tracts (right aortic, left aortic and pulmonary) were cannulated, enabling pressures and flows to be monitored. The perfused heart preparation had an intrinsic heart rate of 34 beats min-1 and generated a physiological power output. Both the left and right sides of the heart were sensitive to filling pressure. Increasing the filling pressure to both atria resulted in an increase in stroke volume and cardiac output (Frank­Starling effect). Increasing the filling pressure to the right atrium also had a positive chronotropic effect. Large right ventricular stroke volumes initiated a right-to-left shunt, despite the left aorta having a pressure 1.5 kPa higher than the pulmonary output pressure. The left ventricle was able to maintain its output and stroke volume up to an output pressure of approximately 8 kPa. However, the right ventricle was significantly weaker. Right ventricular output and stroke volume showed a marked decrease when the output pressure was increased above 5 kPa. A right-to-left shunt occurred when pulmonary output pressure was increased. Surprisingly, a shunt occurred into the left aorta before the pressure in the pulmonary artery became greater than that in the left aorta. Once the pressure in the pulmonary artery exceeded the left aortic pressure, pulmonary artery flow ceased and right ventricular output was solely via the left aorta. A right-to-left shunt could also be initiated by increasing the filling pressure to the left atrium.

Simultaneous measurements of pulmonary blood flow (qPA), coeliacomesenteric blood flow (qCoA), dorsal aortic blood pressure (PDA), heart rate (fH) and branchial ventilation frequency (fv) were made in the Australian lungfish, Neoceratodus forsteri, during air breathing and aquatic hypoxia. The cholinergic and adrenergic influences on the cardiovascular system were investigated during normoxia using pharmacological agents, and the presence of catecholamines and serotonin in different tissues was investigated using histochemistry. Air breathing rarely occurred during normoxia but when it did, it was always associated with increased pulmonary blood flow. The pulmonary vasculature is influenced by both a cholinergic and adrenergic tonus whereas the coeliacomesenteric vasculature is influenced by a beta-adrenergic vasodilator mechanism. No adrenergic nerve fibers could be demonstrated in Neoceratodus but catecholamine-containing endothelial cells were found in the atrium of the heart. In addition, serotonin-immunoreactive cells were demonstrated in the pulmonary epithelium. The most prominent response to aquatic hypoxia was an increase in gill breathing frequency followed by an increased number of air breaths together with increased pulmonary blood flow. It is clear from the present investigation that Neoceratodus is able to match cardiovascular performance to meet the changes in respiration during hypoxia.

The effects of adrenergic agonists on dorsal aortic blood pressure, cardiac output, and coronary blood flow were studied in unrestrained coho salmon, Oncorhynchus kisutch. Resting coronary blood flow was 0.43 ml.min-1.kg body mass-1, which represented 1.1% of cardiac output or approximately 0.5 ml.min-1.g-1 compact ventricular mass calculated on 40% of total ventricle mass. Coronary blood flow was phasic and continuous throughout the cardiac cycle; flow seems to be affected by the ventricular contraction, with a peak flow occurring during diastole and a nadir in early systole. Epinephrine injections into the dorsal aorta resulted in a rapid increase in coronary blood flow in association with a rapid increase in dorsal aortic blood pressure. Subsequently there was also a slower increase in coronary vascular resistance, which could be blocked by phentolamine, indicating an alpha-adrenergic vasoconstriction. Isoprenaline injection produced an increase in coronary blood flow and a large reduction in coronary vascular resistance. The coronary vasodilatation was blocked by propranolol, indicating that it may be partly due to a beta-adrenergic vasodilatation. Preliminary results showed a marked increase in coronary blood flow associated with exposure to environmental hypoxia.

The aim of this study was to investigate cardiac performance and cardiovascular control in two red-blooded nototheniid species of antarctic fishes, Pagothenia bernacchii (a benthic fish) and P. borchgrevinki (a cryopelagic fish), and to make comparisons with existing information on haemoglobin-free antarctic teleosts. In quiescent P. bernacchii at 0 degrees C ventral aortic pressure (PVA) was 3.09 kPa and cardiac output (Q) was 17.6 ml min-1 kg-1, with a heart rate (fH) of 10.5 beats min-1 and stroke volume of 1.56 ml kg-1. Following atropine treatment, Q was maintained but heart rate increased and stroke volume decreased. Resting heart rate resulted from an inhibitory cholinergic tone of 80.4% and an excitatory adrenergic tone of 27.5%. The intrinsic heart rate was 21.7 beats min-1 at 0 degrees C. In quiescent P. borchgrevinki at 0 degrees C, PVA was 3.6 kPa, Q was 29.6 ml min-1 kg-1 and stroke volume was 2.16 ml kg-1. The resting heart rate in P. borchgrevinki of 11.3 beats min-1 resulted from an inhibitory cholinergic tone of 54.5% and an excitatory adrenergic tone of 3.2%. The intrinsic heart rate was 23.3 beats min-1. P. bernacchii maintained Q during a progressive decrease in water oxygen tension from 20 to 6.7 kPa, but fH was increased significantly. Thus, although there is cholinergic control of the heart, no hypoxic bradycardia was observed. Recovery from hypoxia was associated with increases in Q and fH; stroke volume returned to control values. PVA declined in recovery as total vascular resistance decreased. Hypoxic exposure following atropine treatment resulted in progressive increases in PVA, Q and stroke volume; fH decreased during the recovery period. Hypoxic exposure in P. borchgrevinki produced similar cardiovascular responses to those observed in P. bernacchii. During an acute increase in water temperature from 0 to 5 degrees C, P. bernacchii regulated Q and total vascular resistance. Stroke volume decreased as fH increased. The intrinsic heart rate had a Q10 of 1.96 over this temperature range. P. bernacchii maintained chronotropic inhibition up to a temperature of 2.5-3.0 degrees C. However, by 5 degrees C this chronotropic inhibition of the heart rate was lost. Infusion of adrenaline into the ventral aorta of P. bernacchii resulted in significant increases in Q, fH, PVA and total vascular resistance. Infusion of adrenaline after atropine treatment caused similar cardiovascular changes without the change in fH. P. borchgrevinki could sustain swimming in a water tunnel at approximately 1 body length per second for 6-10 min.(ABSTRACT TRUNCATED AT 400 WORDS)

Simultaneous measurements of cardiac output (Q), blood pressures and blood gases were made in the hagfish, Eptatretus cirrhatus, during exposure to hypoxia. The partial pressure of oxygen in the medium (PIO2) was reduced from 20.7 kPa to 8.0 kPa and then lowered to 5.3 kPa. At a PIO2 of 5.3 kPa there was a 40% increase in Q. Part of the increase may have been due to the increased activity of the animal at low PIO2. In recovery, when the animals were inactive, Q continued to rise to 160% of the control values. At 5.3 kPa, oxygen consumption (as determined by the Fick principle) fell to 29% of the normoxic value and was associated with increased branchial vascular resistance (Rg) and an increased diffusion limitation of the gills (Ldiff). Adrenaline increased heart rate and aortic blood pressures. Increased Rg and Ldiff could be provoked in normoxia by the injection of the beta-adrenergic blocking drug propranolol. We suggest that catecholamines may be involved in the tonic control of gill vasomotor tone.

Simultaneous recordings of blood flow in the right and left aorta and carotid and coeliac artery were made in the crocodile, Crocodylus porosus at rest and during various stimuli. In resting animals the right aorta and carotid artery flow profiles resembled the recordings obtained in the caiman (Axelsson et al. 1989a), with an anterograde blood flow throughout the cardiac cycle. As in the caiman, the left aorta flow profile was complex with both anterograde and retrograde blood flow during the cardiac cycle, and a net left aorta blood flow near zero at rest. The coeliac artery blood flow profile did not show the complex pattern seen in the upper aorta, immediately suggesting that most of the coeliac artery blood originates elsewhere. We believe that coeliac artery blood flow in the resting animal derives from the right aorta via the abdominal anastomosis between the two aortas. Feeding induced an increase in the coeliac artery and left aorta blood flow, probably due to a decrease in visceral vascular resistance, and hence coeliac arterial and the left aorta blood pressure, which facilitates blood flow (from right to left aorta) through the foramen of Panizza. During short 'fright dives', heart rate fell and there was a decrease in the recorded blood flows: carotid artery blood flow did not decrease to the same extent as the RAo and coeliac artery flow, indicating some capacity for redistribution of blood to the cephalic circuits during diving. Similarly, a near-unimpaired carotid artery blood flow was maintained after adrenaline injection. Substance P increased the coeliac artery blood flow and produced a right-to-left cardiac shunt, probably by construction of the pulmonary vasculature.

Cardiac output, ventral and dorsal aortic blood pressure, heart rate, and coeliac and mesenteric artery blood flow were recorded simultaneously in the Atlantic cod, Gadus morhua L., at rest, during exercise, during hypoxia and after feeding. In the resting unfed animals, coeliac artery blood flow was 4.1 +/- 0.8 ml min-1 kg-1 and mesenteric artery blood flow was 3.5 +/- 1.1 ml min-1 kg-1 (mean +/- S.E.M., N = 10); together, these flows represent approximately 40% of the cardiac output. Exercise or exposure to hypoxia resulted in increased visceral vascular resistance, leading to reductions in the coeliac and mesenteric artery blood flows. Coeliac and mesenteric blood flows were increased 24 h after feeding and the coeliac and systemic vascular resistances decreased in comparison with the prefeeding values. Phentolamine did not affect the gastrointestinal artery blood flow, but produced a significant decrease in the mesenteric and systemic vascular resistance. Treatment with bretylium and phentolamine revealed differences between the coeliac and the mesenteric vasculature regarding the control mechanisms during hypoxia and during exercise and feeding. During hypoxia, an adrenergic control of the gastrointestinal vasculature with both nervous and humoral components was found, whereas during exercise and after feeding an additional non-adrenergic mechanism controlling gut blood flow was demonstrated.

The thermal expansion of a phosphate-bonded investment material was tested when three heating rates were used during the heating procedure. One of them was too low, one too high, and the third, in the middle. The examination was done through the fit of 12 MOD inlays and 12 full crowns in steel master dies. From the results it can be concluded that rates that are too fast must be avoided in the heating procedure, because they reduce the thermal expansion of the phosphate-bonded investment material and thus produce castings with limited fit.

Atlantic cod were subjected to 12-15 min swimming exercise at 2/3 body lengths s-1 in a Blazka-type swim tunnel. Pre- and postbranchial blood pressures, cardiac output (ventral aortic blood flow) and heart rate were continuously recorded, and blood samples for measurement of arterial and mixed venous oxygen tension were taken before and at the end of the exercise period. In a second group of fish, subjected to similar exercise regimes, blood samples were taken for analysis of the plasma concentrations of catecholamines. Pre- and postbranchial blood pressures and cardiac output increase during exercise, while the mixed venous oxygen tension decreases. The effect on cardiac output is due to an increase of both heart rate and stroke volume. There are no significant changes in either systemic or branchial vascular resistances, or in the plasma concentrations of catecholamines. Injection of the adrenergic neurone-blocking drug bretylium produces a decrease in postbranchial blood pressure in resting cod, due to a decrease in the systemic vascular resistance. Exercising cod treated with bretylium have a significantly lower pre- and postbranchial blood pressure than exercising control cod. This is due mainly to a dramatic reduction in the systemic vascular resistance. The alpha-adrenoceptor antagonist phentolamine does not further affect the blood pressure in cod treated with bretylium. It is concluded that the exercise hypertension observed in cod depends on the effect of adrenergic vasomotor fibres maintaining the systemic vascular resistance, and also on the increase in cardiac output. An adrenergic innervation of the heart may play some role in the control of cardiac performance both at rest and during exercise, but the main cardioregulatory mechanism is likely to be non-adrenergic, most probably including cardiac control via variation of the cholinergic vagal cardioinhibitory tonus.

Prebranchial blood pressure (Pva), heart rate (fH) and plasma catecholamine concentration were measured in the mudpuppy Necturus maculosus at rest and during exercise. During exercise, both fH and Pva increased, as did the plasma noradrenaline concentration. There was no significant effect on Pva after injection of the adrenergic neuron blocker, bretylium, in resting animals, neither did bretylium affect the exercise-induced increase in Pva. This suggests that there is no adrenergic nervous tone on the vasculature at rest or during exercise. The alpha-adrenoceptor antagonist yohimbine had no effect on the resting Pva in the bretylium-treated animals, but it abolished the increase in Pva during exercise. This is compatible with the view of no influence on Pva by the plasma catecholamines at rest, while during exercise the increase in plasma noradrenaline concentration is responsible for the increase in Pva. Injection of atropine elevated resting fH, and reduced or abolished cardiac arrythmia, indicating an inhibitory cholinergic tone on the heart at rest, and that variations in this tone are responsible for the intrinsic variation seen in untreated animals. After the atropine treatment, there was still an increase in fH during exercise. The beta-adrenoceptor antagonist sotalol decreased fH in resting atropinized animals, and inhibited the exercise-induced tachycardia, implying that there is an additional beta-adrenoceptor-mediated adrenergic tone, affecting the heart both at rest and during exercise. The cholinergic tone decreased during exercise with a concomitant increase in adrenergic tone. Falck-Hillarp fluorescent histochemistry was used to study the presence of adrenergic nerve fibres and other catecholamine-storing cells.(ABSTRACT TRUNCATED AT 250 WORDS)

The cardiac innervation of the mudpuppy, Necturus maculosus, was investigated using in vivo recording of blood pressure and heart rate, a perfused heart preparation, isolated paced ventricular and atrial strip preparations, Falck-Hillarp fluorescence histochemistry and measurements of plasma concentrations of catecholamines. The heart of Necturus receives a 'classical' vagal inhibitory innervation by cholinergic fibres which act via muscarinic cholinoceptors. In addition, there appears to be an atropine-resistant inhibitory component in the vagal innervation of the heart. This component is best seen at higher frequencies of vagal stimulation (10-20 Hz), but the mechanism behind this response is not known. There is no direct adrenergic innervation of the ventricle or atria, but by use of Falck-Hillarp fluorescence histochemistry, adrenergic fibres have been demonstrated at the atrio-ventricular border, particularly within the intracardiac ganglion. The histochemical evidence is consistent with a modulation of the ganglionic transmission in the vagal pathways by adrenergic neurons and small intensely fluorescent (SIF) cells, but physiological evidence is wanting. An adrenergic control of the heart via circulating adrenaline may occur during 'stress', when the plasma level of adrenaline is high enough to affect cardiac performance.

Coeliac artery blood flow (Fca) before and after feeding was recorded in the sea raven. To obtain basic information about the scope of cardiovascular adjustment in the sea raven, a separate series of experiments was performed, in which ventral (Pva), and dorsal (Pda) aortic blood pressure, heart rate (HR) and cardiac output (jaz) were monitored during rest and encouraged exercise.Measurements of coeliac artery flow showed that visceral blood flow is substantial, particularly after feeding, and variations in the visceral vascular conductance affect Pda directly. Simultaneous recordings of intestinal and dorsal aortic blood pressures showed no measurable difference in the two arterial pressures, refuting the idea of a vascular control at the level of the main coeliac artery. Thus, in the sea raven, the adrenergic tonus affecting the visceral vasculature presumably acts at the arteriolar level.Sea ravens encouraged to exercise increased theirjaz by 64%; 32% through HR and 25% through stroke volume. The increase injaz during encouraged exercise was sufficient to produce an elevation of both Pva and Pda, despite an increase of systemic vascular conductance, β-adrenoceptor blockade with sotalol, however, severely impaired the increase injaz during exercise, and the change in Pda was reversed.During rest there were both an adrenergic and a cholinergic tonus affecting the HR, as revealed by the effects of injected pharmacological antagonists. Swimming activity decreased the cholinergic tonus, while the adrenergic tonus increased.

A series of 1,022 patients taking part in clinical trials to compare postoperative radiation therapy with postoperative CMF chemotherapy, and postoperative tamoxifen with no adjuvant therapy, had their tumors analyzed for estrogen receptor content. Isoelectric focusing of the receptor in polyacrylamide gel was used for receptor assay and the results were related to tumor DNA content. The estrogen receptor content was significantly correlated to prolonged survival both for premenopausal and postmenopausal women. It was confirmed that postmenopausal women have increased median receptor values, and for this group values of more than approximately 0.3 fmol per microgram DNA were correlated to prolonged survival. For premenopausal women, a lower level of more than 0.1 fmol per microgram of DNA defined patients with prolonged survival. Lymph node involvement and receptor level were independent prognostic indicators. Patients randomized to tamoxifen or CMF tended to live longer as compared with control patients but this was not statistically significant. Moreover, there was no tendency for adjuvant tamoxifen to further increase the survival of patients with receptor-containing tumors as compared with control patients with similar receptor values.

The tonical cholinergic and adrenergic influence on the heart rate was investigated in vivo in seven species of marine teleosts (pollack, Pollachius pollachius; cuckoo wrasse, Labrus mixtus; ballan wrasse, Labrus berggylta; five-bearded rockling, Ciliata mustela; tadpole fish, Raniceps raninus; eel-pout, Zoarces viviparus and short-spined sea scorpion, Myoxocephalus scor pius) during rest and, in two of the species (P. pollachius and L. mixtus), also during moderate swimming exercise in a Blazka-type swim tunnel. Ventral aortic blood pressure and heart rate were recorded via a catheter implanted in an afferent branchial artery, and the influence of the cholinergic and adrenergic tonus on the heart rate was assessed by injection of atropine and sotalol respectively. During rest the adrenergic tonus was higher than the cholinergic tonus in all species except L. berggylta, where the reverse was true. In P. pollachius and L. mixtus, exercise appeared to produce a lowering of the cholinergic tonus on the heart and, possibly, a slight increase of the adrenergic tonus. The nature of the adrenergic tonus (humoral or neural) is not clear, but the low plasma concentrations of catecholamines both during rest and exercise could be interpreted in favour of a mainly neural adrenergic tonus on the teleost heart. These experiments are compatible with the view that both a cholinergic inhibitory tonus and an adrenergic excitatory tonus are general features in the control of the teleost heart in vivo, both at rest and during moderate swimming exercise.

The presence of bombesin-like material in nerves and endocrine cells of the gastrointestinal canal, the circulatory system and the lung of the caiman, Caiman crocodylus crocodylus, has been investigated with immunohistochemistry (IHC) and radioimmunoassay (RIA). The effect of bombesin has been studied on the vascularly perfused lung and on isolated strip preparations of the gut wall of the caiman, and on the circulatory system in vivo in both the caiman and the crocodile, Crocodylus porosus. Bombesin-like immunoreactivity is present in water and acid extracts of the muscle layer and the mucosal layer of the gut. IHC demonstrated a dense network of nerve fibres in the sub-mucosa, circular muscle layer and myenteric plexus of the whole gut. A more sparse innervation by single fibres often following septal edges or small vessels is found in the lung. Systemic vessels are innervated by a loose plexus of small fibre bundles. The levels of immunoreactive material in the lung and heart were low. Bombesin is excitatory on strip preparations of the smooth muscle layers of the intestinal wall, and causes an increase in inflow resistance in the perfused lung. In vivo, bombesin increases the blood flow in the left aorta and the coeliac artery.

The nervous regulation of heart rate and stroke volume in the Atlantic cod Gadus morhua was investigated both in vivo, during rest and exercise, and in vitro. The cholinergic and adrenergic influences on the heart were estimated in experiments with injections of atropine and sotalol. At rest the cholinergic and adrenergic tonus on the heart were 38% and 21%, respectively (ratio 1.81:1). At the end of an exercise period, the cholinergic tonus had decreased to 15% but the adrenergic tonus had increased to 28% (ratio 0.54:1). The results suggest that variation of the cholinergic tonus on the heart is a major factor in the regulation of the heart rate. In one group of fish, cardiac output was also measured, allowing calculation of stroke volume. Cardiac output increased significantly during exercise, and this effect persisted in the presence of both atropine and sotalol, although the increase in heart rate was reduced or abolished. The persisting increase in cardiac output during exercise is due to an increase in stroke volume, reflecting a Starling relationship. In the presence of the adrenergic neurone-blocking agent bretylium, a positive inotropic effect on isolated, paced atrial and ventricular strips was observed. In the atrial preparations the effect persisted after 24 h. The effect was prevented by pretreatment with sotalol or cocaine, but potentiated by phentolamine pretreatment. This shows that bretylium exerts its neurone-blocking action after being taken up into the adrenergic nerves, and suggests that the positive inotropic effect of bretylium observed in vivo is due to release of endogenous catecholamines. The concentration-response curves for adrenaline on isolated spontaneously beating atrial preparations showed that the concentrations of catecholamines necessary to produce appreciable effects on the heart are higher than the concentrations found in cod plasma during 'stress' situations (handling and exhaustive swimming).

We report for the first time the flow events corresponding to the pressure patterns in the left and right aorta (LAo and RAo) during the cardiac cycle in the caiman (Caiman crocodylus ssp). These experiments show a complex LAo flow pattern; an initial small anterograde flow in the early systole is reversed to a backflow at midsystole. At the end of systole there is again a small anterograde flow. This second flow pulse corresponds to a pressure peak ("foramen spike") in the LAo pressure trace. The observed pattern is compatible with the view that the foramen Panizzae is obstructed by the medial cusp of the RAo valve during part of the systole. LAo pressure remains normally above right ventricular pressure throughout the cardiac cycle and there is thus no contribution to LAo flow from the right ventricle. The net flow in the LAo normally equals the flow through the foramen Panizzae and is very small compared with the systemic flow in the RAo.