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Prosthetic hip surgery was performed under subarachnoidal anaesthesia with bupivacaine 16–20 mg and morphine 0.2 mg. Preoperatively, metoclopramide 1 mg · kg-1 was given i.v., followed by an infusion of 1.5 mg · kg-1 over 9 h (n= 17). Control patients received corresponding volumes of solvent (n = 23). The design of the study was double blind. The characteristics of the spinal block (level of analgesia to pinprick and muscular block) and postoperative VAS pain scores were similar in both groups. During the 24 h following the start of the infusion, four patients receiving metoclopramide required i.v. opioids, compared to 15 in the control group (P

Intraabdominal surgery tends to lower circulating plasma volume by mechanisms unrelated to bleeding and evaporation. In chloralose-anesthetized rats, the tissue clearance of radiolabelled albumin was determined by a double isotope method. Animals were subjected to a standardized abdominal trauma, eliciting minimal bleeding and evaporation, and others served as controls. The trauma significantly increased tissue albumin extravasation in abdominal skin, abdominal wall, pancreas, small intestine, colon, mesentery and diaphragm. Considering the mass of the respective tissues, a substantial portion of the albumin extravasation took place in the abdominal wall. No increased albumin clearance was found in extra-abdominal tissues. It is suggested that abdominal surgery decreases plasma volume by extravasation in the operation field.

Intravascular volume expansion is followed by loss of fluid from the circulation. The extravasation of albumin in this readjustment is insufficiently known.Twelve male volunteers participated, each in three separate sessions, in a controlled, randomised, open fashion. They received one of the following: albumin 40 g/L,(7.1 mL/kg, i.e. 500 mL per 70 kg); Ringer's acetate (21.4 mL/kg), or dextran 30 g/L (7.1 mL/kg). The fluids were infused during 30 min and the subjects were followed for 180 min. ECG, arterial oxygen saturation and non-invasive arterial pressure were recorded. Haemoglobin, haematocrit, serum albumin and osmolality, plasma colloid osmotic pressure and hyaluronan concentration were determined in venous samples.The serum albumin concentration decreased (P0.05, anova) following Ringer's acetate or dextran, whereas serum osmolality was unchanged in all groups. The colloid osmotic pressure decreased (P0.05) after the Ringer solution. The blood volume increase was estimated from the decrease in haemoglobin concentration and did not differ between the three fluids. The cumulated extravasation of albumin was largest following albumin (10.4 +/- 5.4 g, mean +/- SD), less following dextran (5.6 +/- 5.0 g) and negligible in the Ringer group (0.5 +/- 10.0 g; P0.05 against albumin). However, the Ringer solution increased the plasma concentration of hyaluronan drastically.Infusion of hypotonic colloidal solutions entails net loss of albumin from the vascular space. This is not the case after Ringer's acetate. Increased interstitial hydration from the latter fluid is followed by lymphatic wash out of hyaluronan.

Excess production of nitric oxide (NO) by the inducible NO synthase (iNOS) has been implicated in the pathophysiology of septic shock. Using methaemoglobin (metHb) and the stable NO metabolite nitrate as markers of NO formation, we assessed the effect of iNOS blockade by aminoguanidine (AG) on hypotension and NO formation in endotoxaemic rats.In 32 male Wistar rats under chloralose anaesthesia, MetHb (at 15 and 330 min, respectively) and plasma nitrate (at 330 min) were determined. Mean arterial pressure, heart rate and haematocrit were monitored. The LPS group (n=8) received bacterial endotoxin (LPS), 3 mg kg(-1) i.v. and was subsequently monitored for 5 h. At 2 h after LPS, the LPS+AG20 group (n=8) received AG, 5 mg kg(-1), and 5 mg kg(-1) h(-1) for the remaining 3 h. The LPS+AG100 group (n=8) instead received 25 mg kg(-1), followed by 25 mg kg(-1) h(-1). The NaCl group (n=8) was given corresponding volumes of isotonic saline.AG decreased the LPS-induced rise in plasma nitrate by about 50% in the LPS+AG20 group. MetHb levels, however, were not appreciably reduced by this dose. Both NO metabolites reached control levels after the higher dose of AG. LPS caused a progressive decrease in haematocrit. AG did not influence the LPS-induced hypotension, tachycardia or haemodilution.AG inhibited NO formation in a dose-dependent way. Yet, AG had no haemodynamic effects, suggesting a minor cardiovascular influence of iNOS in this endotoxin model, in parallel to what has been found in microbial sepsis.

It is generally maintained that protein and fluid are lost from the circulation under septic conditions. The role played by an increased production of nitric oxide, by the inducible nitric oxide synthase (iNOS), in this process is unclear.Chloralose anaesthetised male Wistar rats received E. coli lipopolysaccharide (LPS), 3 mg kg(-1) i.v., and were studied for 5 h. Mean arterial pressure (MAP) and heart rate (HR) were monitored and haematocrit (Hct) was determined intermittently. Tissue plasma volume and tissue clearances of radiolabelled albumin over the last 2 h of the experiment were determined by a double-isotope method. In 8 rats, 2 h after LPS, aminoguanidine, an iNOS selective blocker, was given i.v. at a dose of 5 mg kg(-1). This was followed by a continuous infusion for the duration of the experiment; altogether 20 mg kg(-1) was administered. In the control group (n=8), a corresponding volume of saline was infused.Aminoguanidine did not significantly influence Hct, MAP and HR, as evidenced by inter-group comparisons (Mann-Whitney test). Tissue plasma clearances of albumin and tissue plasma volume were similar in both groups.Aminoguanidine at 20 mg kg(-1) did not reverse the haemodynamic changes induced by LPS. Neither did the drug affect the tissue plasma clearance of albumin or the tissue plasma volume.

The effects of mild hypothermia on blood loss are little known.Patients, undergoing primary prosthetic hip surgery under spinal anaesthesia, were randomised to the operative procedure, with (n=25) or without (n=25) forced air warming. Core temperature was repeatedly measured from the tympanic membrane. The blood loss was calculated by three different methods; the intraoperative loss was estimated visually. The loss during and after the operation was obtained by determination of lost haemoglobin (the Hb-method). The blood loss during hospital stay was also calculated from the haemoglobin balance.Among controls, core temperature decreased by 1.3+/-0.6 degrees C (mean+/-SD) and in the warmed patients 0.5+/-0.4 degrees C (P0.0001). Preoperative variables and the number of allogeneic units transfused did not differ between the groups. In controls, the blood loss during operation was, with the visual method, 698+/-314 ml, compared with 665+/-292 ml in warmed patients. With the Hb-method, the loss was 662+/-319 and 657+/-348 ml, respectively. With this method, the external loss during the entire hospital stay was, in controls, 1066+/-441 ml and in the warmed group, 1047+/-413 ml. The balance method yielded 1674+/-646 ml and 1507+/-652 ml, respectively. Indices of blood loss did not differ significantly between groups and there was no covariation between those variables and the decrease in core temperature.Forced air warming did not decrease the blood loss. Methods for determination of blood loss yielded widely differing results.

Thirteen patients undergoing elective orthopedic surgery were studied regarding anaphylatoxin (C3a and C5a) and terminal complement complex (TCC) formation in association with red cell salvage. The auto-transfusion equipment gave a centrifuged and washed erythrocyte fraction. The concentrations of C5a and TCC were not increased but elevated C3a levels were found in the suspension. After infusion of the erythrocyte fraction to the patient, no signs of systemic complement activation were observed. Thus, plasma levels of C3a, C5a and TCC were within the normal range in all the patients before and after autotransfusion. This study indicates that the complement system is activated in the cellsaver equipment. The washing procedure, however, seems to eliminate most of the anaphylatoxins and terminal complement complexes. No extensive systemic activation of complement seems to occur in association with autotransfusion to patients undergoing elective surgery.

Background: The efficacy of intraoperative salvage and washing of wound blood and the predictors of allogeneic red cell transfusions in prosthetic hip surgery are insufficiently known. Methods: In 96 patients, undergoing primary or revision surgery, salvaged and washed red cells and, if necessary, allogeneic blood were used to keep haematocrit not lower than 33%. The bleeding of red cells during hospital stay was calculated from the red cell balance. The preoperative red cell reserve (millilitres of red cells in excess of a haematocrit of 33%) was estimated and the difference between this volume and the total bleeding of red cells was retrospectively used to classify patients with regard to the need for red cells. Stepwise regression analysis was used to define patient-related variables associated with allogeneic blood transfusion. Results: Preoperative knowledge of the type of operation (primary, revision), the preoperative red cell reserve, and the body mass could predict roughly half of the need for banked blood (r2=0.45). Only one-third of the total bleeding of red cells was retransfused. For complete avoidance of allogeneic blood, autotransfusion was most effective in patients with a moderate need (0–4 u). However, 32% of such patients required allogeneic blood. Conclusions: Autotransfusion has a limited efficacy to decrease the need for allogeneic blood, and other blood-saving methods should be added for this purpose. It is difficult to predict the need for allogeneic blood preoperatively.

Local anesthetics block propagation in nerve fibers but may also inhibit inflammation. Inflammatory phenomena such as warmth, reddening, and swelling are intimately connected with blood flow. Our primary aim was to investigate the effect of mepivacaine on cutaneous blood flow in a situation involving hyperemia, but no inflammation, namely, after arterial occlusion.The subjects were healthy volunteers (9 men, 7 women). Pain was evaluated by visual analog scale every 5 minutes. A laser Doppler probe was applied on each forearm. After baseline flow measurements during 30 minutes, a bilateral regional intravenous block (Bier block) was performed by injecting mepivacaine (1.4 mg/kg in 40 mL) in one arm and normal saline in the other in a randomized, controlled, double-blind manner. Arterial occlusion was maintained for 20 minutes, and flow was followed for 60 minutes after release of the block.The ischemic pain, though modest, was less (P = .045) in the treated arm. Following release of the cuff, the blood flow had essentially stabilized after 20 minutes. The reactive hyperemia (1-20 minutes) was attenuated in the mepivacaine-treated arm (mean, 68% of placebo, P = .025). In the 21-60-minute period, flow in this arm stabilized at a lower level (mean, 73% of placebo, P = .0013).Mepivacaine is a vasoconstrictor of long duration. This has to be taken into account when antiinflammatory effects of mepivacaine are assessed.

Objective To evaluate whether the use of dextran or the combination of low molecular weight heparin and dextran increases the blood loss in elective transurethral resection for benign prostatic hyperplasia. Patients and methods This open randomized controlled study included 198 patients operated under spinal anaesthesia who were allocated to four groups differing in the combination of prophylactic treatment used for thrombosis and for the substitution of blood loss. The prophylactic treatment was either dalteparin sodium, continued each day until mobilization, or 3% Ringer dextran-60 just before operation and continued with 6% dextran-70 for 2 days post-operatively, and the volume substitute was Ringer dextran or Ringer's acetate. Thus, the four treatments (by prophylaxis and volume substitute, respectively) were dalteparin and Ringer's acetate, dalteparin and dextran, dextran and Ringer's acetate, and dextran and dextran. The haemoglobin lost to the irrigation fluid was measured and used to calculate blood loss. Results Patients receiving dextran had a larger post-operative and total blood loss than those who did not. The need for transfusion did not differ between the treatment groups. Conclusion The combination of dalteparin and dextran was not associated with an increased blood loss above that with dextran alone.

A study was conducted in patients undergoing surgery for idiopathic scoliosis, to determine whether combining blood-saving methods would decrease the need for homologous blood. Five groups were compared in a prospective, randomized fashion. In control patients (n=13), blood loss was replaced by colloids. Preoperative haemodilution (PHD group) was used in ten patients. In the intraoperative autotransfusion (IAT) group (n=11), washed red cells were returned to the patient. In the PHD+IAT group, both methods were combined (n=13). In the fifth group, in addition, arterial hypotension was maintained with sodium nitroprusside (the PHD+IAT+HA group, n=10). The haemoglobin value was kept above 79 g/l. Total blood loss did not differ between groups. The use of homologous blood in the PHD+IAT and PHD+IAT+HA groups was significantly less than in controls. It is concluded that blood-saving measures can be combined with an augmentative effect.

Intra-abdominal surgery causes plasma extravasation which, in the rat, is prevented by combined histaminergic H1 and H2 blockade. We evaluated the relative importance of H1 and H2 blockade in this situation. Cloralose-anaesthetized Wistar rats were subjected to a standardized abdominal trauma. Mean arterial pressure (MAP), heart rate (HR) and haematocrit (Hct) were monitored and plasma volume (PV) was determined before and 1 h after the trauma. Compared to non-traumatized rats (n = 8), the trauma decreased PV and increased Hct (n = 8). MAP decreased during the actual trauma, whereas HR remained stable throughout. In animals given cimetidine 25 mg kg-1 i.v. just prior to the trauma (n = 8), PV, Hct and MAP changed, as in the non-blocked rats. In contrast, pyrilamine, 10 mg kg-1, completely prevented the decrease in PV and the increase in Hct (n = 7), but not the decrease in MAP. The findings suggest that a histaminergic H1 mechanism is of importance for the plasma loss elicited by intra-abdominal trauma.

The authors studied whether metoclopramide decreases the incidence of emesis after spinal anesthesia supplemented with subarachnoid morphine.Patients underwent total hip arthroplasty under spinal anesthesia using tetracaine with norepinephrine and morphine 0.2 mg. Forty-eight patients were included in the study conducted with a paired design, using sequential analysis. Patients were allocated randomly and double-blinded to the treatment with metoclopramide or to the control group. In one group, metoclopramide 20 mg intramuscularly was given before and after surgery; patients in the control group were given equal volumes of saline. The presence of emesis for 5 hours postoperatively was recorded.In the postoperative period, emesis was noted in 58% of control patients but in only 17% of patients given metoclopramide (P.05).The data suggest that metoclopramide is effective against postoperative emesis after spinal anesthesia supplemented with subarachnoid morphine.

Intra-abdominal surgery causes a loss of plasma into tissues within and around the abdomen, predisposing to a decreased tissue viability and postoperative complications. In a rat model of intra-abdominal trauma, we investigated whether neuropeptides released from thin afferent nerve endings may contribute to this extravasation. Newborn male Wistar rats were pretreated with capsaicin 50 mg/kg s.c., leading to a lifelong degeneration of thin afferents. The same animals, when adult, were subjected to experiments under chloralose anesthesia in which tissue clearances of radiolabelled albumin were determined by a double isotope technique. Non-pretreated animals served as controls. In non-traumatized animals, pretreated rats had a higher loss of labelled albumin in calf muscle. In animals subjected to the standardized intra-abdominal trauma, the pretreatment did not decrease the trauma-induced loss of albumin. In neck skin, the loss of protein was higher in pretreated animals, possibly due to a decreased trauma-induced sympathetic activation. In conclusion, degeneration of thin afferent fibers may alter the autonomic reflex response to intra-abdominal trauma, but neuropeptide release from afferents apparently plays no role in the relocation of albumin.

Endotoxin (LPS) is a powerful activator of the inducible nitric oxide (NO) synthase. Whereas NO seems to be one factor behind the decreased responsiveness of the circulation to adrenergic stimulation in septic shock, the role of NO in increased vascular permeability is less clear. In a former study [1] we have shown that although NO production increased after LPS there was no increased extravasation of albumin in a wide variety of rat tissues examined; on the contrary clearance was decreased in the entire gastrointestinal tract. In this study tissue extravasation was examined after administration of the nitric oxide synthase inhibitor L-NAME.

Metoclopramide may enhance opioid analgesia, but it is not known if the drug is analgesic itself. This question was examined in a double-blind, randomized study of 38 patients undergoing knee arthroscopy with opioid-free anaesthesia comprising propofol, isoflurane and nitrous oxide in oxygen. At the end of surgery, patients received either metoclopramide 0.5 mg kg-1 or placebo i.v. After operation, they received patient-controlled analgesia with pethidine for 3 h, during which period, pain score was assessed on a visual analogue scale (VAS). There were no significant differences between the groups in the patterns of pethidine consumption. However, the VAS-pain scores tended to be smaller in the metoclopramide group; this difference was significant 30 min after operation. These results do not demonstrate conclusively a clinically relevant analgesic action of metoclopramide.

Postoperative paralytic ileus is in part mediated by the sympathetic gastrointestino-gastrointestinal (GI-GI) reflex. The modulation of this reflex by epidural fentanyl (50 micrograms) was studied in chloralose-anesthetized, ventilated cats. The vagi were cut in the neck but could be efferently stimulated. Gastric volume, arterial pressure and heart rate were followed and the GI-GI reflex was elicited by intestinal distension, mesenteric afferent nerve stimulation or heating or capsaicin administered intra-arterially to an intestinal loop. Epidural fentanyl enhanced the gastric contraction response to efferent vagal stimulation and considerably counter-acted the GI-GI reflex inhibition of vagally induced tone. These effects were reversed by epidural naloxone (10 micrograms). In contrast, 50 micrograms of fentanyl i.v. only enhanced the effect of vagal stimulation but had no influence on the inhibitory GI-GI reflex responses. Apparently, epidural fentanyl may inhibit the GI-GI reflex by a spinal point of action.

In preoperative haemodilution, blood is withdrawn before surgery while normovolaemia is maintained by infusion of cell free fluid. A surgical bleeding then entails a smaller loss of red cells. Reinfusion of the saved blood maintains normovolaemia, raises hematocrit and decreases the need for donor blood. Dilutional anaemia may endanger the oxygenation of the tissues. Tissue oxygenation can be upheld by an augmented and redistributed cardiac output and by a raised oxygen extraction. These compensatory mechanisms are less efficient in the presence of vascular stenosis, in particular in the myocardium which relies virtually exclusively on coronary vasodilatation. Major contraindications to preoperative haemodilution are, apart from coronary insufficiency, ventricular failure and valvular disease. Deleterious increases in cardiac oxygen consumption and/or heart rate may result from e.g. hypovolaemia, arterial desaturation and painful stimuli. The haemodilution procedure requires knowledge and vigilance in all involved personnel and gives best results if combined with other blood saving measures, like blood predeposit and intraoperative red blood cell salvage.

Experiments were performed to analyse to what extent diving mammals, represented by the coypu (nutria), exhibit similar characteristics with regard to cardiovascular nervous control as earlier found in diving birds such as the duck. As in this latter species, submersion of the un-anesthetized coypu led to a profound and prompt bradycardia and reduction of cardiac output at a largely unchanged arterial pressure. - Graded stimulations of the vasoconstrictor fibres to skeletal muscle, kidney and intestine in anesthetized animals produced far stronger responses at given stimulation rates than in non-diving mammals (cats), and virtual flow obstruction could be achieved by rates as low as 6 imp/sec. The coypu thus possesses a vascular neuro effect or system, so organized as to shut off almost completely the blood supply to the mentioned tissues during a dive and hence distribute available oxygen reserves by means of a greatly reduced cardiac output preferentially to the brain and myocardium. Further, the vagal nerves exert on the heart ventricles a negative inotropic effect besides the profound negative chronotropic effect, helping to keep cardiac output very low during submersion. - The cardiovascular nervous control in the coypu is therefore in important respects more related to that in diving birds than to that in non-diving mammals, which probably is a prerequisite for the endurance of prolonged submersion.

Experiments were performed on chloralosed, adrenalectomized cats with recording of gastric volume, blood pressure and skeletal muscle blood flow. The vagal nerves were cut, but the vagal excitatory fibres to the stomach could be activated by electric stimulation. Topical stimulation of the hypothalamic defence area, or surrounding “pressor” areas, produced not only the characteristic known circulatory responses, but also a prompt and often complete inhibition of a vagally induced increase of gastric motility.-But when the stomach was not under the influence of continuous vagal excitatory activity, corresponding stimulation of the hypothalamus rarely had any effect on gastric volume, and then only an insignificant and sluggish increase despite considerable “myogenic” tone of the stomach. Stimulation of the adjacent hypothalamic sympatho-inhibitory area, on the other hand, augmented the vagally induced gastric motility and thereby suggested the presence of a centrally induced suppression of a prevailing sympathetic inhibitory influence on the stomach.-All the above mentioned effects on gastric volume, produced by central nervous stimulation, could be blocked by guanethidine in these vagotomized cats. It is concluded that the hypothalamus contains neural mechanisms, which can affect stomach motility by changing in both directions the impulse frequency in the inhibitory adrenergic outflow to this organ. Simultaneous activity of vagal excitatory fibres to the stomach was found to be a prerequisite for reducing significantly gastric motility and tone when the adrenergic fibres were excited. This is compatible with the hypothesis that the adrenergic fibres exert their inhibitory effect mainly, or only, by acting on the parasympathetic ganglionic cells, which mediate the vagal excitatory influence to the gastric smooth muscles.

Djojosugito, A., B. Folkow, B. Lisander and H. Sparks. Mechanism of escapc of skeletal muscle resistance vessels from the influence of sympathetic cholinergic. vasdilator fibre, activity. Acta physiol. scand. 1968. 72. 148–156. Experiments on the calf muscle circulation of cats and dogs indicate that the return of muscle blood flow to control level during sympathetic vasodilator fibre stimulation (the “escape” phenomenon) occurs only when antoregulation of flow in response to pressure changes is Well developed, i.e. when vascular smooth muscle “reactivity” is pronounced. When this is not the case, sustained vasodilatation is induced by prolonged activation of these fibres. The “escape” is therefore dependent on a counter regulation of the vascular effectors themselves. Precapillary sphincter activity is increased by, but does not significantly affect, the neurogenically reduced flow resistance. Further, sphincter activity returns to control when the “escape” develops, showing that this phenomenon is a property of smooth muscle located upstream of the sphincters, in the precapillary resistance vessels proper. The combined evidence suggests a very restricted site of action of the sympathetic cholinergic vasodilator fibres, directly suppressing only “pacemaker” smooth muscle cells and/or key sites of the upstream myogenic propagation of excitation from such pacemakers. Since pacemaker activity seems to be best developed in the smallest precapillary resistance vessels. neurogenic inhibitory action at this site would lead to dilatation of proximally situated resistance sections, which for their basal tone are dependent on propagated excitation. “Escape” would then occur if latent pacemarkers in this resistance section gradually became dominant and reestablished myogenic tone. Thig is a mechanism very similar to the “vagus escape” phenomenon of the heart.

As the interrelationship of autonomic patterns involving cortico-hypothalamic and bulbar levels is of general interest, the interaction between the hypothalamic defence reaction and the homeostatic baroreceptor reflexes was explored in cats with respect to cardiac as well as vascular effects. The results suggest, in conformity with Hilton's observations (1963), that defence area stimulation suppresses the baroreceptor reflex inhibition of the heart. On the other hand, the baroreceptor influence on vasoconstrictor fibre discharge was largely the same, whether defence area stimulations were performed or not. This had important haemodynamic consequences, especially for muscle blood flow, since the reflex inhibition of regional constrictor fibre tone could greatly enhance the cholinergic vasodilatation. Therefore such a differentiated interaction between oppositely directed central and reflex autonomic mechanisms has the consequence that the baroreceptor reflexes, rather than damping the defence reaction, act in synergism with it with respect to net haemodynamic effects; some further implications of this are dealt with in the subsequent paper (Kylstra and Lisander 1969).

Folkow, B., B. Lisander, K. S. Tuttle and S. C:. Wang. Changes in cardiac output upon stimulation of the hypothalamic defenca araa and the medullary depressor area in the. cat. Acta physiol. scand. 1968. 72. 220–233. The hypothalamic defence area and the bulbar depressor area, with related hypothalamic sympatho-inhibitory structures, were topically stimulated while changes in cardiac output (C. O.). heart rate, stroke volume, central venous pressure and peripheral blood flow were studied in anesthetized-curarized cats and dogs. Defence area stimulation induced up to two-fold increases in C. O. and up to threefold increases in calculated work load for the left ventricle. The major part of the C. O. increase was directed to the skeletal muscles, where active cholinergic vasodilatation increased flow up to fivefold. Gastrointestinal and renal blood flows were promptly reduced and since this neurogenic flow reduction slightly prereded muscle vasodilatation, the C. O. increase could be preceded by a very brief phase of C. O. decrease. β-adrenergic blockade could reduce the threefold increase in left ventricular work load by 50–60 per cent by eliminating the sympathetic drive on the heart. Depressor area stimulations produced an often profound reduction in C. O., sometimes prereded by a brief C. O. increase. Flow resistance fell, especially so in skeletal musrles, where an initial flow increase coincided with the transient C. O. increase; further, blood was pooled within the capacitance section. Blood loss or raised venous transmural pressure greatly potentiated these changes so that imminent cardiovascular collapse could be induced by this central depressor stimulation. The mechanisms involved in the mentioned, diametrically opposite cardiovascular patterns are. discussed.

Experiments were performed on chloralosed, adrenalectomized cats, paralysed with gallamine and artificially ventilated. Gastric motility was recorded by the balloon method. Efferent stimulation of the cut greater splanchnic nerve, well proximal to the celiac ganglion, could either increase or decrease gastric tone. The excitatory responses called for higher stimulation intensities than the inhibitory ones but were as a rule observed at lower frequencies only (1-4 Hz). They could be abolished by atropine but were not prevented by bilateral vagotomy, hexamethonium nor guanethidine. The latter two drugs rather reversed inhibitory responses to excitatory ones which exhibited a hyperbolic frequency-response relationship with maximal effects already at 2-4 Hz. Heating of a nerve trunk selectively activates thin afferents of the delta group and C-class. Heating of the greater splanchnic nerve caused an increase in gastric motility which, like that caused by electric stimulation, was not prevented by hexamethonium nor guanethidine; nor was it eliminated by cutting the nerve centrally, nor by vagotomy, while it was abolished by atropine. These results suggest that the excitatory gastric responses to efferent splanchnic nerve stimulation are due to antidromic activation of thin afferent fibres. Their functional significance remains obscure but their peripheral arborizations may convey 'axon reflexes' influencing gastrointestinal motility.

Intraabdominal surgery tends to lower circulating blood volume by mechanisms unrelated to bleeding. This phenomenon was investigated in chloralose anesthetized rats. Plasma volume was determined with radiolabelled albumin. Animals were subjected to a standardized abdominal trauma, eliciting minimal bleeding and evaporation, and others served as controls. The trauma decreased plasma volume and increased hematocrit significantly, whereas the plasma concentration of labelled albumin followed a similar time course in traumatized animals and in controls. It is concluded that experimental abdominal trauma may decrease blood volume by a loss of fluid with virtually the same albumin concentration as that of plasma.

Experiments were performed on chloralosed cats, which had been vagotomized 9–102 days previously. In contrast to the situation in acutely vagotomized cats, recordings of gastric motility revealed pronounced and regular contractions, which persisted after exclusion of spinal pathways but could be completely blocked by small doses of atropine. These contractions therefore appeared to be the result of enhanced activity of the intramural cholinergic ganglionic cells, presumably due to sensitization to local excitatory influences after decentralization.–This type of motility could be markedly inhibited by even weak activation of the gastric adrenergic supply. Intestinal distension, or afferent stimulation of me:enteric nerve fibres as well as efferent low frequency stimulation of the splanchnic supply to the stomach, promptly inhibited the stomach contractions. After administration of atropine the above types of adrenergic activation elicited at most only very weak inhibitory response of the stomach, and then only after a long latency.–The data presented are compatible with the view that the adrenergic fibres to the stomach exert their primary action on stomach motility by inhibiting the intramural cholinergic ganglion cells rather than the smooth muscle cells, responsible for gastric myogenic tone, or by any “presynaptic inhibitory action” on the preganglionic vagal nerve endings.