Search

The relative roles of acetate and leucine in the provision of a carbon source for fatty acid and sterol biosynthesis in several trypanosomatid species were investigated using 14C- and 13C-labelled acetate, glucose and leucine as substrates. Promastigotes of Leishmania species synthesized a large proportion of their sterol from leucine. L. major (LV39), L. amazonensis and L. mexicana were the most efficient utilizers of leucine, producing at least 70-77% of their sterol from leucine; L. braziliensis, L. donovani and L. tropica apparently produced less sterol from leucine (23-36%) and L. major (LV561), L. adleri and L. panamamensis were intermediate, utilizing leucine to provide 51-58% of their sterol. In all the cases the balance of the sterol produced was apparently synthesized from carbon arising from acetate. The related trypanosomatid Endotrypanum monterogeii also produced a large amount (77%) of its sterol from leucine rather than acetate. By contrast Trypanosoma cruzi elaborated only 8% of its sterol from leucine and used acetate far more effectively than the Leishmania species for sterol biosynthesis. The fatty acid moieties of the triacylglycerols and phospholipids were produced from acetate. Leucine was also incorporated into the fatty acids to varying extents in the different organisms showing that leucine can also be metabolized in trypanosomatids to generate acetyl-CoA.

The man-biting midge Leptoconops spinosifrons (Diptera: Ceratopogonidae) is a major nuisance on many beaches in Seychelles and, with a developing tourist industry, control is required. Malathion, applied weekly as a spray at 1000 g a.i./ha or twice a week with u.l.v. equipment at 1750 g a.i./ha, was not effective; this finding was supported by laboratory studies. DDT exercised control for five months when applied as a spray at 2200 g a.i./ha, at 1100 g a.i./ha control lasted less than one month. DDT residues were detected in Donax cuneatus, an intertidal filter-feeding mollusc, 15 months after the last application. Diazinon, applied as a spray at 6000 g a.i./ha produced good control for five months and applied at 600 g a.i./ha every two weeks gave excellent control. The importance of correlating times of spraying with the lunar tide cycle was confirmed.

Treatment with naloxone improves cardiovascular function and survival in a variety of shock models, and numerous sites and mechanisms for its action have been proposed. Data presented in this article support the hypothesis that in hemorrhagic shock naloxone exerts its beneficial hemodynamic effects by acting primarily at cardiac opiate receptors. Naloxone or its stereoisomer (d-naloxone) were administered intravenously (iv) and directly into the coronary circulation (ic) in dogs anesthetized with pentobarbital sodium and subjected to hemorrhagic shock. Treatment with naloxone (2.0 mg/kg iv or 0.2 mg/kg ic) resulted in significant improvements in arterial pressure, myocardial contractility, and cardiac output. Treatment with saline or naloxone (0.2 mg/kg iv) were without beneficial effect. The hemodynamic responses to naloxone administered into the coronary circulation were dose dependent and stereospecific. These data support the hypothesis that naloxone exerts its salubrious effects in canine hemorrhagic shock by acting at cardiac opiate receptors.

The effects of adrenergic stimulation and blockade on the gastric circulation were studied in anesthetized dogs. Blood flow through the right and left gastric artery was measured electromagnetically. Norepinephrine and isoproterenol were injected intra-arterially and intravenously before and after alpha- and beta-adrenergic blockade. Isoproterenol caused vasodilation of both right and left gastric circulations and this effect was attenuated by beta blockade. Epinephrine and norepinephrine induced constriction followed by dilation in both circulations. The constrictor components were attenuated or abolished by alpha-adrenergic blockade and the dilator components were attenuated by beta-adrenergic blockade. The right and left gastric vascular beds demonstrated quantitatively different responses to the same dose of each adrenergic amine. The left gastric circulation had a greater vasodilator response than did the right gastric circulation. These data support the classical concepts that epinephrine and norepinephrine are "mixed" adrenergic agonists and isoproterenol is a "pure" beta-adrenerigic agonist. The data further suggest that there is a differential in beta-adrenergic receptor distribution with the left gastric vasculature demonstrating greater dilator responses than the right.

Ore occurs in veins along cross-cutting normal faults and in contiguous replacement bodies. Three stages of mineralization are recognized--arsenopyrite, quartz; pyrite; and pyrrhotite, chalcopyrite, gold and silver, bismuthinite, bismuth complexes, quartz. If zoning is present, it is masked by differences dependent on wall-rock composition. The high-temperature mineralization is believed to be related to granitic intrusions like those exposed north of the mine.

Populations of Culex pipiens fatigans Wied. were exposed to infection by Plistophora culicis (Weiser) by allowing eggs to hatch in water containing a known concentration of spores. At 26°C–28°C (mean 27°C) exposure of newly hatched larvae to a concentration of 6 000 spores/ml resulted in a 12–9% reduction in the net reproduction rate, and exposure to a concentration of 12 000 spores/ml to a reduction of 24·0%. These reductions were due to an increase in the rate of female mortality and an increase in the number of eggs laid which were non-embryonated and hence did not hatch. At 33°C–35°C (mean 34°C), although the spores of the microsporidian were not killed, development of P. culicis in the mosquito was inhibited. At 19·5°C–20·5°C (mean 20°C), the net reproduction rate of a population exposed as newly hatched larvae to a concentration of 1 890 spores/ml was reduced by 35·6%, due to a greatly increased rate of female mortality. P. culicis, with the inocula tested, is not considered of practical use against C.p. fatigans; more infective spore inocula are not feasible with the present methods of propagating the parasite.

The effects of 60-min intraarterial infusion of vasopressin (0.005 U per kg-min) and epinephrine (0.05 mu per kg-min) on gastric hemodynamics were studied in anesthetized baboons. Total gastric blood flow was measured electromagnetically and radioactive microspheres (15 +/- 5 mu) with three labels were used to determine regional distribution of gastric blood flow and arteriovenous shunting. Control flow was 55 +/- 8 ml per min, with 77.4 +/- 2.7% of flow going to the gastric mucosa and 1.7 +/- 0.4% of injected spheres appearing in the liver. Epinephrine infusion resulted in a sustained vasoconstriction to 18 +/- 5 ml per min with no autoregulatory escape and no changes in arterial pressure or cardiac output. Vasopressin resulted in a decrease in flow to 14 +/- 3 ml per min with no excape. Whereas cardiac output did not change, there was a singificant hypertensive effect during the vasopressin infusion. There was neither redistribution of flow nor change in arteriovenous shunting with either epinephrine or vasopressin. Transmucosal electrical potential difference was 62 +/- 8 mv and did not change significantly with either infusion.

Five anesthetized cynomolgus monkeys were subjected to hemorrhagic shock (42 +/- 3 mm Hg) for four hours and then resuscitated with shed blood and intravenous fluids to restore mean arterial pressure and arterial pH to control levels. Regional gastric blood flow was measured by radioactive microspheres. Responses were similar in all regions, except mucosal blood flow increased significantly (from 20.1 +/- 5.1 to 42.1 +/- 7.6 ml/min 100 gm of tissue) in response to resuscitation in the antrum but not in the fundus or corpus. This difference in response may explain the occurrence of stress ulcers in the proximal stomach with sparing of the antrum.

We tested the hypothesis that thyrotropin releasing hormone (TRH) would improve cardiovascular function and survival in circulatory shock by opposing the adverse effects of endogenous opioids and other pathophysiologic mediators. Cynomolgus monkeys and mongrel dogs were anesthetized and catheterized to measure mean arterial pressure (MAP) and left ventricular contractility (LV dp/dtmax). Hemorrhagic shock was induced by bleeding into a reservoir to achieve and maintain MAP at 45 mm Hg for one hour. Endotoxic shock was produced by the iv injection of an LD80 dose of Escherichia coli lipopolysaccharide endotoxin (3 mg/kg in dogs and 5 mg/kg in monkeys). Animals were treated iv with either TRH (2 mg/kg plus 2 mg/kg X h) or equivolume saline. TRH significantly increased MAP and LV dp/dtmax in primate hemorrhagic and endotoxic shock. In primate hemorrhagic shock, TRH significantly (p = .02) improved survival (alive/total = 4/5 vs. 0/5). However, TRH had no effect on survival in endotoxemic primates. In contrast, TRH treatment in dogs produced only a transient hemodynamic response after endotoxemia and no significant hemodynamic effect after acute hemorrhage (even at twice the TRH dose). TRH did not affect survival in either dog model of circulatory shock. Based on extensive evidence with the opiate receptor antagonist naloxone in other studies, endogenous opioids play a role in the cardiovascular depression in primate and canine circulatory shock. From these studies with TRH, we conclude that TRH is relatively ineffective in canine circulatory shock, and physiologic antagonism of the adverse effects of opioids and other cardiodepressant substances by TRH administration may prove to be a useful alternative treatment of primate hemorrhagic shock.

Urokinase, the plasminogen activator from human urine, produces a dose-dependent increase in blood flow in the canine superior mesenteric artery when injected intraarterially at doses from 10(-1) to 10(3) units kg-1. This vasodilation persists despite blockade of beta-adrenergic and histamine H1 and H2 receptors as well as inhibition of plasminogen activation, suggesting that these mechanisms are not involved. Infusion of urokinase at 10(2) CTA (Committee on Thrombolytic Agents) units kg-1 min-1 does not produce a sustained vasodilation, but is effective in achieving complete lysis of thrombi within 100 min in the superior mesenteric arterial circulation. Increasing the dose slightly to 125 CTA units kg-1 min-1 results in unwanted clotting abnormalities without attaining a vasodilator level. Decreasing the dose to 75 CTA units kg-1 min-1 still results in complete thrombolysis. In contrast to the results in the femoral circulation, the dose required for fibrinolysis-thrombolysis does not overlap with that for vasodilation in the superior mesenteric artery. Nevertheless, these experiments provide some basis for the use of intraarterial urokinase infusion in the treatment of nonocclusive mesenteric ischemia and, perhaps, thrombotic occlusion of the superior mesenteric artery.

Microvascular architecture of the small intestine of New World monkey, ape, and man was examined with the silicone rubber injection technique and the results compared to previous observations in dogs and Old World monkeys. In man, chimpanzee, and New World monkey the small intestine villus contains a single centrally located vein draining a subepithelial capillary plexus converging at the apex of the villus. These villi also contain a single eccentrically located artery rising to the midlevel of the villus, where it branches into subepithelial capillaries over the rest of its length. This vascular architecture most closely resembles that observed in the gut of Old World monkeys in which the villus artery is absent altogether. This observation contrasts the microvascular architecture of canine intestinal villi in which marginal arteries surround a centrally located vein. These patterns of microvascular anatomy are analyzed in terms of the role of the gut in the pathogenesis of experimental shock. The differences observed may account for the known species variations in canine and primate experimental shock.

Endogenous opioids are released during stress and appear to contribute to the cardiovascular suppression seen in shock. When the opiate receptor antagonist naloxone is administered intravenously to anesthetized dogs subjected to hemorrhage, mean arterial pressure, maximal left ventricular dp/dt, and cardiac output increase. This study tests the hypothesis that naloxone acts by potentiating the effects of neurally and adrenally released catecholamines. If this hypothesis is correct, then blockade of endogenous catecholamine release should attenuate the response to naloxone, and administration of exogenous adrenergic agonists prior to naloxone treatment should restore the response. Catecholamine release was attenuated by a combination of surgical adrenal denervation and pharmacological ganglionic blockade. Adrenal denervation or chlorisondamine alone attenuated and, in combination, blocked the response to naloxone in hemorrhaged dogs. Infusion of alpha- and beta-adrenergic agonists at a constant rate prior to treatment restored the response to naloxone. Naloxone appears to improve cardiovascular function in hemorrhagic shock by potentiating the effect of released catecholamines and not by increasing sympathoadrenal discharge.

The mechanism of decreased lymphocyte responsiveness after major surgery is unclear. Because sodium pentobarbital, and intermediately long-acting barbiturate, will reproducibly induce anesthesia in experimental animals, we utilized a canine model to investigate its effect on lymphocyte proliferation induced by the mitogenic lectins erythroagglutinating phytohemagglutinin (E-PHA) and leukoagglutinating phytohemagglutinin (L-PHA). Although no effect was observed at 10 minutes or 1 hour after an anesthetic dose of sodium pentobarbital, after 1 and 3 hours of anesthesia, canine lymphocytes were significantly suppressed, as demonstrated by decreased responsiveness to E-PHA and L-PHA mitogen stimulation. After 3-hours the majority of animals had mitogenesis values of less than 50% of the preanesthetic control values. Recovery, as measured by a return to at least 70% of the preanesthetic mitogenesis value, was noted in the majority of animals at 24, 48, and 72 hours. In order to investigate the machanisms of the in vivo capability of sodium pentobarbital to induce immunosuppression of lymphocyte transformation, in vitro studies were carried out. Sodium pentobarbital was found to significantly inhibit mitogen-induced canine mononuclear cell blastogenesis at anesthetic (1.5 to 3.0 mg%) drug concentrations in vitro. Lymphocytes pretreated with barbiturate and washed prior to plating did not show this inhibiting effect. Our findings suggest that depression of the immune response reported in patients after operation could result from short-acting barbiturates administered during the induction phase of clinical anesthesia. Furthermore, the suppression may involve in vivo metabolism of pentobarbital, hormones or other in vivo factors, since washed lymphocytes from the in vivo but not the in vitro experiments demonstrated suppression. These results indicate that anesthesia may be an important factor in the immunosuppression reported after major surgery.

The effects of intra-arterial injections and infusions of three adrenergic amines upon hepatic arterial blood flow were measured in anesthetized baboons before and after alpha and beta adrenergic blockade with intravenous phenoxybenzamine and propranolol. Injections of norepinephrine or epinephrine caused dose-dependent decreases in hepatic arterial blood flow. These responses were attenuated by alpha adrenergic blockade and were unchanged by beta adrenergic blockade. Injections of isoproterenol caused dose-dependent increases in hepatic arterial flow. These increases were relatively small and were reversed to constriction at low doses and attenuated at high doses of the agonist by beta adrenergic blockade. Intrahepatic arterial infusions of constrictors were unaccompanied by autoregulatory excape. The degree of constriction was attenuated by alpha adrenergic blockade but was not potentiated by beta adrenergic blockade. Intrahepatic arterial infusion of a relatively large dose of isoproterenol was required to evoke a relatively modest, but sustained, increase in hepatic arterial blood flow. This response was not potentiated by alpha adrenergic antagonism, but was attenuated by beta adrenergic blockade. These observations suggest an apparent and relative decrease in beta adrenergic receptor activity in the hepatic arterial bed of the baboon when compared to other regional circulations such as the mesenteric and femoral beds. These beta receptors are relatively resistant to both stimulation and blockade.

The endogenous opiate ligand, beta-endorphin, is released during stress. We tested the hypothesis that endorphins may be involved in the pathophysiology of hemorrhagic shock by using the opiate receptor blocking agent, naloxone. Two groups of five anesthetized dogs were instrumented to monitor cardiovascular performance and subjected to a protocol in which they were bled into a reservoir to lower mean arterial pressure to 45 mmHg and maintained at that pressure for one hour. At that time the reservoir was clamped and on group of dogs received an intravenous bolus of naloxone (2 mg/kg) and an infusion at 2 mg/kg-hr. These dogs demonstrated a prompt increase in arterial pressure, left ventricular dp/dtmax and cardiac output. The shed blood was returned at t = 2 hr and drug infusion continued for 2 hours. The control group of dogs received saline in equivalent volume. The control dogs died within 30 minutes of clamping the reservoir while all five treated dogs survived beyond 72 hours (P less than 0.02). These data suggest the involvement of endorphins acting on opiate receptors as part of the pathophysiology in this shock model.

We used naloxone to investigate the role of central nervous system opiate receptors in the cardiovascular depression of canine hemorrhagic and endotoxic shock. Shock was induced by bleeding dogs into a reservoir to achieve and maintain a mean arterial pressure (MAP) of 45 mmHg for 30 min; at 30 min the reservoir was clamped and the animals were treated with intracerebroventricular (ICV) perfusion of naloxone 0.1 mg/kg (n = 5) or artificial CSF (n = 5) for 30 min. Endotoxemic shock was induced by the iv injection of E. coli endotoxin 1 mg/kg; 15 min later the animals were given naloxone 0.1 mg/kg (n = 5) or artificial CSF (n = 5) ICV for 30 min. ICV naloxone significantly increased MAP, cardiac output (CO), and left ventricular performance (LV dP/dt max) compared to artificial CSF in canine endotoxic shock but not hemorrhagic shock. Naloxone 0.1 mg/kg (n = 5) given into the cisterna magna failed to significantly improve MAP, CO, or LV dP/dt max in dogs subjected to reservoir hemorrhagic shock for 60 min compared to artificial CSF (n = 5). These results are compatible with opiate-receptor-mediated central cardiovascular depression in endotoxic shock and peripheral cardiovascular depression in hemorrhagic shock. Accordingly, the sites of action of naloxone are mainly central in endotoxic shock and peripheral in hemorrhagic shock.

We noted the effects of the mixed opiate agonist/antagonist nalbuphine on cardiovascular function and survival in canine hemorrhagic shock. Anesthetized adult mongrel dogs were bled to a mean arterial pressure (MAP) of 45 mmHg, which was maintained with a reservoir for 1 hr before the reservoir was clamped and the animals treated with 0.9% NaCl as a control or nalbuphine at various doses. Shed blood was reinfused 1 hr after the reservoir was clamped, and survival was followed for three days. Nalbuphine at 1-4 mg/kg bolus plus 1-4 mg/kg hr infusion intravenously for 3.5 hr increased MAP, cardiac output, left ventricular contractility, heart rate, and survival. At doses above 8 mg/kg plus 8 mg/kg hr nalbuphine had deleterious effects on these parameters and survival. These effects were dose-dependent and support the hypothesis that endorphins acting on opiate receptors contribute to the cardiovascular pathophysiology of canine hemorrhagic shock. Nalbuphine, furthermore, may be a logical alternative to naloxone, since its analgesic properties obviate the theoretical objection of enhanced pain perception with the use of naloxone in shock.

The etiology of renal vasoconstriction in acute pancreatitis remains obscure. The canine model of bile pancreatitis was used to determine whether hypovolemia or increased circulating levels of catecholamines are responsible for this phenomenon. Treatment of the pancreatitis was either with volume loading or alpha adrenergic blockade with Prazosin given both before and after the induction of pancreatitis. Neither pretreatment nor post-treatment with either volume loading or Prazosin protected the kidneys from the standpoint of mitigating renal vasoconstriction. To the contrary, treatment with alpha blockade produced the greatest decreases in renal blood flow.

Based upon clinical observations, we hypothesize that the plasminogen activator urokinase is vasoactive in addition to being fibrinolytic and thrombolytic. The effects of intra-arterial injections and infusions of urokinase were investigated in the canine femoral circulation. Injections of human urine urokinase increased femoral artery blood flow in a dose-related fashion that was not significantly attenuated by beta adrenergic blockade, antihistamine treatment, heating, atropine treatment or kallikrein inactivation. The Ploug preparation of urine urokinase was somewhat more effective than the Abbott or Sterling-Winthrop preparations in causing this dilation. Some nonspecific inhibition of the vasodilator responses was produced by inhibition of plasminogen activation with epsilon-aminocaproic acid. The continuous infusion of urokinase increased femoral arterial flow but there was some tendency to escape. Further experiments seem indicated to determine potential application of local urokinase in clinical conditions where vasodilation and fibrinolysis-thrombolysis might be of value.

The hemodynamic effects of Escherichia coli endotoxin (LD80) were measured in the large intestine of anesthetized Rhesus monkeys to determine whether this organ contributes to the pathogenesis of experimental shock. Inferior mesenteric arterial blood flow (IMF) was measured with an electromagnetic flowmeter. Pressures within the aorta (AP) and portal vein (PP) were recorded. Distribution of colon blood flow was measured with radioactive microspheres: Ce, Sr, and Cr were injected into the left heart. Reference blood samples were obtained from a femoral artery. Mean control IMF was 22.9 +/- 2.2 (SE) ml/min. Aortic pressure was 113 +/- 11 mm Hg, and PP was 6 +/- 1 mm Hg. Arterial blood pH was 7.43 +/- 0.02; pO2 and pCO2 were 93.4 and 37.1 mm Hg, respectively. All parameters were measured at hourly intervals for 4 hr. Neither IMF nor its distribution within the colon changed during the entire observation period. Aortic pressure fell to a low of 60 +/- 6 mm Hg (p less than 0.02) at 3 hr; PP, pO2 and pCO2 were unchanged by endotoxin. Arterial blood pH fell to 7.315 +/- 0.020 at 4 hr (p less than 0.01). These observations indicate that the colon is not a "target organ" of endotoxic shock in subhuman primates, despite considerable hypotension and metabolic disturbances subsequent to near lethal endotoxemia.

The effects of intra-arterial infusions of epinephrine, norepinephrine, and isoproterenol upon right and left gastric blood flow were studied in anesthetized dogs. Blood flow was measured electromagnetically before and after adrenergic blockade. Infusion of epinephrine (0.05 mug Kg.(-1) min.(-1)) resulted in vasoconstriction (-50 +/- 6 ml. min.(-1)) with autoregulatory escape in the right gastric artery (RGA) and constriction (-41 +/- 8 ml. min.(-1)) followed by significant dilation (+ 56 +/- 10 ml. min.(-1)) in the left gastric artery (LGA). Alpha adrenergic blockade with phenoxybenzamine produced only a dilator response in both RGA and LGA to epinephrine infusion and beta adrenergic blockade resulted in a constrictor response with no autoregulatory escape. Norepinephrine infusions produced a constrictor response of similar magnitude as epinephrine but with little evidence of autoregulatory escape in either RGA and LGA. Alpha adrenergic blockade significantly attenuated this response in both circulations. Isoproterenol is a dilator in both circulations and its response is attenuated only by beta adrenergic blockade. This study demonstrates that the canine stomach has two regionally distinct circulations with the fundus and body exhibiting a greater dilator response than the antrum and pylorus.

The effects of graded occlusion of the portal vein upon hepatic arterial blood flow were studied in anesthetized dogs to evaluate the so-called "reciprocal relationship" between portal venous flow and hepatic arterial flow in maintaining oxygenation of the liver. An obstruction that increased portal venous pressure to 20 mm Hg was accompanied by a transient increase in hepatic arterial blood flow without changing the other hemodynamic parameters. Release of portal venous occlusion was accompanied by a transient fall in hepatic arterial blood flow in this group of experiments. Increasing portal venous pressure to 30 mm Hg caused a gradual but progressive fall in arterial pressure accompanied by a significant fall in hepatic arterial blood flow. With complete obstruction of the portal vein there is a reduction in arterial pressure to the same level of portal venous pressure and a significant and sustained diminution in hepatic arterial blood flow. These observations conflict with previously described theories of a relationship between diminution in portal venous flow and increases in hepatic arterial blood flow.

Between December 1976 and September 1977 the Seychelles group of islands in the Indian Ocean was struck by an extensive epidemic of dengue fever. The peak of the epidemic was in the last week of February. Type 2 dengue virus was isolated from patients and mosquitos. Aedes albopictus was the sole vector. The clinical picture was that of classical dengue. Haemorrhagic fever and the shock syndrome were not observed.Absenteeism from schools and offices, anamnestic questioning, and prevalence of antibodies in sera collected after the epidemic was over, indicated that approximately 75% of the population had been infected. Serological evidence was obtained of an epidemic of dengue in the islands more than 40 years earlier. This was confirmed by archival records.

The hypothesis that opiate receptors are involved in the cardiovascular pathophysiology of hypovolemic shock was tested by using the opiate receptor antagonist naloxone. Naloxone increased mean arterial pressure, cardiac output, stroke volume and left ventricular dP/dtmax in a canine hemorrhagic shock model. Naloxone treatment also prolonged survival time. All these responses were dose-dependent and were independent of blood reinfusion. It is concluded that endorphins activated by stress act on opiate receptors to bring about some of the cardiovascular abnormalities in hypovolemic shock.

The possible involvement of opiate receptors in the cardiovascular depression associated with hypovolemic shock was investigated. Opiate receptor blockade with naltrexone increased mean arterial pressure, cardiac output, stroke volume and left ventricular contractility in dogs bled to a mean arterial pressure of 45 mm Hg. Naltrexone also increased survival rate. At high doses, naltrexone adversely affected cardiac performance which may outweigh its advantages of greater potency and putatively longer action than naloxone, at least in the dog. Similar actions with another opiate antagonist gives further proof for endogenous opiate involvement in the cardiovascular pathophysiology of hypovolemic shock.

Portacaval shunt increases hepatic arterial blood flow, and the magnitude of this response is important clinically. To document persistence of this hyperemia we measured splanchnic regional blood flow by the microsphere technique before and after end-to-side portacaval shunt in dogs. The immediate postshunt increase in hepatic arterial blood flow returned to control 3 wk later, replaced by increases in pancreatic, duodenal, and jejunal blood flow. Any hypothesis for the compensatory relationship between hepatic arterial and portal venous blood flows needs to encompass these results.

Endogenous opioid substances are activated in and may contribute to the cardiovascular depression of hemorrhagic shock. In order to determine the importance of the adrenal gland in the beneficial effects of the opiate antagonist naloxone in shock we studied 23 adrenalectomized dogs subjected to hemorrhagic shock. Adrenalectomy abolished the salubrious cardiovascular responses to naloxone. Naloxone responses (increased mean arterial pressure, cardiac output, and left ventricular contractility) were restored by giving hydrocortisone 50 mg intravenously before naloxone. Survival was also prolonged in animals receiving naloxone and hydrocortisone compared to naloxone or saline alone; hydrocortisone alone decreased survival. The adrenal glands are necessary for naloxone's beneficial effects, probably via adrenal corticosteroid secretion.

BIOLOGICAL control is assuming an ever-increasing importance as a means of augmentation of, or substitution for, the use of pesticides in the control of both medically and economically important arthropods. This applies in particular to Culex fatigans, the main vector of Wuchereria bancrofti throughout most of the tropics and subtropics. Control of this mosquito is complicated by the widespread occurrence of resistance to most insecticides, together with the complexities of larval control by sanitation or other non-insecticidal methods.