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D G Reynolds

Publications and source records attributed to D G Reynolds.

At least 37 records · Page 2Linked to original sources
PubMed1982

Histamine H1- and H2-receptor blockade does not maintain electrochemical gradients across canine gastric mucosa exposed to bile salt.

We tested the hypothesis that histamine mediates the changes in cation permeability and potential difference characteristics of gastric mucosal barrier disruption. Canine Heidenhain pouches were exposed to 20 mM sodium taurocholate both with and without combined histamine H1- and H2-receptor blockade with diphenhydramine 2 mg/kg and metiamide 10 mumol (2.5 mg)/kg/hr. Histamine-receptor blockade did not attenuate the flux, clearance rate, or permeability of hydrogen ion due to bile salt exposure and had no effect on the fluxes of sodium, chloride, and volume. Although the potential difference was higher with combined histamine-receptor blockade, the fall in potential difference due to bile salt was not attenuated. Using a pH-stat system to measure acid loss with the incremental addition of sodium taurocholate to final concentrations of 0, 5, 10, and 20 mM, we failed to observe any difference between control and histamine-receptor blockade in hydrogen flux or permeability. Increases in gastric blood flow due to intraarterial injection of histamine were attenuated with diphenhydramine, 2 mg/kg. Further attenuation of this vasodilation was observed with the addition of a histamine H2 antagonist but not with increasing the dose of the H1 antagonist to 10 mg/kg. Thus we were unable to document that doses sufficient to antagonize histamine H1 and H2 receptors prevent the increase in sodium-hydrogen flux and decrease in potential difference observed with exposure of the canine stomach to bile salt.

Animals↗
PubMed1982

Naltrexone improves survival rate and cardiovascular function in canine hemorrhagic 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.

Animals↗
PubMed1982

Naloxone without transfusion prolongs survival and enhances cardiovascular function in hypovolemic shock.

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.

Animals↗
PubMed1982

Pancreatitis induced renal vasoconstriction.

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.

Acute Kidney Injury↗
PubMed1981

Opiate receptors and endorphins in the pathophysiology of hemorrhagic shock.

We investigated the hypothesis that endorphins released by stress act on opiate receptors to depress cardiovascular function during hemorrhagic shock. Anesthetized adult mongrel dogs were bled into a heparinized reservoir to achieve a mean arterial pressure (MAP) of 45 mm Hg. The reservoir was adjusted to maintain MAP for 1 hour and then clamped for 1 hour, at the end of which time the shed blood was reinfused. While the reservoir was clamped we treated the animals with an intravenous bolus followed by 3-hour infusion of either 0.9% NaCl (as control) or the specific opiate receptor antagonist naloxone at three dose regimens (0.5, 1, or 2 mg/kg plus 0.5, 1, or 2 mg/kg . hr). Naloxone produced dose-dependent increases in MAP, cardiac output, stroke volume, and left ventricular contractility. Survival at 72 hours was related to the dose of naloxone used. None of six dogs treated at 0 mg/kg . hr survived, one of six survived at 0.5 mg/kg . hr, four of five at 1 mg/kg . hr, and five of five at 2 mg/kg . hr. Since naloxone has minimal effect on cardiovascular function in nonshocked dogs, these results implicate opiate receptors and perhaps endorphins in the cardiovascular pathophysiology of hemorrhagic shock.

Animals↗
PubMed1980

Failure of immunosuppression to prolong venous allograft survival.

The role of allograft veins in vascular reconstruction remains ill defined. The present experiment was undertaken to evaluate the role of immunosuppression in maintaining allograft patency in the canine femoral venous circulation. Twenty-seven mongrel dogs had segments of both femoral veins excised and each dog received one allograft and one autograft. The dogs were randomly assigned to a control group or to one of three treatment regimens of azathioprine. Low doses of azathioprine were of no benefit in improving patency of venous alografts. Microscopic evaluation of these grafts suggests that substantial intimal repopulation by host cells occurs by six to eight weeks in the canine model. Other methods of preserving patency until intimal repopulation occurs deserve further investigation.

Animals↗
PubMed1980

Naloxone reversal of hypovolemic shock in dogs.

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.

Animals↗
PubMed1980

An outbreak of type 2 dengue fever in the Seychelles, probably transmitted by Aedes albopictus (Skuse).

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.

Adolescent↗
PubMed1980

Alteration of lymphocyte function due to anesthesia: in vivo and in vitro suppression of mitogen-induced blastogenesis by sodium pentobarbital.

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.

Animals↗
PubMed1980

Acute and chronic splanchnic blood flow responses to portacaval shunt in the normal dog.

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.

Animals↗
PubMed1979

Effect of altered intestinal water transport on rabbit ileal blood flow.

A method is described for measuring ileal blood flow in the anesthetized (pentobarbital sodium) rabbit by the intraventricular injection of microspheres (15 micrometer) labeled with cerium-141 or chromium-51; with this method the amount of labeled microspheres lodging in the tissue is proportional to the blood flow. Blood flow to the ileal mucosa plus submucosa could be separated from flow to the ileal muscularis propria plus serosa by this technique. Simultaneous and sequential injections of radiolabeled microspheres gave similar measurements of ileal blood flow and did not affect ileal water absorption. Increasing ileal water absorption by treatment with the glucocorticoid methylprednisolone (3 mg/100 g per day for 3 days) increased blood flow to both compartments of the ileum and also to the colon, liver, and kidneys; methylprednisolone treatment did not alter blood flow when studies were performed before the methylprednisolone-induced increase in ileal water absorption had occurred. In contrast, intestinal secretagogues that induced both active ileal secretion (purified cholera toxin and serotonin) and passive ileal secretion (hypertonic mannitol) did not affect ileal blood flow. These studies indicate that increased ileal water absorption is associated with increased ileal blood flow, whereas intestinal secretion is not necessarily associated with an alteration in ileal blood flow.

Animals↗