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Biomedical subjects

D G Reynolds

Publications and source records attributed to D G Reynolds.

At least 55 records · Page 3Linked to original sources
PubMed1978

Microvascular architecture of anthropoid primate intestine.

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.

Adult↗
PubMed1978

Regional gastric blood flow in cynomolgus monkeys with hemorrhagic shock and resuscitation.

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.

Animals↗
PubMed1978

Vasodilation, fibrinolysis, and thrombolysis with intraarterial infusion of urokinase in the canine superior mesenteric artery.

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.

Animals↗
PubMed1977

Endotoxemia and large intestinal blood flow in subhuman primates.

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.

Animals↗
PubMed1977

The effect of hemorrhagic shock and resuscitation on regional blood flow in cynomulgus monkeys.

The effect of hemorrhagic hypotension and resuscitation on regional blood flow was studied in the Macaca fascicularis monkey. The majority of the splanchnic vasculature demonstrated a profound decrease in flow. Following fluid expansion and correction of acidosis, flow increased in these circulations but did not reach control values. Exceptions were the small bowel flow which fell only moderately and hepatic arterial flow which did not significantly change. Both coronary and adrenal circulations maintained flow during the shock and resuscitation periods, whereas brain and kidney blood flows fell significantly without recovery. There was a significant rise in serum glucose, lactate, and pyruvate during shock, with an increase in the lactate/pyruvate ratio. Following resuscitation, the ratio decreased, implying a return toward aerobic metabolism.

Animals↗
PubMed1977

Adrenergic mechanisms in the hepatic arterial circulation of baboons.

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.

Animals↗
PubMed1977

Vasodilation due to urokinase in the canine femoral circulation.

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.

Animals↗
PubMed1976

Primate gastric circulation: effects of catecholamines and adrenergic blockade.

The effects of intra-arterial injections and infusions of epinephrine, norepinephrine, and isoproterenol on gastric blood flow were studied in anesthetized baboons. Blood flow was measured electromagnetically before and after adrenergic blockade. The results for injected epinephrine and norepinephrine indicate these agents to be pure vasoconstrictors in the primate gastric circulation, and this response is attenuated by alpha-adrenergic blockade with phenoxybenzamine. Isoproterenol is a pure vasodilator, and its response is attenuated following beta-adrenergic blockade with propranolol. Intra-arterial infusions of epinephrine and norepinephrine (.05 mug kg-1 min-1) resulted in sustained vasoconstriction with no evidence of autoregulatory escape and no postinfusion "over-shoot." This study suggests that epinephrine and norepinephrine might provide alternatives to vasopressin as a vasoconstrictor for the control of upper gastrointestinal bleeding.

Animals↗
PubMed1976

Distribution and arteriovenous shunting of gastric blood flow in the baboon: effect of epinephrine and vasopressin infusions.

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.

Animals↗
PubMed1975

Adrenergic mechanisms in canine gastric circulation.

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.

Adrenergic Agonists↗
PubMed1975

Contractility of renal cortex following complete ureteral obstruction.

Contractility of strips of renal cortex obtained from rabbit kidneys obstructed by complete ureteral ligation for 8 and 32 days was tested and compared with control tissue. Concentration-response data were obtained for norepinephrine, angiotensin, and 5-hydroxytrypamine, and were expressed as mg tension/cm of tissue. Control tissue tested simultaneously revealed minimal responses, but obstructed tissue containing modified interstital cells revealed statistically significant evidence of contraction in response to all three drugs studied. The response to norepinephrine could be blocked by the alpha adrenergic antagonist, phenoxybenzamine, but this drug did not significantly affect the response to angiotensin or 5-hydroxytryptamine. The findings are related to similar observations reported in stimulated fibroblasts of granulation tissue and are discussed in terms of the possible role this phenomenon may play in the pathogenesis of renal interstitial injury.

Angiotensin II↗
PubMed1975

Hemodynamics of experimental portal venous occlusion in dogs.

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.

Animals↗