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Biomedical subjects

T S Harrison

Publications and source records attributed to T S Harrison.

17 recordsLinked to original sources
PubMed1979

Cage size and exercise affects infarct size in rat after coronary artery cauterization.

Left coronary occlusion in the rat was performed by cornary artery cauterization. A small amount of myocardial damage at the site of occlusion was noted, and myocardial infarction occurred in the distal distribution of the obstructed coronary. The effects of cage size and level of physical activity on estimated infarct size (as measured by creatine kinase depletion) 48 h after occlusion were determined. Isolation in small cages and moderate treadmill exercise resulted in an approximate doubling of the amount of infarction when compared to grouping of rats in large cages. Mild exercise did not increase infarct size. Total urinary catecholamines in normal rats placed in small cages for 48 h were elevated when compared to unconfined rats in larger cages. Cornary artery occlusion by cauterization is an easily performed technique. Cage size and level of activity (and their effects on sympathoadrenal function) are important independent determinations of infarct extent after coronary occlusion in the rat.

Animals↗
PubMed1978

Converting enzyme inhibition augments and competitive inhibition of angiotensin II partially restores reflex adrenal catecholamine release in anephric dogs.

Adrenal epinephrine (E) release after hemorrhage in anesthetized dogs is blunted by acute nephrectomy and restored by angiotensin II infusion. In the present study, we report the effect of converting enzyme inhibition by SQ 20881, a decapeptide, and of competition inhibition of angiotensin II by saralasin (1-Sar-8-Ala-Ang-II) on reflexly stimulated adrenal release of E and norepinephrine (NE) in three groups of acutely anephric dogs. Aortic catheters and adrenal vein to femoral vein Silastic shunts were placed in dogs anesthetized with pentobarbital and mechanically ventilated. Adrenal secretion rates were calculated from adrenal vein to aorta catecholamine concentration differences divided by measured adrenal venous flow. Catecholamine concentrations were determined with trihydroxyindole technique. Blood samples were obtained before and 15, 30, and 60 min after rapid hemorrhage to a stable mean arterial pressure of 50 mm Hg. Saralasin infusion (10 microgram/kg/min) supported adrenal E release in anephric hemorrhaged dogs toward secretion rates comparable to those seen in intact dogs. Anephric SQ 20881 (approximately 0.5 microgram/kg) recipients had delayed (60 min) augmented adrenal E and NE release after hemorrhage. In resting animals not reflexly stimulated by hypovolemia, neither drug provoked adrenal E or NE release. These results suggest an agonist effect of saralasin on reflex adrenal E release and increased responsiveness of the stimulated adrenal medulla under the influence of converting enzyme inhibition.

Adrenal Medulla↗
PubMed1977

Blood pressure vulnerability to volume contraction: regulation by adrenal cortical hormones.

Although the unique sensitivity of blood pressure to hemorrhage after adrenalectomy can be overcome by adrenocortical hormones the specificity of this steroid effect is not known. Under pentobarbital anesthesia five groups of six adult male Sprague-Dawley rats were bled into a 0.9% saline-primed pressure-balanced reservoir. A mean arterial pressure of 50 Torr was maintained for 3 h. When compared to normal rats, those with adrenalectomy showed significantly lowered bleeding volume (P less than 0.05 to less than 0.001). In untreated adrenalectomized rats 120 min following hemorrhage, saline was consistently taken up from the reservoir to maintain blood pressure at 50 Torr. Deoxycorticosterone-cortisol (intravenous bolus coupled with infusion) restored bleeding volume to normal in adrenalectomized rats. Aldosterone (constant infusion) also protected bleeding volume after adrenalectomy, P less than 0.05 to less than 0.01, but this effect was significantly less striking than that of cortisol 180 min after the onset of bleeding, P less than 0.001. Sham adrenalectomy did not affect bleeding volume. Aldosterone appears to be effective in restoring normal bleeding volume sensitivity after adrenalectomy but this effect of aldosterone is less sustained than that seen with cortisol.

Adrenal Glands↗
PubMed1977

Cardiac output following adrenomedullary deprivation.

This study was performed to determine whether or not the adrenal medulla supports cardiac output and total peripheral vascular resistance after acute hypovolemia. Two groups of anesthetized dogs were studied. The first group underwent right adrenalectomy and the second, left adrenal denervation in addition. Adrenocortical function, as reflected by compound F and dihydroepiandrosterone determinations, was equally maintained in both groups for 120 minutes after hemorrhage. Arterial plasma concentrations of norepinephrine and epinephrine were low in group 2, p greater than 0.05 to greater 0.01. Cardiac index and peripheral vascular resistance were comparable in both groups before and for two hours after the induction of hypovolemia to a mean arterial pressure of 50 millimeters of mercury. The findings indicate that cardiac output and total peripheral resistance do not require adrenomedullary catecholamine release after acute hypovolemia.

Adrenal Cortex↗