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Biomedical subjects

R Keeler

Publications and source records attributed to R Keeler.

34 records · Page 2Linked to original sources
PubMed1981

Circulatory effects of acute or chronic endotoxemia in rats.

A study was made of the effects of acute (4 h) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastorintestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced. Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.

Animals↗
PubMed1981

Effects of methysergide or phenoxybenzamine on the renal and cardiovascular responses to endotoxin in rats.

Renal and cardiovascular responses to an intravenous infusion of endotoxin (2.5 mg/kg/hr for four hours) were studied in unanesthetized rats. Cardiac output was reduced while total body and renal vascular resistance increased. Mean systemic blood pressure was only slightly reduced. The renal excretion of sodium, potassium, and water were reduced with no significant effect on urine concentration. Glomerular filtration rate, renal plasma flow, and filtration fraction were also reduced. alpha-Adrenergic blockade with phenoxybenzamine did not prevent any of the above changes, but a 5-HT blocking agent, methysergide, greatly reduced the effect of endotoxin on total peripheral resistance and blocked the effect of endotoxin on renal vascular resistance and renal blood flow. In rats treated with phenoxybenzamine or methysergide, endotoxin caused a large fall in the filtration fraction and extreme reduction in the rate of sodium excretion. These changes possibly resulted from decreases in the glomerular ultrafiltration coefficient or in capillary hydrostatic pressure.

Animals↗
PubMed1976

Vasopressin contamination as a cause of some apparent renal actions of prolactin.

The injection or infusion of NIAMDD prolactin (NIH P-S-10) into unanesthetized rats resulted in water and electrolyte retention with a large increase in urine osmolality but no effect on glomerular filtration rate. Since these effects on urine output were also observed in homozygous Brattleboro rats, the antidiuretic activity could not have caused by the release of endogenous antidiuretic hormone. Radioimmunoassay of NIH prolactin showed that it was contaminated with vasopressin (20 ng/mg of prolactin). By comparison, Sigma prolactin had no observed effect on urine excretion and contained very little vasopressin (2.5 ng/mg). It is concluded that some of the renal effects of prolactin have been reported in the literature may have been caused by the contaminating vasopressin.

Animals↗
PubMed1975

Effects of carotid baroreceptor stimulation and renal denervation on the medullary concentration gradient in rat kidneys.

Unilateral stimulation of carotid baroreceptors in unanesthetized rats treated with desoxycorticosterone acetate caused highly significant decreases in solute content and osmolar concentration in the inner renal medulla. There was also a corresponding decrease in urine osmolality and a large increase in the excretion of sodium. In rats subjected to water diuresis, the changes in medullary tissue composition were similar but sodium excretion was very low, indicating that the natriuretic response was not a result of medullary "washout" per se. Renal denervation had no significant effect on medullary tissue composition and did not prevent the dissipation of the cortico-medullary concentration gradient following carotid baroreceptor stimulation. It is concluded that the changes in inner medullary composition are mediated by a humoral agent.

Animals↗
PubMed1975

Failure of vasopressin to prevent the natruiretic and diuretic response to unilateral stimulation of carotid baroreceptors.

Unanesthetized rats treated with deoxycorticosterone acetate were continuously infused with a maximally effective dose of vasopressin (50 muU/min per 100 g). After a control period of 2 h the animals were subjected to a 2 h period of unilateral stimulation of the carotid baroreceptors. There was a large natriuretic response accompanied by diuresis and a fall in urine osmolality. It was concluded that neither the natriuretic nor the diuretic response could be explained by inhibition of vasopressin secretion. Analysis of kidney tissue indicated that the diuresis was associated with partial dissipation of the inner medullary concentration gradient.

Animals↗
PubMed1975

Effect of chronic preoptic lesions on the renal excretion of sodium in rats.

Rats with bilateral lesions in the preoptic area showed a normal pattern of urineand electrolyte excretion under resting conditions but complete absence of a natriuretic response to unilateral carotid baroreceptor stimulation and also a significant reduction in the rate of sodium excretion after saline loading and after a high-sodium intake. Measurements of renal clearance did not show any significant differences in glomerular filtration rate, renal plasma flow, or filtration fraction between normal and preoptic-lesion rats. Apart from the test situations used above, rats with preoptic lesions were apparently able to regulate their sodium metabolism normally because after 3 wk on a high-sodium intake their plasma and extracellular fluid volumes, plasma electrolytes, osmolaity, and mean arterial pressures were indistinguishable from normal rats. It is suggested that the preoptic component of the baroreceptor reflex pathway mighthave an input into a hypothalamic area controlling sodium excretion.

Animals↗