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Biomedical subjects

E E Selkurt

Publications and source records attributed to E E Selkurt.

At least 19 recordsLinked to original sources
PubMed1986

Effects of histamine-receptor antagonists on histamine-stimulated renin secretion.

The effects of histamine H1- and H2-receptor antagonists on histamine-stimulated renin secretion were examined in anesthetized dogs. Tripelennamine (H1 blocker) further enhanced renin secretion in the presence of exogenous histamine. Moreover, tripelennamine alone increased renin secretion. These effects are probably due to non-specific properties of the drug and not to interaction of tripelennamine with H1 receptors. Conversely, cimetidine (H2 blocker) significantly inhibited histamine-induced increases in renin secretion, renal blood flow, and sodium excretion without any changes in mean arterial blood pressure or glomerular filtration rate. Cimetidine alone had no effect. We conclude that H2 receptors mediate the effect of histamine on renin secretion in dogs with innervated, intact kidneys.

Animals↗
PubMed1985

Effect of acute pulmonary hypertension on pressure/flow in the canine pulmonary vascular bed.

The relationship of pulmonary blood flow and vascular resistance to pulmonary artery pressure was examined in pentobarbital-anesthetized open-chest dogs. The pulmonary artery perfusion pressure was varied in the range 0-100 mm Hg. This was achieved by perfusion of the lobar artery supplying the left upper lobe of the lung from the subclavian artery. Perfusion pressure was varied by a clamp on the external shunt. The relationship was rectilinear in the lower pressure range, from zero flow at 5 mm Hg, to 45-55 mm Hg. Above this, curvilinearity developed, concave toward the pressure axis. Possible participation of the autonomic nervous system (ANS) in the P/F relationship was examined by treatment with the ganglionic blocking agent, hexamethonium. Although the drug was successful in lowering systemic arterial pressure, it had no effect on the pulmonary P/F relationship. Possibly, the sympathetic nervous system (SNS) tone to pulmonary vessels was low or absent in our preparation. Changes in compliance of the pulmonary arterial supply, resulting from changes in transmural pressure, may explain the results. A myogenic type of response is favored.

Acute Disease↗
PubMed1985

The role of histamine H1 and H2 receptors in the canine kidney.

The functional role of H1 and H2 receptors in mediating the effects of histamine on renal hemodynamics and tubular function was investigated in anesthetized dogs. Histamine, infused directly into the renal artery, caused decreases in renal vascular resistance and increases in total renal blood flow without significant changes in mean arterial blood pressure or glomerular filtration rate. These hemodynamic effects of histamine were inhibited by the H2-receptor antagonist, cimetidine, but not by the H1-receptor antagonist, tripelennamine. Histamine also caused increases in fractional urine flow and the fractional excretion of sodium and calcium with a concomitant decrease in urine/plasma osmolality. These tubular effects of histamine were antagonized by both tripelennamine and cimetidine. Histamine-induced increases in the fractional excretion of potassium were blocked only by tripelennamine. These results suggest that (1) both H1 and H2 receptors mediate the effects of histamine on urinary dilution and tubular reabsorption; (2) H2 receptors mediate the effects of histamine on renal hemodynamics, indicating that H2 receptors are present in the renal vasculature, and (3) H1 receptors may exist in the renal tubules.

Animals↗
PubMed1985

Role of the lung in metabolism of prostaglandin E during severe hemorrhagic shock in the dog.

The pulmonary handling of prostaglandin E (PGE) during a hemorrhagic shock procedure was evaluated in pentobarbitalized dogs. Net extraction [(V - A)/V] and turnover [(V - A) X total plasma flow] of endogenous PGE were measured. Following hemorrhage to 40 mm Hg arterial pressure, the endogenous arterial plasma PGE level rose from ca 400 to ca 700 pg/ml, and net extraction fell from 42.5% to -30%, indicating a shift from preponderant removal of endogenous PGE by the lung to net release. Reflecting this, turnover decreased from a control average of 480 ng/min to -60 ng/min. At two hours post-reinfusion, net extraction and turnover were still essentially zero. These findings support the hypothesis that changes in net metabolism of PGE by the lung in hemorrhagic shock result in increased systemic arterial blood levels of PGE, which may contribute to peripheral vasodilation during the decompensatory phase of hypotension, and to the irreversible phase of the post-infusion period.

Animals↗
PubMed1984

Influence of prostaglandin synthetase inhibitors on the renal effects of histamine.

The increase in renal blood flow and accompanying increase in excretion of electrolytes (e.g., Na+, Ca2+, and other osmolar constituents) produced by intra-renal arterial infusion of histamine in dogs are reduced by the inhibitors of cyclooxygenase activity, indomethacin and RO 20-5720, given intravenously. This suggests the possibility that histamine might be acting in conjunction with the renal prostanoids, either by stimulating their release by activating prostaglandin synthesis, or by acting at the PG receptor sites in a similar manner.

Animals↗
PubMed1984

Influence of prostaglandin E and reduction of renal arterial pressure on renin release by the dog kidney.

The influence of PGE1 infusion into the renal artery of dogs n renal hemodynamics and renin release (RR) was examined, with or without simultaneous reduction in renal arterial perfusion pressure. The degree of reduction in renal arterial pressure was such as to remain in the autoregulatory range. PGE1 is a known stimulator of RR. The objective of the experiment was to attempt to determine whether or not PGE1 and reduction of renal arterial pressure (baroreceptor mechanisms) operated by a similar receptor-effector mechanism, or by different mechanisms. Evidence is supplied that supports the former case (similar receptor-effector mechanism).

Animals↗
PubMed1979

Influence of PGE1 on renal function in severe hemorrhagic shock.

The influence of intravenously administered PGE1 on renal function in standardized hemorrhagic shock in dogs was examined in this study. Infusion rates as high as 1.04 micrograms/min/kg were evaluated. Although arterial blood levels as high as 2.47 ng/ml of plasma compared to control values of less than 0.20 ng/ml were attained during postreinfusion treatment, no beneficial influences on renal functional parameters (hemodynamics, electrolyte and water handling) were observed. In fact, treated animals took up blood from the arterial reservoir more quickly and expired sooner following blood transfusion than an untreated series. A further deleterious change in renal function was a decrease in renal concentrating capability. It is concluded that with the severe grade of hemorrhagic shock employed in these studies, organ blood perfusion was restricted to the extent of limiting effective PGE action.

Animals↗
PubMed1978

Role of the kidney and lung in the handling of prostaglandin E in hemorrhagic shock.

The polyuria and hyposthenuria noted particularly following blood transfusion after prolonged periods of hypotension (dog, monkey) seem best explained by a prostaglandin-antidiuretic hormone (PG-ADH) antagonism, operating primarily in the renal medulla. The kidney releases greatly enhanced amounts of PGE at this time, which probably act primarily in the renal medulla, then secondarily influence the systemic (arterial) levels by passing in greater amounts through the lungs. The lungs normally metabolize the major portion of PGs delivered to them. Our data suggest impairment of the lung's "up-take-metabolizing" mechanism, but also could be interpreted as involving enhanced release of PGE from the lung, so net pulmonary extraction, (V--A)/V, shifts from positive to zero or even negative values in the hypotensive shock phase. This ratio tends to improve after transfusion, but systemic PGE levels remain elevated. It is speculated that in hemorrhagic shock enhanced concentration of PGE and other vasodilator PGs, produced in increased amounts by the kidney (and possibly other organs and tissues), appear in greater amounts in the systemic plasma because of the lung's altered function. These exert a decompensatory action on the peripheral vasculature.

Animals↗
PubMed1976

Primate kidney function in hemorrhagic shock as influenced by dibutyryl cyclic AMP.

Standardized hemorrhagic shock was employed to study alterations in electrolyte and water handling in the owl monkey, either normally hydrated or moderately dehydrated. Increase in fractional clearance of osmolarity,sodium, and calcium occurred with retransfusion after the hypotensive phase. In the hydrated animals, free-water clearance became positive, and the urine-to-plasma osmolarity ratio [(U/P)osM] decreased below 1.0. In the dehydrated animals, free-water reabsorption (TCH2O) decreased but remained negative,while (U/P)osM remained above 1.0. Dibutyryl cyclic AMP (DBcAMP) was infused into the renal arterial supply in an attempt to correct a possible deficiency of cyclic AMP production. In the hydrated group, free-water clearance (CH2O) became more positive with infusion, and (U/P)osM decreased even further, with no effect on fractional sodium clearance. Effects were less or absent in the dehydrated group. Possible explanations for the observed effects of DBcAMP are considered. It was concluded that the loss of concentrating power seen in hemorrhagic shock occurs at a step beyond the production of cyclic AMP by adenylate cyclase.

Animals↗
PubMed1976

Effect of hemorrhagic shock on renal release of prostaglandin E.

The effect of hemorrhage and reinfusion on renal release of prostaglandin E (PGE), arterial [PGE], mixed-venous [PGE], and renal function was observed in anesthetized dogs. Following hemorrhage to 60 mmHg arterial pressure, arterial [PGE] rose significantly from 405 to 740 pg/ml. Renal release of PGE remained near control (8 ng/min), as renal blood flow (RBF) decreased from 4.7 to 2.2 ng/min per gram kidney weight (KW). Mixed-venous [PGE] remained near the control value (960 pg/ml). Reinfusion of shed blood restored RBF to 4.0 ml/min per KW. Renal release of PGE rose significantly to 190 ng/min. Arterial [PGE] remained elevated, but mixed-venous [PGE] was not significantly different from control. Indomethacin, a prostaglandin synthesis inhibitor, caused a significant decrease in renal release of PGE. Arterial [PGE] remained elevated following treatment. The inhibition of PGE release from the kidney by indomethacin indicates that increased renal release of PGE following reinfusion is the result of accelerated PGE synthesis. The data suggest that the elevated arterial [PGE] may be the result of alteration of the handling of PGE by the lung.

Aminohippuric Acids↗