John F. Gerkens

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The influence of sodium balance and furosemide administration on acute amphotericin B-induced nephrotoxicity has been investigated in the anesthetized dog. In sodium-depleted dogs, amphotericin B (1 mg/kg i.v.) reduced renal blood flow by 32% and glomerular filtration rate by 90% 40 min after the infusion and 32 and 65%, respectively, 140 min after(More)
The influence of intra-renal infusions of prostaglandin (PG) I2, PGE2 and PGD2 on renin secretion and renal blood flow was investigated in renally denervated, beta-adrenergic blocked, indomethacin treated dogs with unilateral nephrectomy. All three prostaglandins when infused at doses of 10(-8) g/kg/min and 10(-7) g/kg/min resulted in marked renal(More)
Blood was withdrawn at a constant rate from the cannulated carotid artery of an anaesthetized rat and perfused an ex vivo segment of tail artery cannulated at both ends and contained in an organ bath. Blood returned to the rat via a cannulated jugular vein. The tail artery was constricted and perfusion pressure increased by peri-arterial stimulation at 5 Hz(More)
Three groups of rats were fed a low-sodium diet. Groups 1 drank water and was treated with cyclosporine, 100 mg kg-1 48 h-1 p.o. for 3 weeks (low-salt-treated group). Group 2 drank 0.15 M saline and was also treated with cyclosporine (high-salt-treated group). Group 3 drank water and was treated with the vehicle (low-salt-vehicle group). Measurements were(More)
Several studies indicate that prostaglandin (PG) I2 is involved in the control of renin release. This investigation was performed to determine if the active possible metabolite of PGI2, 6-keto-PGE1, is also a renin secretagogue. The relative potencies of PGI2, 6-keto-PGE1 and 6-keto-PGF1 alpha on renin secretion rate (RSR) and renal blood flow (RBF) were(More)
The relationship between renal prostaglandin (PG)I2 biosynthesis and renin release was examined in conscious dogs before and during renal artery constriction. Dogs were chronically instrumented with femoral vein, femoral artery and left renal vein catheters and an inflatable cuff and electromagnetic flow probe were positioned on the left renal artery. After(More)
  • J F Gerkens
  • Clinical and experimental pharmacology…
  • 1987
1. Mesenteric perfusion pressure was measured in the in situ mesentery perfused at a constant rate with blood drawn from the carotid artery of the same anaesthetized rat. Increases in perfusion pressure were produced by mesenteric periarterial electrical stimulation. These responses were measured before and 30 min after the administration of frusemide (5(More)
A major limitation in the use of amphotericin B is its potential to cause nephrotoxicity. In animals, increased dietary sodium reduces renal toxicity. Experience with five patients in whom impaired renal function developed early during amphotericin B therapy is reported. In four of the patients, there was evidence of sodium depletion due to low sodium(More)
Administration of the antifungal agent amphotericin B causes a pronounced reduction in renal blood flow (RBF). Since amphotericin B induced renal vasoconstriction may contribute to the clinical nephrotoxicity of this drug, the purpose of these studies was to investigate the mechanism of amphotericin B induced renal vasoconstriction. To determine if the(More)
The polyene antibiotic, amphotericin B, causes an acute reduction in renal blood flow and glomerular filtration rate. The purpose of this study was to evaluate the hypothesis that the renal vascular response to amphotericin B can be blocked by aminophylline. Toward this end, the effect of aminophylline on the renal response to amphotericin B in(More)