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Biomedical subjects

H E Williamson

Publications and source records attributed to H E Williamson.

At least 19 recordsLinked to original sources
PubMed1988

Interaction of cyclosporine and indomethacin in the rat.

The renal toxicity of cyclosporine has been reported to be due, at least in part, to a decrease in renal blood flow. Inasmuch as nonsteroidal antiinflammatory compounds also decrease renal blood flow, cyclosporine and such an agent (indomethacin) were given together to determine if there was an interaction in the kidney. Rats, 250-300 g, were divided into 4 groups: control, indomethacin (5 mg/kg), cyclosporine (25 mg/kg) and cyclosporine + indomethacin. At weekly intervals, renal excretion of creatinine/24 hrs and N-acetyl-beta-D-glucosaminidase activity in urine (NAG) were determined as well as body weights. At one week, values for creatinine, NAG and weight did not differ between the groups. At two weeks, the animals in the cyclosporine + indomethacin group showed decreased creatinine excretion and increased NAG excretion. At three weeks, 90% of the animals in the cyclosporine + indomethacin group were dead. Thus, when indomethacin and cyclosporine are given together, they interact to produce an increase in renal toxicity and lethality.

Animals↗
PubMed1986

Interaction of furosemide and phenytoin in the rat.

The interaction of phenytoin and furosemide was examined in rats. After 2 or more weeks of pretreatment with phenytoin, the diuretic activity of furosemide given orally was decreased. This was due primarily to a generalized decrease in absorption from the gastrointestinal tract. Following intravenous administration of furosemide to phenytoin pretreated rats, a decrease in diuretic activity also occurred. Excretion of furosemide was not altered. Thus, phenytoin pretreatment would also appear to interfere directly with the renal action of furosemide.

Administration, Oral↗
PubMed1985

Diuretic update.

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Acute Kidney Injury↗
PubMed1979

Renal actions of oxyphenbutazone.

Oxyphenbutazone decreased the renal excretion of sodium and water in anesthetized dogs. As these excretions decreased, the drug also produced a decrease in renal blood flow and in the glomerular filtration rate. Blood pressure increased slightly. These changes are consistent with an inhibition of renal prostaglandin synthesis and could explain why oxyphenbutazone is reported to produce weight gain and edema when used clinically.

Animals↗
PubMed1979

Effect of indomethacin and meclofenamate on canine mesenteric and celiac blood flow.

Two nonsteriodal antiinflammatory agents, indomethacin and meclofenamate, were found to produce a marked decrease in mesenteric blood flow, an increase in blood presure and no significant change in celiac blood flow. The initial effect of indomethacin on mesenteric blood flow differed from that seen with meclofenamate. Whereas meclofenamate induced a fall in mesenteric blood flow that was gradual in onset, indomethacin induced a marked vasoconstriction of the mesenteric bed that was immediate in onset and of short duration, which was followed by a decrease of slower onset similar to that seen with meclofenamate.

Animals↗
PubMed1979

Effect of furosemide on canine splenic arterial blood flow.

Furosemide has been reported to cause pathological changes in the intestines as a consequence of the decrease in splanchnic blood flow that it produces. In view of the pancreatic toxicities of this diuretic, it was of interest to examine the effect of the agent on blood flow to this organ. An electromagnetic flow probe, was placed around the splenic artery, a vessel which supplies a major fraction of pancreatic blood flow. Within 60 min after furosemide (1 mg/kg, iv) administration, splenic blood flow (SBF) decreased by 20% and the decrease paralleled the drug-induced diuresis. When the diuresis was prevented, the agent failed to affect SBF. Thus, furosemide causes a reduction in SBF, which appears to involve a mechanism dependent upon the volume reduction produced by the drug-induced diuresis.

Animals↗
PubMed1979

Decrease in hepatic blood flow during furosemide-induced diuresis.

The effect of furosemide on hepatic hemodynamics was investigated using electromagnetic flow probes positioned around the hepatic-portal vein and common hepatic artery of anesthetized dogs. Furosemide administration induced a vigorous diuresis and concomitantly decreased total hepatic blood flow. Hepatic arterial blood remained relatively stable. Thus, the decrease in total hepatic blood flow was due primarily to a decrease in portal blood flow. When furosemide was given to animals with ureters ligated to prevent extracellular volume contraction, the drug did not reduce total hepatic blood flow, portal blood flow or hepatic arterial blood flow. Thus, furosemide induces a decrease in total hepatic blood flow that appears to involve a mechanism dependent upon the volume contraction produced by the diuretic. The contraction causes a reduction in venous blood flow but not arterial blood flow to the liver.

Animals↗
PubMed1979

Effect of furosemide on peripheral venous compliance following ureteral ligation in the adult dog.

The effect of furosemide on peripheral venous compliance in the absence of the diuretic effect of the drug was examined. Following bilateral ligation of the ureters, adult dogs were given furosemide, 2 mg/kg. A significant increase in peripheral venous compliance was observed as early as ten minutes after the drug was given (120% of control), and an additional increase was seen at 60 minutes after administration of the drug (136% of control). No change in peripheral venous compliance was observed in animals receiving only the furosemide vehicle, nor was there any change in animals in which bilateral nephrectomy had been performed prior to the administration of furosemide. These results indicate that furosemide produces a significant increase in peripheral venous compliance, which is independent of its diuretic action. However, the presence of the kidneys appears to be necessary for this effect.

Animals↗
PubMed1978

Phenylbutazone-induced decrease in renal blood flow.

Phenylbutazone (Butazolidin), and anti-inflammatory agent, has been reported to decrease renal excretion of sodium and water. Whether or not an alteration in renal hemodynamics could be involved in producing these effects was tested in anesthetized dogs. Renal blood flow (RBF) was monitored with electromagnetic flow probes. After i.v. administration of phenylbutazone, 2 mg/kg, RBF fell by 20%. Glomerular filtration rate, sodium and water excretion were also decreased and blood pressure increased slightly. The reduction of RBF and glomerular filtration rate by phenylbutazone indicates that a hemodynamic mechanism could be involved in the retention of sodium and water induced by this agent. The decreased blood flow was correlated with a depressed renal secretion of prostaglandin E. Also, in animals pretreated with indomethacin, another inhibitor of prostaglandin synthesis, administration of phenylbutazone did not result in any additional changes in renal hemodynamics or excretion of sodium and water. In addition, phenylbutazone antagonized the ability of furosemide to increase RBF, an inhibition which has previously been shown to occur with indomethacin. Thus, phenylbutazone appears to alter renal mechanisms in a manner similar to indomethacin.

Animals↗
PubMed1978

Effect of furosemide on mesenteric blood flow in the dog.

Diuretic therapy has been implicated as a possible inciting factor in nonocclusive mesenteric infarction. In view of this possibility, the effect of furosemide on superior mesenteric arterial blood flow (MBF) was investigated using electromagnetic flow probes in pentobarbital anesthetized dogs. After administration of furosemide, 1 mg/kg iv, MBF decreased by 44%. To assess the role of extracellular volume depletion induced by the diuresis in reducing MBF, volume depletion was prevented by infusing isotonic saline at a rate matching urine flow. In these experiments, MBF was not decreased by furosemide. Thus furosemide induces a marked decrease in mesenteric blood flow and this hemodynamic action involves a mechanism that is dependent upon the volume depletion induced by the drug.

Animals↗
PubMed1976

Ethacrynic acid induced release of prostaglandin E to increase renal blood flow.

Ethacrynic acid administered to anesthetized dogs was found to increase the level of prostaglandin E as determined by radioimmunoassay in renal venous blood at the time when renal blood flow was increased by this agent. No change was found in the renal venous level of prostaglandin F. When ethacrynic acid was administered after treatment with indomethacin, which blocks the increase in renal blood flow induced by the natriuretic agent, no increase in the renal venous level of prostaglandin E was seen. Thus, the dilation of the renal vasculature would appear to be caused by a stimulation of synthesis and release of prostaglandin E by ethacrynic acid.

Animals↗
PubMed1975

Furosemide induced release of prostaglandin E to increase renal blood flow.

Levels of PGE in renal venous blood were found to be significantly elevated at the time RBF was increased by furosemide. Following indomethacin, a second dose of furosemide failed to increase RBF and levels of PGE in renal venous blood were not elevated. Levels of PGF and PGA were not affected by furosemide. The increase of PGE in renal venous blood at the time of renal dilation supports the hypothesis that furosemide increases RBF by releasing PGE. An intrarenal action of the released PGE is implied by this mechanism.

Animals↗