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Biomedical subjects

W A Bourland

Publications and source records attributed to W A Bourland.

8 recordsLinked to original sources
PubMed1992

Trauma to the proximal superior mesenteric artery: a case report and review of the literature.

Visceral arterial injuries account for a small but important portion of major abdominal vascular trauma. A case of proximal superior mesenteric artery trauma is presented. The advantages and drawbacks of the surgical approaches to these injuries are discussed. On the basis of a review of the literature describing the management of these injuries, ligation of the proximal superior mesenteric artery for trauma cannot be recommended. Prompt surgical intervention with revascularization offers the best chance for the survival of these critically injured patients.

Adult↗
PubMed1982

Pancreatitis induced renal vasoconstriction.

The etiology of renal vasoconstriction in acute pancreatitis remains obscure. The canine model of bile pancreatitis was used to determine whether hypovolemia or increased circulating levels of catecholamines are responsible for this phenomenon. Treatment of the pancreatitis was either with volume loading or alpha adrenergic blockade with Prazosin given both before and after the induction of pancreatitis. Neither pretreatment nor post-treatment with either volume loading or Prazosin protected the kidneys from the standpoint of mitigating renal vasoconstriction. To the contrary, treatment with alpha blockade produced the greatest decreases in renal blood flow.

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↗
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↗
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↗