Key result
Prostaglandin inhibition during suprarenal aortic cross-clamping in dogs increased plasma endothelin, reduced GFR, and caused marked renal vasoconstriction, which was prevented by renal artery clamping.
Why the study?
Does prostaglandin inhibition affect circulating endothelin and renal hemodynamics during acute ischemic renal dysfunction from suprarenal aortic cross-clamping in dogs?
Does prostaglandin inhibition affect circulating endothelin and renal hemodynamics during acute ischemic renal dysfunction from suprarenal aortic cross-clamping in dogs?
Prostaglandin inhibition during suprarenal aortic cross-clamping in dogs leads to increased circulating endothelin, reduced GFR, and marked renal vasoconstriction.
Alerts to prostaglandin-endothelin interplay in canine ischemic injury; leaves open human relevance during aortic surgery.
This study was undertaken to investigate circulating endothelin (ET) and associated renal hemodynamics in the acute ischemic renal dysfunction associated with suprarenal aortic cross-clamping (ACC) in the presence and absence of prostaglandin inhibition in the anesthetized dog. Second, the modulating action of exogenous atrial natriuretic factor (ANF) was also investigated. In Group I (ACC; N = 6), ACC was performed in the absence of prostaglandin inhibition. No change in mean arterial pressure, GFR, RBF, renal vascular resistance, or ET was noted 2 h after reperfusion when compared with baseline values. In the presence of prostaglandin inhibition with indomethacin (10 mg/kg iv) (Group II, ACC + INDO; N = 10), an increase in plasma ET was first noted to be elevated above baseline ET in Group I as well as during and 2 h after ACC in association with a reduction in GFR, marked renal vasoconstriction, and a sustained increase in arterial pressure. To evaluate the role of the kidney in this increase in ET, another group (Group III, ACC + INDO + NEPH; N = 6) was investigated in the presence of prostaglandin inhibition, and bilateral renal artery clamping was performed 30 min before ACC and maintained throughout the protocol to simulate nephrectomy. In this group, plasma ET concentrations did not increase during ACC. Because ANF may antagonize the renal actions of ET in vivo and may suppress ET release in vitro, the action of ANF upon GFR and plasma ET was evaluated in Group IV (ACC + INDO + ANF; N = 6).(ABSTRACT TRUNCATED AT 250 WORDS)
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Sandok et al. (1992) studied Acute ischemic renal dysfunction (n=28). Prostaglandin inhibition (indomethacin) during suprarenal aortic cross-clamping vs. Suprarenal aortic cross-clamping without prostaglandin inhibition was evaluated on Circulating endothelin and renal hemodynamics. Prostaglandin inhibition during suprarenal aortic cross-clamping in dogs increased plasma endothelin, reduced GFR, and caused marked renal vasoconstriction, which was prevented by renal artery clamping.
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