Prevention of renal cortical ischemia during aortic clamping with prostaglandin E1

E. J. Arbid, A. G. Hakaim, W. W. LaMorte and J. O. Menzoian
Section of Vascular Surgery, Boston Mass University Medical Center.

OBJECTIVES: To investigate the effects of aortic clamping and prostaglandin E1 on systemic hemodynamics and renal cortical and medullary blood flow by means of continuous intraparenchymal laser Doppler fluorometry. DESIGN: Experimental animal study in a porcine model. With the animal under general anesthesia after hemodynamic monitoring was instituted, surgical exposure was obtained through a small left retroperitoneal incision. The kidney was left undisturbed. Intraparenchymal laser Doppler probes (0.44 mm in diameter) were inserted in the renal cortex and medulla. In the first group of six animals, systemic hemodynamic variables, urine output and renal cortical and medullary flow were measured at baseline after 60 minutes of equilibration, and after 15 minutes of aortic clamping and unclamping. Data are given as mean +/- SE. INTERVENTION: In another six animals, prostaglandin E1 (20-micrograms intravenous bolus given over 1 minute) was given before clamping, and the same variables were recorded. RESULTS: In the first group, aortic clamping caused no change in cardiac output or filling pressures. Cortical blood flow decreased from 40.4 +/- 3.7 to 33.3 +/- 2.7 mL/100 g per minute (P < .0004) after clamping, and to 27 +/- 2.3 mL/100 g per minute (P < .0001) after unclamping, and was associated with a decrease in urine output from 3.2 +/- 0.5 to 2 +/- 0.2 mL/min (P < .0013). Medullary flow remained the same at 9.2 +/- 0.8, 10 +/- 0.3, and 9.8 +/- 0.6 mL/100 g per minute, respectively. These adverse effects were prevented when prostaglandin E1 was given before clamping. There was an initial drop in blood pressure (100 +/- 4 to 89 +/- 5 mm Hg, P < .0004), but cardiac output (43.3 +/- 5.8 L/min) and filling pressures (6 +/- 1 mm Hg) were unchanged. Cortical flow was preserved during the entire period of clamping and unclamping (43.3 +/- 5.8 mL/100 g per minute). Medullary flow remained unchanged (10 +/- 0.8 mL/100 g per minute). Urine output increased from 2 +/- 0.3 to 3.4 +/- 0.6 mL/min (P < .006). CONCLUSIONS: In this animal model, infrarenal aortic clamping causes a significant decrease in renal cortical flow and urine output with no significant changes in filling pressures, cardiac output, or medullary blood flow. These adverse effects are prevented by pretreatment with prostaglandin E1, which prevents cortical ischemia and maintains brisk diuresis.