Bilateral Nephrectomy Impairs Cardiovascular Function and Cerebral Perfusion in a Rat Model of Acute Hemodilutional Anemia.

Anemia and renal failure are independent risk factors for perioperative stroke, prompting us to assess the combined impact of acute hemodilutional anemia and bilateral nephrectomy (2Nx) on microvascular brain pO2 (PBrO2) in a rat model. Changes in PBrO2 (phosphorescence quenching) and cardiac output (CO, echocardiography) were measured in 2 different groups of anesthetized Sprague-Dawley rats (1.5% isoflurane, n = 5-8 per group) randomized to Sham 2Nx or 2Nx and subsequently exposed to acute hemodilutional anemia (50% estimated blood volume exchange with 6% hydroxyethyl starch) or time based controls (no hemodilution). Outcomes were assessed by ANOVA with significance assigned at p<0.05. At baseline, 2Nx rats demonstrated reduced CO (49.9±9.4 vs. 66.3±19.3 mL/min) and PBrO2 (21.1±2.9 vs. 32.4±3.1 mmHg)relative to Sham 2Nx rats (p<0.05 for both). Following hemodilution 2Nx rats demonstrated a further decrease in PBrO2 (15.0±6.3 mmHg, p<0.05). Hemodiluted 2Nx rats did not demonstrate a comparable increase in CO (74.8±22.4 vs 108.9±18.8 mL/min, p<0.001) after hemodilution which likely contributed to the observed reduction in PBrO2. This impaired CO response was associated with reduced fractional shortening (33±9 vs. 51±5 %) and increased left ventricular end systolic volume (156±51 vs 72±15 µL, p<0.001) suggestive of systolic dysfunction. By contrast, hemodiluted Sham 2Nx animals demonstrated a robust increase in CO and preserved PBrO2. These data support the hypothesis that the kidney plays a central role in maintaining cerebral perfusion and in initiating the adaptive increase in CO required to optimize PBrO2 during acute anemia.