INTRARENAL HEMODYNAMICS IN LOW-OUTPUT AND HIGH-OUTPUT CARDIAC-FAILUREIN RATS

Cardiac failure is multifactorial in causation, and the underlying phy siologic mechanisms are variable, yet their renal effects have been co nsidered more homogeneous. To investigate and compare the intrarenal h emodynamic characteristics in two experimental types (low and high-out put) of cardiac failure, renal micropuncture studies were performed in rats after myocardial infarction (MI) and arteriovenous fistula, resp ectively. Myocardial infarction was produced by ligation of the left m ain coronary artery and arteriovenous fistula by direct puncture of th e aorta and inferior vena cava below the renal arteries. Pressures and interrenal and glomerular dynamics were obtained using classic microp uncture techniques. Both forms of cardiac failure were characterized b y elevated left ventricular end-diastolic pressure (LVEDP), reduced me an arterial pressure, and increased cardiac mass. Left ventricular end -diastolic pressure was higher in MI rats, and effective renal plasma flow (ERPF) tended to be reduced in both forms of cardiac failure. The re were no apparent differences in effective renal plasma flow between two models. In addition, single-nephron plasma flow and single-nephro n glomerular filtration rate were reduced, and single-nephron filtrati on fraction and glomerular capillary pressure (P-G) were increased in both models. These changes were associated with higher afferent and ef ferent arteriolar resistances and lower ultrafiltration coefficients. Despite these similarities, P-G was higher in MI rats, yet LVEDP corre lated directly with P-G (r = 0.73; P < 0.001) and efferent arteriolar resistances (r = 0.72; P < 0.01). Therefore, although systemic arteria l pressure and effective renal plasma flow were similar in both models of cardiac failure, Po was significantly higher in MI rats with Base on these findings, it is suggested that LVEDP may provide the most sen sitive cardiac and systemic hemodynamic determinants of altered intrar enal hemodynamics in cardiac failure.