title: Intrarenal hemodynamics in low- and high-output cardiac failure in rats.
abstract: Cardiac failure is multifactorial in causation, and the underlying physiologic mechanisms are variable, yet their renal effects have been considered more homogeneous. To investigate and compare the intrarenal hemodynamic characteristics in two experimental types (low- and high-output) of cardiac failure, renal micropuncture studies were performed in rats after myocardial infarction (MI) and arteriovenous fistula, respectively. Myocardial infarction was produced by ligation of the left main coronary artery and arteriovenous fistula by direct puncture of the aorta and inferior vena cava below the renal arteries. Pressures and interrenal and glomerular dynamics were obtained using classic micropuncture techniques. Both forms of cardiac failure were characterized by elevated left ventricular end-diastolic pressure (LVEDP), reduced mean 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. There were no apparent differences in effective renal plasma flow between two models. In addition, single-nephron plasma flow and single-nephron glomerular filtration rate were reduced, and single-nephron filtration fraction and glomerular capillary pressure (PG) were increased in both models. These changes were associated with higher afferent and efferent arteriolar resistances and lower ultrafiltration coefficients. Despite these similarities, PG was higher in MI rats, yet LVEDP correlated directly with PG (r = 0.73; P < 0.001) and efferent arteriolar resistances (r = 0.72; P < 0.01). Therefore, although systemic arterial pressure and effective renal plasma flow were similar in both models of cardiac failure, PG was significantly higher in MI rats with higher LVEDP than in arteriovenous fistula rats.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Hypertension Research Laboratories, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
authors.forename: A
authors.initials: A
authors.lastname: Numabe
authors.forename: T
authors.initials: T
authors.lastname: Nishikimi
authors.forename: K
authors.initials: K
authors.lastname: Komatsu
authors.forename: E D
authors.initials: ED
authors.lastname: Frohlich
mesh_terms: D000818:Animals; D001164:Arteriovenous Fistula / Q000150:complications / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D002303:Cardiac Output, Low / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D005919:Glomerular Filtration Rate / Q000502:physiology; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology; D009399:Nephrons / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology*; D017596:Renal Plasma Flow, Effective / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology