Cardiovascular instability continues to be one of the primary clinical
problems in hemodialysis. Acetate buffer in dialysate is one of the f
actors that may induce hypotension. Since uremia may have a direct eff
ect on the regulation of the cardiovascular system, the present study
was designed to investigate the separate effects of uremia and acetate
hemodialysis on blood pressure in anesthesized dogs, as well as the h
emodynamic parameters determined by invasive cardiovascular monitoring
. Animals were separated into four groups: (I) group I, hemodialysis w
ith acetate in controls; (2) group II, hemodialysis with acetate in ur
emic dogs; (3) group III, hemodialysis with bicarbonate in controls; a
nd (4) group IV, hemodialysis with bicarbonate in uremic dogs. Acute u
remia was induced by bilateral ureteral ligation and a 90-minute hemod
ialysis (acetate or bicarbonate) procedure was performed 72 hours late
r. The results obtained in this study show that, compared with dogs wi
th normal renal function, acute uremia resulted in an elevation in mea
n arterial pressure (MAP; 178 +/- 13 vs. 115 +/- 23 mm Hg, P < 0.01),
which was associated with an increase in cardiac index (CI) and left v
entricular stroke work index (LVSWI). In these dogs, the pulmonary cap
illary wedge pressure (PCWP; preload) and the systemic vascular resist
ance index (SVRI; afterload) were not different than controls. In urem
ic dogs, hemodialysis with acetate, but not with bicarbonate, decrease
d the MAP to values similar to controls. The decrease in MAP induced b
y acetate hemodialysis in uremic dogs was associated with a decrease i
n SVRI and PCWP. These results suggest that in dogs with acute uremia,
acetate hemodialysis (HD) decreases miocardial contractility that was
previously increased by a direct effect of uremia. In controls, aceta
te produced a moderate decrease in MAP that was the result of a mild d
ecrease in CI and SVR. Since PCWP was not significantly decreased afte
r acetate HD, the decrease in CI can be attributed to a mild decrease
in myocardial performance. In conclusion, this study in dogs suggests
that uremia enhances myocardial contractility directly. Acetate hemodi
alysis reduces this elevated miocardial contractility to normal values
.