Showing papers by "Joseph L. Izzo published in 1984"

Hemodynamic response to volume depletion in acutely uremic dogs.

Abstract: Hemodynamic response to volume depletion by isolated ultrafiltration was compared in uremic (U) and nonuremic (N) conscious dogs. Fluid was removed at a constant rate until mean arterial pressure (MAP) decreased to less than 80 mmHg. Initial MAP was higher in the uremic dogs [132 +/- 8.6 (SD) mmHg] than in nonuremic controls (106 +/- 12, P less than 0.001). Initial cardiac index [U 4.97 +/- 0.831 X min-1 X m-2, N 4.44 +/- 0.62] and total peripheral vascular resistance index [(TPRI) U 2,160 +/- 353 dyn X s X cm-5 X m-2, N 1,976 +/- 420] were slightly, but not significantly, higher in uremic animals. Initial central venous pressure, wedge pressure, and plasma norepinephrine level were greater in the uremic dogs. At the end point of volume depletion, both uremic and nonuremic animals had achieved similar levels of TPRI, despite greatly attenuated or absent increases in plasma renin activity in the uremic group. At end point, blood volumes and plasma norepinephrine levels were comparable. The increase in pulse rate was higher in the uremic animals (59 +/- 37 pulses/min) compared with controls (25 +/- 52, P less than 0.05). In an additional group of uremic dogs, cardiovascular responses to hemorrhage and isolated ultrafiltration were compared and found to be similar, after allowance for blood viscosity changes had been made. The data suggest that in acutely uremic conscious dogs, despite reduced renin-angiotensin responses, hemodynamic adaptation to rapid volume depletion is not impaired.

Renal norepinephrine overflow during graded renal nerve stimulation before and after beta-adrenoceptor blockade.

Abstract: These experiments were designed to determine if renal venous norepinephrine (NE) overflow provides a valid index of renal sympathetic nerve activity. In addition, we evaluated the effect of beta-adrenoceptor blockade on renal NE overflow during graded renal nerve stimulation in order to examine the possibility that presynaptic beta-adrenoceptors facilitate neuronal release of NE in the kidney. In 6 pentobarbital-anesthetized dogs, the renal nerves were transected to remove tonic nerve activity and the distal ends were electrically stimulated (8–25 V, 0.5 ms) over the range of 0.3–5.0 Hz for consecutive 4-min periods. NE overflow rate was calculated as the product of the veno-arterial NE concentration difference and renal plasma flow. Control values for NE overflow (−8.7 ± 1.8 ng/min) demonstrated net clearance of NE from the renal circulation. NE overflow rate rose to −3.1 ± 2.2, 1.0 ± 4.0, and 33.2 ± 15.4 ng/min at 0.3, 0.6, and 1.2 Hz stimulation, respectively, with no accompanying change in renal blood flow. At 2.4 and 5.0 Hz, renal blood flow decreased by 21 ± 4% and 37 ± 3%, but there was no further increase in NE overflow rate (38.8 ± 9.4 and 27.8 ± 6.5 ng/min). Propranolol (0.5–1.0 mg · kg−1 plus 0.4–0.5 mg · kg−1 · h−1 i.v., n = 4) did not alter the effect of nerve stimulation on either NE overflow or renal blood flow. Thus we were unable to demonstrate the presence of functional renal presynaptic beta-adrenoceptors. Further, our data indicate that renal norepinephrine overflow rate is not always a reliable index of renal nerve activity, since NE overflow was not proportional to renal nerve stimulation rate at frequencies high enough to cause vasoconstriction.