Splanchnic and splenic erythrocyte volumes decrease during postural changes and exercise to help maintain central blood volume and cardiac output. The contribution of this compensatory mechanism to hemodynamic stability during dialysis has not been studied, however. In 8 ESRD patients, age 51.0 +/- 4.5 years old, we measured changes in the splanchnic/splenic erythrocyte volume during dialysis by tagging the patients' erythrocytes with technetium and following abdominal radioactivity over time. Splanchnic radioactivity decreased to 90.2 +/- 3.8% (mean +/- SEM) of the baseline value after 2 hr of accelerated fluid removal (3.7 +/- 0.4 liters) during dialysis (DUF), while it remained relatively unchanged after two hours of dialysis without fluid removal (DD) [106.5 +/- 2.3%, P (DUF vs. DD) = 0.03]. Splenic radioactivity decreased to 89.2 +/- 5.0% of the initial value during DUF versus 103 +/- 3.8% during DD, but the decrease was noted only during the last 30 minutes of DUF and did not attain statistical significance. Autonomic nervous system integrity was measured by the spontaneous variation of the R-R interval during deep respiration (E/I ratio) and by the Valsalva ratio. The mean E/I and Valsalva ratios in the eight patients were 1.13 +/- 0.03 (+/-SEM) and 1.42 +/- 0.1 respectively, suggesting reasonably adequate autonomic nervous system functioning. The results suggest that contraction of the splanchnic, and possibly the splenic, vascular beds occurs during fluid removal associated with hemodialysis. The resultant addition of erythrocytes to the circulation may help maintain central blood volume and cardiac output.
The vasorelaxant effects of acetate in arginine vasopressin (AVP)-contracted rat tail artery strips were examined in order to study mechanism of action. Dose-dependent relaxation by acetate was found in the clinically important range of 4 to 16 mM. Relaxation was not due to complexing of ionized calcium, persisted after mechanical removal of the endothelium, and was not altered by pretreatment with indomethacin. Although acetate also inhibited contraction by alpha-1 and alpha-2 agonists, the relaxant effect was not altered by destruction of sympathetic nerve terminals using 6-hydroxydopamine. The degree of relaxation in this model by various anions correlated with their lyotropic properties; however, the vasorelaxant effect of acetate exceeded that which would be expected on the basis of its position in the lyotropic series. The vasorelaxant effect of acetate was shared by other short-chain fatty acids that can be conjugated with coenzyme A (CoA), such as propionate and malonate. In contrast, a much lesser or absent relaxant effect was found with nonfatty-acid precursors of acetyl CoA, such as pyruvate, lactate, and alanine. The vasorelaxant effect of acetate was abolished by pretreatment with DIDS, an inhibitor of organic anion uptake, suggesting that cellular uptake of acetate is essential to its vasorelaxant action. The results suggest that the relaxant effect of acetate in vascular smooth muscle is non-specific, is not mediated by prostaglandins, does not depend upon the presence of either endothelium or the sympathetic nervous system, and may be due to metabolism of acetate to acetyl CoA with attendant conversion of ATP to AMP.
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