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To assess the effect of the Na concentration of cerebrospinal fluid (CSF) on arterial pressure regulation under dehydration, the Na concentration in CSF (Nacsf) was measured continuously with an Na-sensitive electrode in the lateral ventricle (LV) together with mean arterial pressure (MAP), central venous pressure (CVP) and cardiac output (CO) during and after hypotonic infusion (INF, approximately 200 mOsm/kg H2O, 5 microliters/min for 10 min) into the LV of dehydrated and pentobarbital anesthetized rats. Total vascular conductance (TVC) was calculated from CO/(MAP-CVP). Sino-aortic denervation was performed to eliminate any influence of arterial baroreflexes on MAP changed by Nacsf. After dehydration, MAP increased by 20 mmHg (p < 0.001) despite a 9% decrease in blood volume (p < 0.001) while Nacsf increased by 13 mEq/kg H2O (p < 0.001). This increase in MAP was attributed to the decrease in TVC. After hypotonic INF began, MAP and Nacsf decreased and the maximal decreases of -13 mmHg (p < 0.001) and -28 mEq/kg H2O (p < 0.001) were found at the end of INF, respectively. The changes in MAP (r = 0.97, p < 0.001), CO (r = 0.97, p < 0.001), and TVC (r = -0.90, p < 0.001) were highly correlated with the change in Nacsf during INF and the following 10-min recovery. These results suggest that the increase in Nacsf is involved in the maintenance of arterial pressure by decreasing TVC and by attenuating the decrease in CO caused by dehydration-induced hypovolemia.
Mian Chen (Mon,) studied this question.