Intravenous infusion of hyperosmotic NaCl solution induces acute cor pulmonale in anesthetized rats

Abstract

Intravenous hyperosmotic NaCl infusion is an effective treatment for circulatory shock. However, a fast infusion rate (2 mL/kg at the rate of 1 mL/s) induces transient hypotension. This response has been reported to be due to decreased total peripheral resistance and/or decreased cardiac performance. Although the hypotension is transient and recovers within 2 min without detrimental consequences, it is important to understand the associated hemodynamics and mechanisms. We found that the hypotensive effect was larger with intravenous NaCl infusion than with intra-aortic infusion, indicating that change in cardiac performance played a more significant role than change in peripheral resistance. NaCl infusion induced an increase in pulmonary vascular resistance and central venous pressure and a decrease in right ventricular dP/dt max, suggesting acute cor pulmonale. Diastolic ventricular crosstalk-induced left ventricular failure was also observed. Hyperosmotic NaCl-induced hypotension was therefore mainly due to a combination of acute cor pulmonale and left ventricular failure.

Abnormal sodium and water homeostasis in mice with defective heparan sulfate polymerization

“…This is supported by previous studies that have demonstrated that the transient BP reduction, which is normally seen after rapid hypertonic NaCl infusion and was present in controls, but absent in Ext1 +/- Ext2 +/- mice, is caused by a decrease in vascular resistance [33–36] This transient BP reduction could not be prevented by hexamethonium, a nicotinic cholinergic antagonist, indicating that the decrease in vascular resistance is not of higher neurological origin but is caused by local factors that influence vasodilation such as nitric oxide. [33, 34]…”

Reduced carotid baroreceptor distensibility-induced baroreflex resetting contributes to impairment of sodium regulation in rats fed a high-fat diet

“…A decrease in arterial compliance is observed in obese subjects and animals (2,8,39,42); thus, it is possible that higher AP is required to activate the baroreceptors. Because infusion of hyperosmotic NaCl solution is known to increase plasma volume and AP (1,43), we hypothesized that sodium regulation via the baroreflex might be impaired in response to chronic hyperosmotic NaCl load in rats fed a high-fat diet. To examine this hypothesis, we conducted the following experiments in rats fed a normal-fat diet or a high-fat diet: 1) we determined mean AP, water, and sodium balance, and norepinephrine excretion in response to chronic infusion of various concentrations of NaCl via a venous catheter, 2) we determined arterial baroreflex characteristics using static openloop analysis, and 3) we determined distensibility of the common carotid artery.…”