Cardiac and vasomotor responses to hypertonic saline

Small volumes of 7.5% hypertonic saline (HTS) have been found effective for resuscitation from various types of shock. Recent studies suggest that the beneficial effects of HTS on the circulation are primarily attributed to peripheral vasodilation and increases in plasma volume and myocardial contractility. In this article, we examine the relative importance of both nitric oxide (NO) and the autonomic nervous system (ANS) to the cardiovascular effects of HTS. When administered rapidly into either normovolemic or hypovolemic dogs, HTS caused a significant and transient hypotension prior to cardiovascular improvement. Mean arterial pressure decreased 49% within 1 min after the onset of HTS intravenous infusion at a rate greater than 1 ml/kg/min. This acute hypotensive response was not caused by cardiac depression and was independent of ANS function. Inhibition of NO synthase activity attenuated the initial decrease in blood pressure associated with rapid infusion suggesting an involvement of NO activity in the vascular effects of HTS. Infusion of HTS at 1 ml/min directly into the circumflex artery increased blood flow (by 64%) and regional myocardial contractility (percent of systolic shortening increased from 11 to 13%). The increases in myocardial blood flow and contractile function were observed in both normovolemic and hypovolemic animals. These responses were independent of ANS blockade. The NO inhibition attenuated the coronary vasodilation induced by HTS, but did not alter,contractile function. Intracoronary infusion of HTS at higher doses were associated with arrhythmias and transient myocardial depression. Laboratory studies suggest that NO synthase activity may play a role in mediating the vasodilator effect of HTS. However, NO inhibition does not alter the effects of HTS on myocardial contractile function.