Afferent Pathways Involved in Cardiovascular Adjustments Induced by Hypertonic Saline Resuscitation in Rats Submitted to Hemorrhagic Shock

Abstract

The peripheral hyperosmolarity elicited by intravenous infusion of hypertonic saline (HS) can be beneficial in treating hemorrhagic shock. However, the neural mechanisms involved in this resuscitation remain unknown. The present study sought to determine the effects of selective baroreceptor denervation on arterial blood pressure response during HS resuscitation in rats submitted to hemorrhagic shock. Male Wistar rats (280-320 g) were anesthetized with thiopental sodium (40 mg/kg, i.v.), and the femoral artery and jugular vein were cannulated for MAP and heart rate recording and HS infusion (3 mol/L NaCl; 0.18 mL/100 g body weight, >2 min). Hemorrhagic shock was obtained by withdrawing blood over 30 min until a MAP of 60 mmHg was obtained. This level of MAP was maintained for a further 30 min through subsequent blood withdrawal or reinfusion. Next, animals were divided into selective aortic and/or carotid denervation or sham groups before infusing HS. Results showed that in the sham group (n = 12), HS infusion increased MAP to levels close to baseline (from 65 +/- 3 to 112 +/- 5 mmHg, 10 min after HS). In the aortic denervated group (n = 10), HS infusion also increased MAP (from 54 +/- 3 to 112 +/- 5 mmHg, 10 min after HS). In contrast, in the carotid denervation group (n = 8), the increase in MAP induced by HS infusion was abolished (from 53 +/- 3 to 73 +/- 12 mmHg, 10 min after HS). These results indicate that in hemorrhaged rats, HS infusion produces a pressor effect that is likely to be mediated through carotid rather than aortic baroreceptors.

Use and Effect of Vasopressors after Pediatric Traumatic Brain Injury

“…However, in this study, we did not find a statistically significant difference in hemodynamics between the vasopressors, although there was a trend for higher MAP and CPP with norepinephrine per our a priori analyses. In post hoc analyses, however, this trend for improved outcome in patients receiving norepinephrine appears to be partly due to the fact that a greater proportion of patients in this group received hypertonic saline, which has been shown to have a vasopressor effect [23,24,25,26,27], and to the longer time to vasopressor start. …”

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

“…A possible action on the carotid bodies is suggested by the finding that sinoaortic denervation attenuated the recovery of MAP in response to hemorrhagic resuscitation with hypertonic saline (6). An intact innervation of the lung has been suggested to be essential for the full hemodynamic response to hypertonic saline (16,39), but other studies have questioned this hypothesis (1).…”

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

“…Several lines of evidence have suggested that, besides their well-known role in arterial blood pressure regulation, aortic and carotid afferents are also involved in cardiovascular adjustments induced by acute changes in volume or composition of the extracellular compartment (2,3,5,(19)(20)(21)(22)(23)(24). In a previous study, Morris and Alexander (2) showed that the ANP release after hypernatremia is severely reduced after sinoaortic denervation (SAD).…”

“…Recently, we showed that selective denervation of carotid afferents abolished the recovery of arterial blood pressure induced by infusion of hypertonic saline in rats submitted to hypotensive hemorrhage (21). In that study, carotid afferents were removed after the induction of hemorrhagic shock and mean arterial pressure was lower than 60 mmHg, i.e., below afferent threshold.…”