The role of the vagus nerve in hypertonic resuscitation of hemorrhagic shocked dogs.

I.T Velasco,R.C Baena

doi:10.1590/s0100-879x2004000300020

Abstract

Previous studies have suggested a critical role for the vagi during the hypertonic resuscitation of hemorrhagic shocked dogs. Vagal blockade prevented the full hemodynamic and metabolic recovery and increased mortality. This interpretation, however, was challenged on the grounds that the blockade also abolished critical compensatory mechanisms and therefore the animals would die regardless of treatment. To test this hypothesis, 29 dogs were bled (46.0 +/- 6.2 ml/kg, enough to reduce the mean arterial pressure to 40 mmHg) and held hypotensive for 45 min. After 40 min, vagal activity was blocked in a reversible manner (0 masculine C/15 min) and animals were resuscitated with 7.5% NaCl (4 ml/kg), 0.9% NaCl (32 ml/kg), or the total volume of shed blood. In the vagal blocked isotonic saline group, 9 of 9 dogs, and in the vagal blocked replaced blood group, 11 of 11 dogs survived, with full hemodynamic and metabolic recovery. However, in the hypertonic vagal blocked group, 8 of 9 dogs died within 96 h. Survival of shocked dogs which received hypertonic saline solution was dependent on vagal integrity, while animals which received isotonic solution or blood did not need this neural component. Therefore, we conclude that hypertonic resuscitation is dependent on a neural component and not only on the transient plasma volume expansion or direct effects of hyperosmolarity on vascular reactivity or changes in myocardial contraction observed immediately after the beginning of infusion.

Highlights

Previous studies have suggested a critical role for the vagi during the hypertonic resuscitation of hemorrhagic shocked dogs
In 1980, we demonstrated that the circulatory effects of severe blood loss (40-50 ml/ kg) in dogs could be successfully reversed to virtually normal function and indefinite survival by a single intravenous injection of a small volume (4-5 ml/kg) of 7.5% NaCl [1]
Our initial findings were confirmed in a canine model of selective lung denervation [3], and reinforced the importance of these neural pathways for the hypertonic resuscitation of hemorrhagic shocked dogs [3]

Summary

Introduction

In 1980, we demonstrated that the circulatory effects of severe blood loss (40-50 ml/ kg) in dogs could be successfully reversed to virtually normal function and indefinite survival by a single intravenous injection of a small volume (4-5 ml/kg) of 7.5% NaCl (hypertonic resuscitation) [1]. We hypothesize that a neural pathway participates directly in the action of hypertonic saline on the recovery from hemorrhagic shock. We acknowledge that this neural pathway does not consist only of a single vagal reflex, but rather includes an integrated response with afferent and efferent responses coming from several tissues and organs. Three distinct protocols of hemorrhagic shock resuscitation were used: 1) hypertonic solution (HS group, 4 ml/kg 7.5% NaCl), 2) isotonic solution (IS group, 32 ml/kg 0.9% NaCl), or 3) total shed blood replacement (blood group) In all these groups, vagal reflex was blocked by cooling the vagus nerve for 15 min, during the whole resuscitation procedure. The response of the vagal blocked animals to the resuscitation treatment provided information about the presence of the neural component in the action of hypertonic saline

Material and Methods

Results

Discussion