Sympathetic responses during hemorrhagic shock

Introduction

Hemorrhagic shock is associated with adrenergic discharge that has been linked to neurohumoral and immune inflammatory responses, vasoconstriction and end-organ perfusion deficits. Our goal is to characterize the sympathetic activity to hemorrhage in tissues with a rich supply of sympathetic nerves (deferens duct).

Methods

Seventy anesthetized male Wistar rats were submitted to femoral artery and vein catheterization for mean arterial pressure (MAP) measurement and blood withdrawal to reach a MAP of 40 mmHg. Deferens ducts were removed from rats after 10 minutes, 30 minutes and 60 minutes, and were placed in isolated organ baths between two platinum electrodes for transmural electrical stimulation (TES) (0.1–20 Hz, 1 ms, 60 V). This technique allows the evaluation of neurotransmissors released by sympathetic nerves (noradrenaline and ATP).

Results

Controls maintained a MAP of 105 ± 3 mmHg in all experimental groups. Hemorrhaged rats presented a MAP of 39 ± 3 mmHg after 10, 30 or 60 minutes. The contraction profile after ATP and noradrenaline after TES were similar between controls and hemorrhaged rats. The amplitude was greater, however, for the three hemorrhaged groups. The addition of tetrodotoxin abolished contractions induced by TES, confirming the neurogenic nature of those contractions. The ATP-mediated contraction was blocked by the selective P₂ purinoreceptor antagonist suramin. Noradrenalin-mediated contraction was blocked by the prazosin, a selective α-adrenoreceptor.

Conclusion

We conclude that, based on the increased amplitude contraction induced by both noradrenaline and ATP, sympathetic nerve activity is increased in hemorrhagic shock animals.