engleski

HYPOTENSION AND SYMPATHOINHIBITION MEDIATED BY SEROTONIN RECEPTORS IN THE ROSTRAL VENTROLATERAL MEDULLA DURING SEVERE HEMORRHAGE

Introduction: Acute loss of blood volume evokes a drastic fall in blood pressure and heart rate, which can be life threatening. Hypotension and sympathoinhibition can be evoked by stimulation of serotonin 1A receptors in rostral ventrolateral medulla. Background data suggests that a central serotonergic mechanism mediates the sympatho-inhibitory response to severe hemorrhage, yet the site of actions and receptor subtype remain to be determined. Present study was undertaken to examine the role of serotonin 1A receptors in the rostral ventrolateral medulla in the mediation of the hypotensive and sympathoinhibitory responses to severe hemorrhage. Materials & Methods: Hemorrhage was performed in pentobarbital sodium-anesthetized rats withdrawing the blood from arterial line (1 ml/min to 50 mmHg). Blood pressure was monitored and sympathetic nerve activity recorded before, during and 20 min after hemorrhage. Results: Response to hemorrhage consists of a fall in arterial blood pressure and an initial baroreflex increase in renal sympathetic nerve activity followed by a rapid decline in blood pressure and decrease in renal sympathetic nerve activity. In animals in which the specific serotonin 1A receptor antagonist WAY-100635 was microinjected into the rostral ventrolateral medulla, the fall in blood pressure after hemorrhage was delayed and attenuated while renal sympathetic nerve activity was increased and maintained above baseline. Conclusion: These data suggest that hypotension and sympathoinhibition in response to severe hemorrhage are mediated by serotonin 1A receptors in the rostral ventrolateral medula.

sympatethic nerve activity; serotonin; sympathoinhibition; hemorrhage

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