Changes in the neural drive to abdominal expiratory muscles in hemorrhagic hypotension.

Abstract

The purpose of this study was to test the hypothesis that hemorrhage-induced hypotension increases the neural drive to the abdominal expiratory muscles in chloralose-urethan-anesthetized cats that are studied under conditions of constant arterial PCO2 (PaCO2) and hyperoxia. A secondary aim was to describe in detail the concomitant changes in inspired pulmonary ventilation (VI) and the pattern of breathing under these conditions. The rectified and integrated electromyogram (EMG) of the external oblique and rectus abdominis muscles and VI were recorded in moderate and severe hemorrhagic hypotension, leading to reductions in mean blood pressure of approximately 30 and 60%, respectively. The PaCO2 was prevented from falling, and the arterial PO2 was maintained at a hyperoxic level (> 200 mmHg) by adding CO2 and O2 to the inspired gas mixture. VI increased by 2.5- and 5-fold in moderate and severe hypotension (P < 0.05). The changes in VI were mediated exclusively by changes in tidal volume, indicating that the reflex did not alter the activity of respiratory rhythm-generating structures. The EMG of external oblique muscles averaged 2, 44, and 100% in control conditions and in moderate and severe hypotension, respectively; corresponding values in rectus abdominis muscles were 10, 28, and 100% (P < 0.05 for both muscles). Bilateral cervical vagotomy caused a one- to three-fold decrease in the ventilatory response to hemorrhage and abolished the increase in abdominal muscle EMG activities. In conclusion, hemorrhagic hypotension reflexly increases pulmonary ventilation and the neural drive to the abdominal muscles. The reflex is vagally mediated, but the location of the receptors was not identified.