Role of central nervous system in renal nerve activity during prolonged hemorrhagic shock in dogs.

The contribution of sympathetic efferent outflow through the central nervous system (CNS) during prolonged hemorrhagic hypotension of 50 mmHg was examined in anesthetized dogs. Mean blood pressure, heart rate, and renal nerve activity (RNA) were recorded simultaneously after arterial bleeding for 2 h. In animals with an intact neuraxis, hemorrhage to approximately 50 mmHg increased RNA to 180 +/- 12% of control level at 5 min after bleeding, but returned close to control level after 10 min. A secondary increase in RNA followed, with its maximum (280 +/- 12%) at 30 min after bleeding. Then RNA gradually decreased so that at end of experiment (120 min after bleeding) RNA was 10 +/- 9% of control. The initial increase in RNA was abolished by denervation of afferents from carotid sinus and cardiopulmonary regions, but secondary RNA response during hemorrhagic hypotension was similar to that in the intact group and occurred when the head region of animals was exposed to a hypotension of 50 mmHg, and perfusion to peripheral regions of the body was maintained near normal range. However, when perfusion to the head was maintained at a steady level and peripheral regions were exposed to hypotension of 50 mmHg, RNA response did not change significantly. These results provide evidence that prolonged hemorrhagic hypotension, which induces severe brain ischemia, causes biphasic sympathetic outflow via the CNS. The increase in sympathetic activity was followed by decrease with time. This decrease may contribute to the pathogenesis of vasomotor paralysis occurring at the irreversible stage of hemorrhagic shock.