Severe hypotension during the decreasing phase of Gz stress in anesthetized rats wearing an anti-G suit.

INTRODUCTION: Physiological responses to +Gz stress have been reported in several studies. However, no reports exist on differences in arterial pressure responses between increasing and decreasing G phases. We hypothesized that +Gz stress and/or an anti-G support might disturb the circulation system and cause potential brain hypoperfusion, even if the anti-G support protects against G-induced loss of consciousness. METHODS: Dependency of +Gz magnitude, hemodynamic changes, renal sympathetic nerve activity (RSNA), and aortic blood flow (AoBF) were estimated in anesthetized rats to analyze the effects of +Gz stress and/or an anti-G support on arterial pressure at a level of the brain (APLB). The rats were exposed to +Gz using a centrifuge for small animals while wearing an anti-G suit. RESULTS: APLB remained at the control level while the anti-G suit was inflated. However, a decrease in APLB was observed twice during increasing and decreasing G phases using the anti-G suit. Hypotension in the decreasing C phase at +5 Gz was significantly deeper than that in the increasing G phase (47.5 +/- 7.7 vs. 29.6 +/- 3.0 mmHg). RSNA responses to Gz loads were greater in the decreasing G than in the increasing G phase (129.7 +/- 8.6 vs. 147.3 +/- 10.4%). Both AoBF and calculated vascular resistance were suppressed more significantly in the decreasing G than in the increasing G phase (38.3 +/- 4.4 vs. 34.4 +/- 3.4 ml x min(-1), 1.44 +/- 0.22 vs. 1.09 +/- 0.14 mmHg x min(-1) x ml(-1)). DISCUSSION: We conclude that transient excessive decreasing G hypotension may occur during the decreasing G phase, which may be due to anti-G suit functioning.

Teeth clenching and positive acceleration-induced cerebral arterial hypotension in rats.

INTRODUCTION: High positive acceleration (+Gz) stress is known to cause cerebral hypoperfusion, resulting in brain insults. Muscular contraction is reported to induce a pressor response. The effects of teeth clenching on cerebral hypoperfusion were examined. METHODS: The masseter muscle of anesthetized Sprague-Dawley rats was electrically stimulated to cause maximum clenching of the teeth. Arterial pressure at the level of the brain (APBr), heart rate, and central venous pressure were measured when rats were exposed to +1.5 Gz by using a centrifuge without an anti-C system. RESULTS: Acceleration of +1.5 Gz decreased APBr by 18.3 +/- 2.0 mmHg, which was reduced to 1.9 +/- 2.0 mmHg by masseter muscle contraction, but was not reduced by femoral muscle contraction. Stimulation of the masseter muscle but not the femoral muscle induced a pressor response of 11.8 +/- 2.1 mmHg, which was eliminated by dantrolene, a postsynaptic skeletal muscle relaxant. When masseter contraction was blocked by dantrolene, masseter stimulation did not reduce cerebral hypotension in the presence of +1.5-Gz acceleration (delta 18.9 +/- 2.6 mmHg). CONCLUSION: Our results suggest that teeth clenching induced a pressor response that prevented +Gz-induced cerebral hypotension, which suggests the possible development of a new anti-G method.