The effects of negative pressure to the lower body (LBNP) which can well simulate the effects of positive acceleration on the cerebral blood flow and temperature were studied in 24 unanesthetized rabbits. Cerebral blood flow measured by the doubled heated thermoelectric flow probes increased during the application of lesser LBNP (-10-20 mm Hg). The increase of the flow was especially prominent in the animals not repeatedly exposed to greater negative pressure, and indicated the participation of some intrinsic regulatory mechanisms of increasing blood flow against the diminution of carotid arterial blood pressure. Cardiac acceleration with no change in brain temperature was also a characteristic feature under exposure to lesser LBNP.
When the animals were subjected to greater stress of LBNP (-50-80 mm Hg), cerebral blood flow decreased with rather complicated changes in brain temperature. Cardiac acceleration progressed, but in some cases a relative bradycardia appeared by the end of the 1 minute of application. With the release of LBNP, cerebral blood flow increased, but the increase was not prominent, despite of a marked overshoot of carotid arterial pressure.
A marked bradycardia with irregular cardiac rhythm, which might be a sign of cardiac decompensation developed by repeated exposures to greater LBNP. Cerebral blood flow decreased markedly under exposures to LBNP after which it increased profoundly. Brain temperature fell approximately by 0.3°C. after the release of negative pressure. The increase of cerebral blood flow after the release of negative pressure is probably due to passive dilatation of cerebral vessels after direct inhibition of neurogenic casoconstrictor center in which developed some irreversible functional destruction by the repeated exposure to greater LBNP.
Brain temperature was rather closely but inversely related to the changes in cerebral blood flow in many cases. It seems, therefore, very likely that in such circumstances the cerebral tissues may be cooled by the arterial blood passing through the vascular trees of the brain, and in this way this investigation could throw a little light on the central mechanism of temperature regulation. The mechanism of the epileptiform seizures frequently observed during and after exposures to positive acceleration may be interpreted by the changes in cerebral hemodynamics as described in this paper.