Correlation of cerebral microvascular circulation with vital signs in cerebral compression and the validity of three concepts: vasodilation, autoregulation, and terminal rise in arterial pressure.

Abstract

Vasodilation, autoregulation, and rising arterial pressure are three common concepts in cerebral compression, believed to improve cerebral blood flow to maintain the brain's nutrition. However, these concepts are unclear, unproven, and based on assumptions. This study aimed to correlate cerebral circulation with alterations of vital signs and to evaluate the above concepts based on physics and hemodynamics. Without new animal experiments, a large amount of data: recording of vital signs, long movies of cerebral circulation, and numerous photos of histological examination and microvessels obstruction in cerebral compression in cats was studied, and only partial and preliminary results were reported in 1970. The experiments were supported by an NIH grant for head injury, done before the 1985 Institutional Animal Care and Use Committee requirement. The advent of digital technology facilitated digitizing and stepwise correlating them and evaluating the validity of the above concepts. As cerebral compression increased intracranial pressure (ICP), veins dilated, not arteries, and arterial microvessels obstructed, diminished, and stopped cerebral circulation. Simultaneously, vital signs deteriorated, and pupils became fixed and dilated. There was no evidence for what is believed as autoregulation. In cerebral compression, rising ICP obstructs cerebral arterial microvessels while simultaneously deteriorating vital signs. There is no evidence for dilatation of the arteries; only veins dilate, best-called venodilation. There is no evidence of autoregulation; what occurs is a cerebral compartmental syndrome. The terminal rise of arterial pressure is the hemodynamic result of cerebral circulation cessation, overloading the aorta. None of the concepts benefit the brain's nutrition.