Hematocrit changes in the extra- and intraparenchymal circulation of the feline brain cortex in the course of global cerebral ischemia.
Based on distinctly different hemodynamic behavior of erythrocytes and plasma affecting properties of the circulating blood in vivo, such as apparent viscosity, flow resistance, axial streaming of erythrocytes, plasma skimming, etc., hematocrit (Htc) can have an apparent impact on tissue perfusion. Hematocrit also shows a diameter dependent decrease along the extraparenchymal arterial vascular routes that levels off being markedly lower in the microcirculation than in the central arterial blood. It was postulated that the impact of Hct may become a critical aspect of the macro- and microcirculatory compensatory mechanisms under ischemic conditions, when excessive fluid shifts between the extra- and intravascular compartments can in fact alter both systemic and local Htc, and when a decreased perfusion pressure sets the stage for sluggish flow velocities at which orientation of erythrocytes in the plasma stream can abruptly change and impair the macro- and microcirculation alike. To test this hypothesis, systemic (Htcs), feed (Htcf) and local hematocrit (Htcl) were simultaneously monitored in anesthetized and mechanically ventilated cats from the abdominal aorta, a pial artery of 100 micra in diameter and 500-600 cerebrocortical microareas of 0.01 cubic mm each respectively, by a television densitometric method while global cerebral ischemia was induced and maintained by adjusting the systemic mean arterial blood pressure to 40-50 mmHg by controlled arterial hemorrhage. Global cerebral ischemia was terminated when cerebrocortical microcirculation collapsed or shed blood completely got reinfused to the animal. The data show that under control conditions Htcf is 44% of Htcs, while hemoconcentration in the tissue brings Htcl up to 67% of Htcs. Under ischemic conditions, in cases of short survival time, the extraparenchymal arterial hemoconcentration can not be sufficiently compensated by intraparenchymal hemodilution and the microcirculation collapses under the conditions of lowering or moderately rising local tissue hematocrit. In case of longer survival , the rate of extraparenchymal hemoconcentration is increasingly lower and therefore the intraparenchymal hemodilution becomes more effective and prolonged. Due to factors most likely pertinent to the tissue proper, microcirculation collapses under abruptly developing secondary tissue hemoconcentration. Since terminal Htcl was only slightly higher than that at the beginning of the ischemic episode, attention to other hemodynamic and rheological factors in the microcirculation--not directly influenced by Htc--have been turned to.(ABSTRACT TRUNCATED AT 400 WORDS)
Eke
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2nd Department of Physiology, Semmelweis Medical University, Budapest, Hungary.
D000818:Animals; D001794:Blood Pressure; D002545:Brain Ischemia / Q000097:blood / Q000503:physiopathology*; D002415:Cats; D002540:Cerebral Cortex / Q000098:blood supply*; D002560:Cerebrovascular Circulation; D004912:Erythrocytes / Q000502:physiology; D005260:Female; D006400:Hematocrit; D006470:Hemorrhage / Q000503:physiopathology; D008297:Male; D010953:Plasma Volume; D012039:Regional Blood Flow