Total Cerebral Ischemia: Effect of Alterations in Arterial PCO₂ on Cerebral Microcirculation

Abstract

Radiolabeled 15-μm microspheres were used to examine alterations in regional CBF and cerebrovascular resistance in response to changes in arterial PCO2. Flow measurements were obtained before and 1–3 and 24 h after 12 min of total cerebral ischemia. Striking sensitivity of blood flow in all areas of the central nervous system was shown to changes in arterial PCO2 between 24 and 50 mm Hg during the control nonischemic period. Following 12 min of total cerebral ischemia, cerebrovascular resistance increased, producing a decrease in regional blood flow when the important controlling variables for CBF were held constant. One to 3 h after total cerebral ischemia, the effect of variations in arterial PCO2 on cerebral blood flow was almost completely abolished. Within 24 h after total cerebral ischemia, the sensitivity of CBF to changes in PCO2 was almost completely restored, whereas the secondary severe neurologic deficit remained. Therapeutic interventions following global cerebral ischemia, designed to ameliorate the “no-reflow” phenomenon and minimize residual ischemic neurologic damage, must take into account this marked early postischemic reduction in sensitivity to normally potent cerebrovasodilatory influences.

Response of the Cerebral Circulation to Hypocarbia in Postasphyxia Newborn Lambs

“…Nemoto et al (1 5), using a model of 15 min of global ischemia in dogs, showed no change in CBF from normocarbia as Paco, was lowered to 2.7 kPa (20 mm Hg) during the period of postischemic recirculation. Koch et al (16) …”

Mechanisms of ischemic brain damage

“…Such models have included ventricular fibrillation [11], aortic occlusion [12], brachiocephalic, and subclavian arterial occlusion in combination with hypotension, elevated intracranial pressure by neck cuff insufflation and intraventricular infusions [13], four-vessel occlusion (permanent occlusion of vertebral arteries with transient occlusion of carotids), or bilateral carotid occlusion in combination with hypotension [14,15]. In these animal models, specific neuronal populations in the brain are susceptible to injury.…”

Post–Cardiac Arrest Care

“…68 In addition to an increased intracranial pressure, perivascular edema, intravascular coagulation, and a loss of blood flow autoregulation may also be responsible for the beneficial effect of supranormal cerebral perfusion pressures after prolonged cardiac arrest. [95][96][97] In contrast, with shorter durations of cerebral ischemia or later after reperfusion, CO 2 responsiveness was maintained or restored such that hyperventilation after ROSC reduced cerebral blood flow and worsened neurologic outcomes compared with normoventilation. 33 Experimental evidence suggests that the CO 2 responsiveness of cerebral arteries is disturbed for the first several hours after prolonged ischemia such that arterial vasodilation in response to increasing PaCO 2 is abolished.…”