Reperfusion after cerebral ischemia: influence of duration of ischemia.

Abstract

SUMMARYThe influence of the duration of ischemia on the pattern of cerebral blood flow in recirculation was studied in anesthetised rats. Severe incomplete cerebral ischemia (mean ischemic flow = 5.8 ± 0.4 ml/100 g/min) was produced by four-vessel occlusion and recirculation permitted after 15,30 or 60 minutes ischemia. All three groups showed an immediate hyperemia followed by hypoperfusion. Hyperemia was maximal following 15 minutes ischemia and least pronounced following 60 minutes ischemia (p = 0.0249). Hypoperfusion started most quickly following 15 minutes ischemia and was delayed following 60 minutes ischemia (p < 0.001). In established hypoperfusion there was no difference in flow between the three groups. The possible mechanisms of these changes in flow are discussed.Stroke Vol 17, No 3, 1986RECIRCULATION after cerebral ischemia is a common clinical event. It occurs after the spontaneous break-up of cerebral emboli and follows the removal of clips used for temporary hemostasis during surgery for aneurysm and arteriovenous malformation. Operations such as extracranial-intracranial by-pass are designed to increase circulation to chronically ischemic brain. The initial period of recirculation after ischemia is of paramount importance and two patterns of post-ischemic circulatory disturbance have been described, the 'no-reflow phenomenon' and 'hyperemia-hypoperfusion'. The no-reflow phenomenon was originally demonstrated as an absence of carbon black staining after 5-7 minutes global cerebral ischemia in rabbits 1 and has also been demonstrated in primates 2 and rats. 3 Noreflow can be reversed or prevented by recirculation at a satisfactory blood pressure, even if ischemia is prolonged. -3 Explanations for the no-reflow phenomenon have included blockage of the vascular lumen by platelets or red cell aggregates; 6 -7 change in blood viscosity; 8 local intravascular coagulation; 9 and direct capillary compression from edematous endothelial and glial cells. "12 The alternative pattern of post-ischemic circulatory disturbance is where an initial increase in cerebral blood flow, 'reactive hyperemia', is followed by a reduction in flow, 'delayed hypoperfusion'. This secondary hypoperfusion has been demonstrated in the isolated canine brain;13 following global cerebral ischemia in the cat, 14 dog, 15 monkey 16 and rat 17 and following focal cerebral ischemia in the cat. 18It has been difficult to reconcile these two postischemic circulatory changes. Recent work has suggested that the no-reflow phenomenon will follow complete cessation of cerebral blood flow and does not It is important to define the factors in ischemia that influence post-ischemic circulatory changes. In these studies, we have chosen to vary the duration of ischemia with a fixed ischemic flow in order to decide whether post-ischemic hyperemia and hypoperfusion are universal phenomena or whether the degree and duration of these events are influenced by the duration of the preceding ischemia. Methods Animal PreparationExperiments were performed in ...

Combined Contrast-Enhanced Ultrasound and rt-PA Treatment is Safe and Improves Impaired Microcirculation after Reperfusion of Middle Cerebral Artery Occlusion

“…reperfusion into a maximally vasodilated arterial bed (Dirnagl et al, 1994;Todd et al, 1986). In this context, it has been suggested that recovery of vascular smooth muscle tone may contribute to subsequent hypoperfusion (Todd et al, 1986).…”

“…In this context, it has been suggested that recovery of vascular smooth muscle tone may contribute to subsequent hypoperfusion (Todd et al, 1986). Animal studies have shown that ultrasound application can significantly improve tissue perfusion in rabbit muscle and myocardial ischemia after fixed arterial occlusion (Siegel et al, 2004;Suchkova et al, 2002).…”

Deterioration of baroreceptor reflex by transient global cerebral ischemia in dogs.

“…On the other hand, however, Smith et al (12) showed that some mor phological damages developed in the cerebral cortex during the 7-day recovery period fol lowing 4 to 10-min ischemia in the rat Transient cerebral ischemia is known to be followed by regionally heterogeneous circula tory disturbances such as the no-reflow phenomenon (1.3-15) and the post-ischemic hypoperfusion syndrome (15)(16)(17)(18)(19)(20), which may disturb functional recovery of the brain. Therefore, another possible explanation would be that the degree of post-ischemic hypoperfusion in the baroreflex pathway might be greater than that in the cerebral cortex, resulting in the selective attenuation of the baroreflex activity.…”

A new model of global postischemic reperfusion in rabbit

“…Although many models of global cerebral ischemia have been reported in gerbils (Yoshida et al, 1980), rats (Pulsinelli and Brierley, 1979;Todd et al, 1986), cats (Paschen et al, 1983), dogs (Jackson and Dole, 1979), and the primates (Branston et al, 1980), we consider that the rabbit should be chosen as the best candidate for the model of CPIR because the pattern of brain vessels in the rabbit is more similar to that in the primates and man than that in dogs and cats (Aguilar, 1963;Gu, 1983). In addition, the rabbit's size is bigger than rats, so it is easier to measure intracranial pressure, blood pressure, and to take more blood samples.…”