Abstract
Occurrence of no-reflow phenomenon (NRP) has been repeatedly reported in various experimental models of cerebral ischemia. These models were, however, those of cessation of arterial blood supply to the brain by obliteration of arteries. Since cerebral blood flow (CBF) is lowered by raised intracranial pressure (ICP), occurrence of NRP in such an experimental model is also conceivable. In the present study, the mode of occurrence of NRP was investigated in a raised ICP model in dogs.
After immobilization by intravenous infusion of Galamine, artificial ventilation was continued to maintain the normal level of arterial blood gases. Pressure of 200 mmHg was applied to the cisterna magna for 15 min by infusion of warmed saline. CBF was monitored by a double-needle type thermocouple. The cisterna magna pressure, arterial blood pressure, EEG and cerebral impedance according to the method of Mori et al. were continuously recorded on a polygraph.
Three hours after cisternal infusion, the brain was perfused with carbon black solution (Pelikan biological ink) via the thoracic aorta of a pressure of 120 mmHg. Prior to sacrifice, 50 ml of 5 % Evans blue was injected intravenously. Specimens for electron microscopy were taken by core-biopsy in a few dogs of each experimental groups.
The dogs were divided into three groups. Group I: (5 dogs) Only cisternal infusion was carried out. Group II : (16 dogs) The systemic arterial pressure was lowered to 60-80 mmHg by administration of Arfonad during cisternal infusion. Post-ischemic (PI) arterial pressure was brought up to the normal level by administration of Angiotensin II and Norepenephrine as quickly as possible. Group iII : (5 dogs) Immediately after cisternal infusion combined with arterial hypotension as in group 1 1, cerebral perfusion was carried out.
In group I, very rapid and pronounced appearance of reactive hyperemia (RH) was noted, indicating decrease of cerebral vascular resistance (CVR). EEG activity recovered almost completely and the result of cerebral perfusion was also normal. In the group II, however, the appearance of RH was slower and less pronounced than in group I (group II-A, 10 dogs), or entirely absent (group II-B, 6 dogs). Since PI cerebral perfusion pressure was kept in almost the same range in all the groups, this marked reduction of CBF in group II was ascribed to increase of CVR, i.e., presence of NRP. Occurrence of NRP was further confirmed in group f, in which cerebral perfusion carried out immediately after cisternal infusion revealed extensive non-filling of parenchymal capillary networks.
As seen in the courses of CBF and cerebral impedance, NRP was transient in group II-A and persistent in group II-B. Recovery of CBF and appearance of RH always preceded the normalization of cerebral impedance and recovery of CBF.
Presence of cerebral edema was confirmed in group II-B by macroscopic and electron-microscopic observations.There was also leakage of Evans blue in the cerebral parenchyma. Although this cerebral edema apparently seems due to the result of persistence of NRP, further investigations are required to clarify their causal relationship.
