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The animal model of the bulbar conjunctival and pral microcirculation disturbance induced by high molecular weight dextran in rabbit were reported In this experiment.The interre'ationship between the bulbar conjunctival microcired ation disturbance and the pial miciocirculation disturbance, has been observed. We found that the occurrence of the buibar conjunctival microcirculation was earlier than the pial microcirculation. The degrees of abnormal bulbar conjunctival micro-circulation were more prominent. than that of the pial one, however, the degrees of erythrocyte aggregation in the bulbar conjunctiva Was similar to that of the cerebral microcirculation. The experiment showed the bulbar conjunctival microciculation disturbance, to some degree may reflect the degree of the cerebral microcirulation disturbance in living animals.
RESUMO
In the experiment of atherosclerosis, the change of the cerebrovascular dynamic indexes (CVDI) was observed. In the atherosclerosis group, the values of carotid artery's mean flow (Qmcan), mean velocity (Vmcan), maximal velocity (Vmax), minimal velocity (Vmin) and cerebrovascular compliance for zero pressure (CO) were significantly decreased (P
RESUMO
The levels of platelet-activating factor (PAF) in cerebrospmal fluid (CSF) of patients with acute cerebral infarction were measured by the method of PAF-induced platelet aggregation quantitative analysis. The results indicated that the levels of PAF in CSF of patients with acute cerebral infarction were significantly increased (P
RESUMO
The effects of arginine vasopressin (AVP) on the contents of ir-?-EP and ir-Dyn A1-13 in ischemic brain regions of Mongolian gerbils were observed with radioimmunoassay in this study.The results showed that the contents of ir-?-EP were significantly increased and those of ir-Dyn A1-13 were decreased in ischemic cortex and hypothalamus after injection of AVP into the lateral ventricle. However, the contents of ir-?- EP were markedly decreased and those of ir-Dyn A1-13 were unchanged significantly in the ischemic cortex and hypothalamus after intraventricular infusion of AVP antiserum.
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In this study, the animal model of acute impaired pial microcirculation was stablished by intravenous injection of dextran of high molecular weight. The manifestations of the animal model of acute impaired pial microcirculation were as follows: blood flow in the pial microvessles was slowed down and presented granular or cotton-like pattern, and erythrocyte aggregation occurred.Ninety-eight rabbits were divided into group A (38 rabbits) and group B (60 rabbits).Solution of dextran with an average molecular weight of 25x104 dalton was used in group A and the animal model of acute impaired pial microcircuiation was established in 28 of 38 rabbits, and the successful duplication rate of animal models was only 73.6%.However, solution of dextran with an avera molecular weight of 49x104 dalton was used in group B and the model of acute impaired pial microcirc-ulatiori was established in 59 of 60 rabbits with a duplication rate of about 98.3%. The experimental results suggest that the dextran with an average molecular weight of 49x104 dalton was better than the dextran with an average molecular weight of 25x104 in producing the animal model of acute impaired pial microcirculation. The animal model can be used in the research on the impaired pial microcirculation and agents for improving pial microcirculation.
RESUMO
The purpose of this experiment was to study the role of arginine vasopressin (AW) in acute cerebral ischemic edema in mongolian gerbils. The results showed that intracerebroventricular injection (ICV) of AVP exacerbated the ischemic brain edema, while ICV of AW antiserum significantly decreased the ischemic brain edema. Nimodipine couldn't block this role of AW in ischemic brain edema. The cortical Na+ -K+ ATPase activity was significantly decreased, the contents of cAMP in the ischemic cortex and hypothalamus and the contents of cGMP in the hypothalamus were remarkably increased after ICV of AW. These suggest AW was involved in the pathophysiologic process of acute ischemic brain edema. And its mechanism might be the effect of AW on AW receptor mediated by cAMP, cGMP, and that in turn inhibited the Na+ -K+ ATPase activity of brain cell membrane, then exaggerated the formation of ischemic brain edema.