ABSTRACT
Objective To investigate the effects of prescription of nourishing blood and stretching of stoke (PNBSS) on the levels of TXB2 and 6-Keto-PGF1αin serum of patients with acute ischemic cerebrovascular disease (AICD);To discuss its action mechanism in AICD treatment. Methods Ninety patients with AICD were randomly divided into trial group and control group, 45 cases in each group. The control group received western routine treatment, while the trail group received the western routine treatment plus PNBSS, one dose per day, for one week. Rating scale of neurologic deficit was employed to evaluate treatment effectiveness. Venous blood was collected before the treatment and on the 3rd and 7th days of treatment. Levels of TXB2 and 6-Keto-PGF1αin serum were detected respectively. Results The score of neurologic deficit of post-treatment in two groups apparently decreased compared with baseline (P<0.01), and score of neurologic deficit in trial group on 7th day was lower than that of control group (P<0.05). The total effective rate in trial group was 93.3%, which was apparently higher than that of control group (84.4%). The level of TXB2 in serum and ratio of TXB2/6-Keto-PGF1α (T/P) in two groups on 3rd and 7th days remarkably decreased compared with baseline (P<0.01), while the level of 6-Keto-PGF1α in two groups on 3rd and 7th days was higher than that of baseline (P<0.01). Meanwhile, the level of TXB2 and ratio of T/P in two groups on 7th day were apparently lower than that of 3rd day (P<0.01), and the level of 6-Keto-PGF1αon 7th day was higher than that of 3rd day (P<0.01). The level of TXB2 in serum and ratio of T/P on 3rd and 7th days in trial group were apparently lower than that of control group (P<0.01, P<0.05), while the level of 6-Keto-PGF1α on 3rd and 7th days in trial group was apparently higher than that of control group (P<0.01, P<0.05). Conclusion One of the mechanisms of PNBSS for AICD appears to inhibit overavtivity of thrombocyte, and regulate the misadjustment of ratio of T/P.
ABSTRACT
BACKGROUND: Previous studies have suggested that the phenylalkylamine calcium channel blocker, emopamil, may have neuroprotective properties. This study was designed to examine the effects of emopamil on the neurologic and neuropathologic outcome after transient global cerebral ischemia. METHODS: New Zealand white rabbits were randomly assigned to one of the following groups: emopamil group (n = 6; emopamil 1 mg/kg bolus prior to ischemia and then 0.1 mg/kg/min for 1 hour), hypothermia group (n = 7; 29degreesC prior to, during and until 1 hour after ischemia), or control group (n = 7). All rabbits were subjected to 6.25 minutes of global cerebral ischemia produced by a neck tourniquet inflation (20 psi) combined with hypotension during halothane anesthesia. Neurologic deficit scoring was done at 24 hours and 48 hours after ischemia. The rabbits were then euthanized and perfused with 10% formalin. Coronal sections of brain (6nm) were stained with hematoxylin and eosin. The sections were scored for evidence of ischemic injury by two observers blinded as to the experimental group. RESULTS: The hypothermia group had significantly less evidence of neurologic and neuropathologic injury when compared to the control group (P < 0.05). There were no significant differences between the control and emopamil groups in neurologic or neuropathologic outcome. CONCLUSIONS: These results suggest that the peri-ischemic administration of emopamil had no effect on their neurologic or neuropathologic outcome in this model, but, as anticipated, hypothermia was neuroprotective.