Abstract
A Wedge-Pressure catheter was inserted to 1cm above aortic valve in ascending aorta through left common carotid artery of 36 rabbits. 1.5mg/kg of sodium arachidonate (AA) was injected into the proximal portion of ascending aorta after inflation of balloon which obstructed the ascending aorta. The inflation remained for 5 seconds, the solution was perfused into coronary arteries. 14 rabbits among the 36 rabbits were not pretreated before injection of AA, each 11 rabbits were pretreated intravenously with 10mg/kg of OKY-1580 and OKY-046 (specific inhibitors on TXA2 synthetase) respectively 3 minutes before AA injection. ECG, respiratory movement and blood pressure were recorded. Before, 3 and 60 minutes after AA, 5ml of heparinized blood was collected, added with indomethacin (10μM in final concentration) and centrifuged to collect PPP for measurement of TXB2 and 6-keto-PGF1α using radioimmunoassay (RIA). In control, 5 out of 14 cases died because of apnea. Blood pressure decreased in 5 or 6 seconds after AA, irregular respiration and arrhythmia in some 10 seconds, ST deviation in 20 seconds, apnea appeared in 30 seconds. Arrhythmia and marked ST depression appeared in all cases. Apnea was seen in 10 cases. In OKY groups, arrhythmia, ST depression and apnea were prevented significantly. In control, TXB2 values were 1.2±0.2ng/ml (mean±SE) before, 10.2±3.3 minutes after, and 1.3±0.2 60 minutes after. In OKY-046, 1580 groups, those 3 minutes after were 0.8±0.1, 1.1±0.2 respectively showing complete inhibition of TXB2. In control, 6-keto-PGF1α values were 2.1±0.4ng/ml before, 133.1±40.0 3 minutes after and 2.5±0.8 60 minutes after. In OKY-046, 1580 groups, those 3 minutes after were 41.4±7.5, 74.4±13.0 respectively also showing significant difference with that of control group. ST deviation on ECG had good correlation with the value of TXB2 (r=0.765, p<0.005), but no relation with the value of 6-keto-PGF1α. Histological findings of heart were not so severe as expected, but showed more remarkable ischemic changes in control than OKY groups. These findings clearly show that intracoronary injection of AA causes myocardial ischemic changes through TXA2, because OKY protected cardiopulmonary changes, but also suggest the important role of PGI2.
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