• The Korean Journal of Physiology
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• v.9 no.1
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• pp.33-37
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• 1975

Adult rabbits were anesthetized with nembutal, 30 mg/kg. Carotid artery and jugular vein were exposed surgically and cannulated with polyethylene tubing. Arterial blood pressure was recorded via pressure transducer on the physiograph and $100{\mu}g/ml$ of histamine solution was infused through the jugular vein by using the constant infusion pump with a rate of 0.92 ml/min or 1.40 ml/min. Mean arterial blood pressure was maintained at $40{\sim}70 mmHg$ and hypotension was kept for 2 hours. After the termination of this period, blood was taken and osmotic fragility was mea sured immediately. Also, every sample of normal blood and shocked blood was incubated for 1 hour or 2 hours at $37^{\circ}C$ in order to see whether or not there was some influence of incubation. Furthermore to clarify which component was responsible for the change on the fragility, the mixtures of normal blood cells with shocked plasma and shocked blood cells with normal plasma were also incubated at $37^{\circ}C$ for one or two hours and fragility in such cases was measured. The data obtained were analysed by probit-plot method and the concentration of saline solution at which the hemolysis started to occur, 50% of blood cells were hemolysed and that at which the red blood cells hemolysed completely were determined. The values for the blood of hypotension stage were compared with those of the control blood. The results obtained were as fellows: 1. Osmotic fragility of red blood cell was increased in hypotensive state induced by histamine. 2. The differences of osmotic fragility after two hours of incubation were negligible both in normal blood and in that of hypotensive state. 3. Osmotic resistance of normal red blood cell incubated in shock plasma was less than that of shock red blood cell incubated in normal plasma. It was suggested that plasma in hypotensive state caused by histamine might be primarily responsible for the alteration of red blood cell fragility.

• The Korean Journal of Pharmacology
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• v.22 no.2
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• pp.96-104
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• 1986

Higenamine, dl-1-( 4-hydroxybenzyl)-6, 7-dihydroxy-1 ,2, 3 ,4-tetrahydroisoquinoline has been synthesized and evaluated for hemodynamic actions using rabbits under pentobarbital anesthesia. Concentration-related fall of mean blood pressure was observed, where diastolic blood presure was significantly lowered at 10 ug/kg/min or above (p<.05), while the systolic blood pressure was slightly increased or unaffected, thereby, causing increment of pulse pressure. No significant change was occured in heart rate, however, carotid artery blood flow was significantly (p<.05) increased. These actions were inhibited with pretreatment of 0.3 mg/kg of propranolol, beta-adrenoceptor antagonist, 5 minutes before infusion of higenamine indicating that higenamine compete with propranolol for the so-called beta adrenergic receptor. As comparison, the same procedure was applied to isoproterenol as well, where typical antagonism of propranolol against isoproterenol was shown. From these findings the vasodilating and diastolic blood pressure lowing effects could be explained in terms of cardiac beta stimulating action, however, dopamine receptor activation could not be excluded because no significant changes observed in chronotropism.