• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.123-131
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• 1983

1) To delineate the role of central ${\alpha}_2-adrenoceptors$ in the pressor response to raised intracranial pressure(ICP), the influence of yohimbine, an ${alpha}_2-adrenoceptor$ antagonist, on the pressor response to raised ICP was investigated in urethane-anesthetized rabbits. 2) The ICP was raised by infusing saline into a balloon placed in the epidural space. The rise of ICP was slow in the beginning of the infusion but it became sharp as the infusion proceeded. 3) In response to raised ICP, blood pressure(BP) tended to decrease slightly in the beginning and then increased sharply. BP, however, fell abruptly and markedly if ICP was raised further. The maximal pressor response to raised ICP was the increase of $49{\pm}2.4%$ of the original $BP(mean{\pm}SE\;in\;32\;experiments)$, and at this point the volume of saline infused into the balloon was $1.22{\pm}0.15\;ml$, and the ICP $165{\pm}6.4\;mmHg$. 4) Intraventricular yohimbine $(50{\mu}g)$ by itself did not affect BP. After the administration of this dose of yohimbine the increase of both ICP and BP was observed after the infusion of much smaller volume of saline than in the control animals, i.e., after the infusion of $0.83{\pm}0.02\;ml$ of saline the maximal increase of preesor response$(57{\pm}4.5%\;in\;6\;experiments)$ appeared and at this state the ICP was $164{\pm}9.6\;mmHg$. 5) Intraventricular $clonidine(30{\mu}g)$ markedly decreased BP by itself, and in the clonidine-treated rabbits the increase of ICP induced by the infusion was much less than in the control group and the pressor response to raised ICP was hardly seen. 6) The hypotensive effect of intraventricular clonidine was reversed by a susequent intraventricular $yohimbine(500\;{\mu}g)$. At this state the pressor response to raised ICP appeared as in the control animals. 7) These results show that the pressor response to raised ICP was facilitated when ${\alpha}_2-adrenoceptors$ in the rabbit brain was blocked by yohimbine and that yohimbine antagonized the inhibitory effect of clonidine on the pressor response to raised ICP.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.137-146
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• 1992

The central tryptaminergic system has been shown to play an important role in the regulation of renal function: $5-HT_1$ receptor mediate diuresis and natriuresis, whereas both $5-HT_2$ and $5-HT_3$ mediate antidiuresis and antinatriuresis. Recently, $5-HT_1$ receptors are further subdivided into many subtypes, and central $5-HT_{1A}$ subtype was shown to mediate diuretic and natriuretic effects. The present study was undertaken to delineate the role of $5-HT_{1B}$ subtype. Trifluoromethylphenylpiperazine (TFMPP), a selective $5-HT_{1B}$ agonist in doses ranging from 8 to $750\;{\mu}g/kg$ icv elicited diuresis, natriuresis and kaliuresis in dose-dependent fashion, with the fractional excretion of filtered Na reaching 5.44% with $250\;{\mu}g/kg$ icv. The natriuresis outlasted the transient increases in renal hemodynamics, suggesting humoral mediation in the decreased tubular Na reabsorption. Plasma concentration of atrial natriuretic peptide increased along with the natriuresis. Systemic blood pressure transiently increased. When given intravenously, no diuresis and natriuresis was elicited, indicating the central mechanism. The icv TFMPP effects were not significantly affected by icv methysergide, a nonselective $5-HT_1$ blocker. Both ketanserin and MDL 72222, selective $5-HT_2$ and $5-HT_3$ antagonists, resp., did not abolish the TFMPP effects. Nor did NAN-190, $5-HT_{1A}$ blocker, affect the TFMPP effects. These observations suggest that central $5-HT_{1B}$ receptors may play a role in the central regulation of renal function by exerting diuretic and natriuretic influences, mainly through natriuretic factors.

• Journal of Chest Surgery
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• v.30 no.5
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• pp.471-478
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• 1997

Introduction: The use of rabbits as a cardiopulmonary bypass(CPB) animal model is extremely dif%cult mainly due to technical problems. On the other hand, deep hypothermic circulatory arrest(CA) is used to facilitate surgical repair in a variety of cardiac diseases. Although steroids are generally known to be effective in the treatment of cerebral edema, the protective effects of steroids on the brain during CA are not conclusively established. Objectives of this study are twofold: the establishment of CPB technique in rabbits and the evaluation of preventive effect of steroid on the development of brain edema during CA. Material '||'&'||' Methods: Fifteen New Zealan white rabbits(average body weight 3.5kg) were divided into three experimental groups; control CA group(n=5), CA with Trendelenberg position group(n=5), and CA with Trendelenberg position + steroid(methylprednisolone 30 mglkg) administration group(n=5). After anesthetic induction and tracheostomy, a median sternotomy was performed. An aortic cannula(3.3mm) and a venous ncannula(14 Fr) were inserted, respectively in the ascending aorta and the right atrium. The CPB circuit consisted of a roller pump and a bubble oxygenator. Priming volume of the circuit was approximately 450m1 with 120" 150ml of blood. CPB was initiated at a flow rate of 80~85ml/kg/min, Ten min after the start of CPB, CA was established with duration of 40min at $20^{\circ}C$ of rectal temperature. After CA, CPB was restarted with 20min period of rewarming. Ten min after weaning, the animal was sacrif;cod. One-to-2g portions of the following tissues were rapidly d:ssected and water contents were examined and compared among gr ups: brain, cervical spinal cord, kidney, duodenum, lung, heart, liver, spleen, pancreas. stomach. Statistical significances were analyzed by Kruskal-Wallis nonparametric test. Results: CPB with CA was successfully performed in all cases. Flow rate of 60-100 mlfkgfmin was able to be maintained throughout CPB. During CPB, no significant metabolic acidosis was detected and aortic pressure ranged between 35-55 mmHg. After weaning from CPB, all hearts resumed normal beating spontaneously. There were no statistically significant differences in the water contents of tissues including brain among the three experimental groups. Conclusion: These results indicate (1) CPB can be reliably administered in rabbits if proper technique is used, (2) the effect of steroid on the protection of brain edema related to Trendelenburg position during CA is not established within the scope of this experiment.