• Journal of Veterinary Clinics
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• v.22 no.3
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• pp.220-227
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• 2005

Although ketamine has been used in the field of anesthetic medicine for its safety and favourable respiratory effects, the cardiovascular effects of ketamine is still controversial. To clarify the action and mechanism of ketamine upon cardiovascular system, arterial blood pressure, tension of aortic ring, left ventricular developed pressure and heart rate were measured in rats, Ketamine produced two types of effects on arterial blood pressure in anesthetized rats; monophasic effect (blood pressure lowering) and biphasic effect (initial transient blood pressure increasing following sustained lowering), The ketamine-induced lowering of aterial blood pressure showed a concentration-dependent manner, inhibited by the pretreament of $MgCl_2$ and potentiated by the pretreatment of $CaCl_2$. The ketamine-induced lowering of aterial blood pressure was suppressed by the pretreatment of nifedipine, verapamil or lidocaine. In phenylephrine-precontracted endothelium intact (+E) aortic rings, ketamine sometimes caused a small enhancement of contraction ($112.5{\pm}3.6{\%}$). However, in many experiments, ketamine produced a concentration-dependent relaxation in +E aortic rings precontracted with either phenylephrine or KCl. Ketamine-induced relaxation was significantly greater in KCl-precontracted strips than phenylephrine-precontracted strips. In phenylephrine-precontracted +E aortic rings, the ketamine-induced vasorelaxation was not suppressed by endothelium removal or by the pretreatment of a nitric oxide synthase inhibitors, L-$N^G$-nitro-arginine and a guanylate cyclase inhibitors, methylene blue, suggesting that the ketamine-induced vasorelaxation is not dependent on the endothelial function. In addition, ketamine elicited an increase in left ventricular developed pressure in perfused hearts accompanied by decrease in heart rate. These results suggest that ketamine could evoke a hypotension due to vasorelaxation and decrease in heart rate in rats. The inhibitory effect of cardiovascular system might be associated with modulation of $Ca^{2+}$ homeostasis.

• Korean Journal of Veterinary Research
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• v.44 no.3
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• pp.357-366
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• 2004

We studied the effect of propofol (PPF) on the endothelium-dependent vascular responses in isolated rat thoracic aorta. In aortic rings with endothelium, PPF inhibited the phenylephrine (PE)-induced contraction in a concentration-dependent manner. In PE-precontracted preparations, PPF attenuated the endothelium-dependent relaxation by acetylcholine but not by A23187. And PPF did not attenuate the endothelium-independent relaxation by sodium nitroprusside (SNP). The relaxation induced by acetylcholine in PE-precontracted aortic rings was significantly augmented by zaprinast, a cGMP-specific phosphodiesterase inhibitor, and this augmentation was inhibited by PPF. Although SNP-induced relaxation was significantly augmented by zaprinast, this augmentation was not inhibited by PPF. In preparations preconstricted with PE, the PPF-induced relaxation was inhibited by atropine. In addition, PPF attenuated the vasorelaxation by phosphodiesterase inhibitors (IBMX, Ro20-1724 or zaprinast except milrinone). In vivo, the infusion of acetylcholine and SNP showed decreased arterial blood pressure in rats. The pre-injection of PPF inhibited the acetylcholine-induced blood pressure lowering, but not the SNP-induced blood pressure lowering. These results suggest that PPF can attenuate in part the acetylcholine-induced vasorelaxation and blood pressure lowering through the inhibition of the acetylcholine receptor-mediated endothelium-derived relaxing factor by acting on endothelium. It is considered that the inhibitory effect of PPF on the vasorelaxation is due to the decreased level of cGMP which can be attributed to the inhibition of the muscarinic receptor and/or receptor-G-protein interaction.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.1-11
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• 1989

In this study, it was aimed to investigate the role of serotonergic neurotransmission in nucleus tractus solitarius (NTS) for the central regulation of blood pressure and heart rate and its involvement in baroreceptor reflex activation in rats. A microinjection of 5-hydroxytryptamine (5-HT) into the NTS produced decreases in blood pressure and heart rate. Maximal decreases were $34.4{\pm}1.6$ mmHg and $41.7{\pm}10.2$ beats per min by 300 pmol of 5-HT. Microinjections of ${\alpha}-methylnor-adrenaline$ $({\alpha}-MNE)$ and clonidine manifested similar decreases in blood pressure and heart rate. The hypotensive and bradycardial effects of 5-HT were blocked by previous applications of 5-HT antagonists, ritanserin, methysergide and ketanserin into the NTS, respectively. By pretreatment with reserpine and 6-hydroxydopamine (6-OHDA, i.c.v.), both hypotensive and bradycardial effects of 5-HT were significantly attenuated. Pretreatment with 5, 7-dihydroxytryptamine (5,7-DHT, i.c.v.) enhanced the hypotensive and bradycardial effects of 5-HT. Similarly, following pretreatment with 6-OHDA, the effects of clonidine were increased. Pretreatment either with 5,7-DHT or 6-OHDA significantly attenuated the sensitivity of baroreflex produced either by phenylephrine or by sodium nitroprusside. When either 5,7-DHT or 6-OHDA was injected into the NTS $(5,7-DHT;\;8{\mu}g\;6-OHDA;\;10{\mu}g)$, both of the baroreflex sensitivities were impaired. In the immunohistochemical study, the injection of 6-OHDA into the the NTS led to reduction of axon terminal varicosity, however, the injection did not reduce the numbers of catecholaminergic cell bodies. Likewise, when 5,7-DHT was injected into the NTS, the varicosity of serotonergic axon terminals was markedly reduced. Based on these results, it is suggested that (1) stimulation of serotonergic receptors in the NTS leads to decreases in blood pressure and heart rate as observed with the stimulation of catecholaminergic system, (2) both serotonergic and catecholaminergic receptors may be located postsynaptically, and (3) the serotonergic neurons as well as catecholaminergic neurons may have a close relevance for the activation of baroreflex.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.485-493
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• 2005

We studied the effects of trazodone on arterial blood pressure in anesthesized guinea pigs, and on vascular responses in isolated thoracic aorta. Trazodone produced a concentration-dependent relaxation in phenylephrine-precontracted endothelium intact (+E) rings, but not in a KCl-precontracted aortic rings. These relaxant effects of trazodone on +E rings were significantly greater than those on denuded (-E) rings. The trazodone-induced relaxation was suppressed by glibenclamide and tetrabutylammonium, but not by N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), methylene blue (MB), nifedipine, indomethacin, 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC) and clotrimazole. In vivo, infusion of trazodone elicited a significant decrease in arterial blood pressure. Trazodone-induced blood pressure lowering was markedly inhibited by intravenous pretreatment of prazosin but not by pretreatment of saponin, L-NNA, L-NAME, MB, nifedipine, glibenclamide, clotrimazole and NCDC. In addition, trazodone produced an increase in twitch force of isolated papillary muscle and left ventricular pressure of perfused heart. These findings suggest that the endothelium-independent vasorelaxant effect of trazodone may be explained by activation of $Ca^{2+}$-activated and ATP-sensitive $K^+$ channels, and the hypotensive effect of trazodone is not associated with cardiac contraction.

• Proceedings of the Korean Institute of Navigation and Port Research Conference
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• 2018.05a
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• pp.112-113
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• 2018

스트레스는 스트레스 요인에 반응하는 신체와 정신의 변화과정으로, 외부의 자극을 받으면 혈압, 심박동수, 호흡수가 증가하게 된다. 이러한 생체신호로 인간의 스트레스 요인을 측정할 수 있다. 본 연구에서는 선박조종시뮬레이션을 이용해 예비(견습)도선사가 도선접안 중 체감하는 스트레스의 정도와 특성을 생체신호 변화를 활용하여 실증적으로 분석하였다. 선박조종시뮬레이션에서 추출한 엔진 사용량, 타각 사용량, 속력 및 예선 사용량과 스트레스 분석을 위해 Heart BPM, SDNN, RMSSD의 3가지 심박변이도 파리미터의 상관관계를 분석하였다. 분석결과, 6회 중 4회의 시뮬레이션에서 Heart BPM은 지속적으로 상승하고 SDNN은 하강하여 시간에 따라 스트레스가 상승하는 것으로 분석되었다. 특히 예선 사용시점에서 변화의 폭이 큰 것을 확인하였다. RMSSD는 단기주기(1분간격) 측정 파라메터로 실험자가 느끼는 순간의 위험에 따라 그래프 변화폭이 심한 것으로 분석되었다. 전체적으로 엔진, 타각, 예선의 사용시점에 따라 큰 변화를 보였으며, 실험자들의 선박운용 행위에 따라 생체신호 변화를 보였다고 사료된다. 분석결과를 바탕으로 도선사에게 스트레스를 미치는 요소를 판별하여 도선접안 중 스트레스가 높아지는 순간에 인적사고를 예방할 수 있는 시스템적 보완을 마련하고자 한다.

• 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.

• Journal of Ginseng Research
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• v.32 no.4
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• pp.324-331
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• 2008

Introduction : Korean red ginseng has been shown to have an preventive effect on atheroma formation and enhancing effect on nitric oxide synthesis in endothelial cell inducing vasodilatation. However, there are few studies showing the effect of Korean red ginseng on blood pressure and vascular(endothelial) pathologic changes together. We designed this study to show changes of blood pressure and vascular pathologic findings with Korean red ginseng administration compared with Chinese red ginseng and control for 3 months in rats. Materials and methods : We studied the in vitro hypotensive effect and effect on vascular pathologic changes of Korean red ginseng compared with Chinese red ginseng and control. Rats were randomly assigned to three groups(Korean red ginseng, Chinese red ginseng and control) and evaluated by blood pressure and aortic vascular(endothelial) pathologic changes monthly during 3-month administration. All results were analyzed by paired T-test, ANOVA and post-hoc. Results : Blood pressure lowering effect was noted on Korean red ginseng and Chinese red ginseng compared to control. Especially, in Korean red ginseng group, hypotensive effect was showed in first and second month, but, in Chinese red ginseng group, it was just noted in first month. In case of vascular(aortic endothelial) pathologic finding, endothelial wall thickening and elastic fiber tearing were noted in Chinese red ginseng group compared with Korean red ginseng group and control with statistical significance.(p<0.05) Discussion : These results suggested Korean red ginseng could have more hypotensive effect and maintenance rather than Chinese red ginseng. And the difference of hypotensive effect between Korean red ginseng and Chinese red ginseng might has some association with difference of vascular pathologic findings in each group. However, further evaluation and research of other mechanism will be needed to convince this hypothesis.

• Tuberculosis and Respiratory Diseases
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• v.49 no.6
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• pp.715-723
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• 2000

Background : Obstructive sleep apnea syndrome (OSAS) affects systemic blood pressure and cardiac function. The development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac rhythm, suggests that recurrent hypoxia and arousals from sleep may increase a sympathetic nervous system activity. Continuous positive airway pressure (CPAP) therapy has been found to be an effective treatment of OSAS. However, only a few studies have investigated the cardiovascular and sympathetic effects of CPAP therapy. We evaluated influences of nasal CPAP therapy on the cardiovascular system and the sympathetic activity in patients with OSAS. Methods : Thirteen patients with OSAS underwent CPAP therapy and were monitored using polysomnography, blood pressure, heart rate, presence of arrhythmia and the concentration of plasma catecholamines, before and with CPAP therapy. Results: The apnea-hypopnea index (AHI) was significant1y decreased (p<0.01) and the lowest arterial oxygen saturation level was elevated significantly after applying CPAP (p<0.01). Systolic blood pressure tended to decrease after CPAP but without statistical significance. Heart rates during sleep were not significantly different after CPAP. However, the frequency and number of types of arrhythmia decreased and sinus bradytachyarrhythmia disappeared after CPAP. Although there was no significant difference in the level of plasma epinephrine concentration, plasma norepinephrine concentration significantly decreased after CPAP (p<0.05). Conclusion : CPAP therapy decreased the apnea-hypopnea index, hypoxic episodes and plasma norepinephrine concentration. In addition, it decreased the incidence of arrhythmia and tended to decrease the systemic blood pressure. These results indicate that CPAP may play an important role in the prevention of cardiovascular complications in patients with OSAS.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.27-37
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• 1995

In anesthetized rats, we examined the possibility that endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) released in response to cholinergic mechanism may contribute to the reflex autoregulation of cerebral blood flow. Suffusion with mock cerebrospinal fluid (CSF), containing acetylcholine (ACh, $10^{-9}{\sim}10^{-6}M$) evoked concentration-dependent vasodilatation of the resting pial artery (mean, $19.3{\pm}1.7{\mu}m$, n=36), which was significantly inhibited not only by $N{\omega}$-nitro-L-arginine (L-NNA, $10^{-5}M$) but also by methylene blue ($10^{-6}M$) and oxyhemoglobin ($10^{-6}M$). The muscarinic receptors in the endothelium of pial artery implicated in the release of EDRF were considered to be $M_1\;and\;M_3$ subtypes. When suffused with mock CSF containing L-arginine it caused a transient vasodilatation, which was strongly inhibited by LY 83583 ($10^{-5}M$), but not by L-NNA ($10^{-5}M$). Additionally, both ACh- and L-arginine-induced vasodilation were significantly inhibited by glibenclamide, a specific ATP-sensitive $K^+$ channel blocker. On the other hand, changes in pial arterial diameter were plotted as a function of changes in systemic arterial blood pressure. The slopes of regression lines for vasodilation and vasoconstriction were not affected by pretreatment with $10^{-5}M$ L-NNA, but significantly reduced by $3{\times}10^{-6}M$ glibenclamide. Thus it is suggested that the reflex vasodilation of rat pial arteries in response to a transient hypotension is not mediated by EDRF (NO).

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.1
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• pp.371-375
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• 2019

The role of resuscitative endovascular balloon occlusion of the aorta (REBOA) in hemodynamically unstable pancreatic trauma is unclear. We report here a case of traumatic pancreatic bleeding controlled with REBOA and angioembolization of the splenic artery before surgery. A 65-year old man experienced blunt trauma upon falling from a height of 20 m. Computed tomography (CT) revealed distal pancreatic trauma (grade III) and contrast extravasation around the splenic artery. Shortly after CT, his systolic blood pressure was 60 mmHg and REBOA was performed for hemodynamic stability. His systolic pressure increased to 130 mmHg after balloon inflation and angioembolization of the splenic artery was performed. On angiography, no further arterial bleeding was identified and the balloon was removed. Subsequently, the patient underwent emergent laparotomy with distal pancreatectomy. There was no active bleeding during surgery and distal main pancreatic duct injury was identified. After surgery, the patient recovered without complication. In this case, hemodynamically unstable hemorrhagic pancreatic trauma was treated effectively and safely with distal pancreatectomy after REBOA with angioembolization.