• Natural Product Sciences
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• 제20권3호
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• pp.216-225
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• 2014

The present study was designed to investigate whether ethylacetate (EtOAc) fraction extracted from Rubus coreanum affect the contractility of the isolated thoracic aortic strips and blood pressure of normotensive rats. The EtOAc fraction ($400{\mu}g/mL$) significantly depressed both phenylephrine (PE, $10{\mu}M$)- and high $K^+$ (56 mM)-induced contractile responses of the isolated thoracic aortic strips in a concentration-dependent fashion. In the simultaneous presence of L-NAME (an inhibitor of NO synthase, $300{\mu}M$) and EtOAc ($400{\mu}g/mL$), both PE- and high $K^+$-induced contractile responses were recovered to the corresponding control level in comparison with inhibition of EtOAc-treatment alone. Moreover, in the simultaneous presence of EtOAc after pretreatment with 0.4% CHAPS, both PE- and high $K^+$-induced contractile responses were recovered to the corresponding control level compared to the inhibitory response of EtOAc-treatment alone. Also, in anesthetized rats, EtOAc fraction (0.3~3.0 mg/kg) injected into a femoral vein dose-dependently produced depressor responses. This hypotensive action of EtOAc fraction was greatly inhibited after treatment with phentolamine (1 mg/kg), chlorisondamine (1 mg/kg), L-NAME (3 mg/kg/30 min) or sodium nitroprusside ($30{\mu}g/kg/30 min$). Intravenous infusion of EtOAc fraction (1.0~10.0 mg/kg/30 min) markedly inhibited norepinehrine-induced pressor responses. Taken together, these results demostrate that EtOAc causes vascular relaxation in the isolated rat thoracic aortic strips as well as hypotensive action in anesthetized rats. These vasorelaxation and hypotension of EtOAc seem to be mediated at least by the increased NO production through the activation of NO synthase of vascular endothelium, and the inhibitory adrenergic modulation.

• The Korean Journal of Physiology
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• 제26권1호
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• pp.45-54
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• 1992

Effects of pH, $PCO_2$, and adenosine on the vascular contractility were investigated in the pig coronary arteries. The helical strips of isolated coronary arteries were immersed in the HEPES or $HCO_3^-/CO_2$-buffered Tyrode's solution equilibrated with 100% $O_2\;or\;95%\;O_2-5%\;CO_2\;at\;35^{\circ}C$. The contraction was recorded isometrically using a force transducer. The amplitudes of contraction induced by ACh, high $K^+$, and electrical Held stimulation (EFS) were decreased by elevating extracellular pH (pHo) and were increased by lowering pHo. A shift from $0%\;CO_2\;to\;5%\;CO_2$ at constant pHo (pH 7.4) reduced the contractions induced by ACh, high $K^+$, EFS. However the contraction induced by 100mM $K^+$ was less influenced by the change of pHo or $CO_2$. The contraction induced by ACh in $Ca^{2+}$free Tyrode's solution as well as the contraction developed by the addition of extracellular of $Ca^{2+}$ were decreased by lowering pHo and were increased by elevating pHo. High $K^+$ (25mM) induced contraction at pH 6.8 was not returned to the level of the contraction at pH 7.4 by the elevation of extracellular. calcium $[Ca^{2+}]_o$. Adenosine-induced relaxation was more significant with 5% $CO_2$ than 0% $CO_2$ in the high $K^+$-induced contraction and was more significant with low pHo than high pHo in the contraction induced by EFS. From the above results, it is suggested that $H^+$ and $CO_2$ inhibit $Ca^{2+}$ influx as well as $Ca^{2+}$ release from intracellular $Ca^{2+}$ storage sites and enhance the relaxing effect of adenosine in the pig coronary artery.

• 대한약리학회지
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• 제11권2호
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• pp.19-27
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• 1975

Haloperidol, a butyrophenone, was synthetized by Janssen and introduced for the treatment of psychosis. Although structurally different from the phenothiazines, the butyrophenones share many of their pharmacological properties, such as inhibition of conditioned avoidance response, blocking effect of amphetamine reaction, producing catalepsy, antishock effect and protection against the lethal effects of catecholalmines. Chlorpromazine can lower the arterial blood pressure through its adrenergic blocking activity, its direct effect in relaxing vascular smooth muscle, its direct effect in depressing the myocardium and its action in a complex manner on the central nervous system. In the case of haloperidol, however, was not clarified the mechanism of lowering the blood pressure. The present paper describes the effects of haloperidol on cardiovascular system to investigate the mechanisms of its actions on the arterial blood pressure. The results are followings; 1. In anesthetized cats, intravenous administration of haloperidol and chlorpromazine in the dose of 0.1mg/kg produced a slight decrease in the blood pressure, which followed by complete recovery within $30{\sim}60$ minutes. In the dose of 3mg/kg, however, both produced an abrupt and marked decrease of the blood pressure, which followed by delayed recovery. 2. Haloperidol in the dose ranges of 0.1mg to 3.0mg/kg tended to produce the heart rate slowing in the cats, while chlorpromazine has no effect on the rate. 3. Following administration of haloperidol or chlorpromazine, epinephrine reversal in the arterial blood pressure was observed in the cat, however the responses of norepinephrine and acetylcholine were little affected. 4. In the isolated rabbit atrium the contractility was depressed by haloperidol in the doses over 0.5mg per 100ml, but the rate was not affected. In contrast, the epinephrine-induced contractility was not depressed after haloperidol treatment. However, the increased rate of atrium by epinephrine was partially blocked after haloperidol. 5. In the isolated rabbit aortic strip, epinephrine-induced contraction was blocked by haloperidol. With the above results, it may be concluded that the hypotensive effect of haloperidol was largely due to ${\alpha}$-adrenergic blocking properties and the direct effect in depressing the myocardium as well as its action on central nervous system.

• Journal of Chest Surgery
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• 제34권7호
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• pp.515-523
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• 2001

배경: 당뇨병 환자에서 사망률과 이환률의 원인은 70%이상 혈관계의 합병증에 기인한다. 이러한 합병증은 혈관 내피세포 이완 작용 이상과 연관되어 있으며 이는 oxygen free radical의 직접적인 독성으로 추정되어 본 연구는 당뇨를 유발시킨 백서 복부 대동맥 운동성에 대한 Vit C의 보호효과를 연구 목적으로 한다. 대상 및 방법: 백서 60마리를 실험군(n=33)과 대조군(n=27)으로 나누고 실험 군은 streptozotocin을 투여하여 당뇨를 유발시켰다. 각각 실험 군과 대조군을 ascorbic acid를 투여한 군과 투여하지 않은 군으로 세분한 후 ascorbic acid투여 직후, 6주, 9주, 12주후의 복부 대동맥 혈관근육의 운동성을 측정하였다. 결과: 대조군의 경우 6주째 복부 대동맥 절편에서 acetylcholine투여 후 정상적인 이완반응이 나타났으나 실험군의 경우 현저히 저하됨이 관찰되었다. 9, 12주 째 절편에서는 실험군 중 ascorbic acid투여군에서 acetylcholine에 의한 이완반응이 거의 대조군에서의 결과와 일치할 정도로 회복되었다. 결론: 이상의 결과로 당뇨병을 유발한 백서에서 내피세포 의존적인 장애가 나타남을 확인할 수 있었으며 이러한 장애는 ascorbic acid의 투여로 회복됨을 알 수 있었으며 그 효과는 항산화 작용에서 비롯된 것으로 생각되므로 ascorbic acid가 당뇨환자의 혈관성 질환에 대해 보호적 효과를 보일 수 있을 것으로 사료된다.

• 대한장애인치과학회지
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• 제9권1호
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• pp.30-35
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• 2013

The four principles of treatment of odontogenic infection are as follows : (1) removal of the cause, (2) establishment of drainage, (3) institution of antibiotic therapy, and (4) provision of supportive care, including proper rest and nutrition. A separate incision is required to establish drainage, especially in the case of extensive fascial space infections. There are four principle causes for active bleeding in the immediate incision & drainage phase; (1) vascular wall alteration (infection, scurvy, chemicals), (2) disorder of platelet function, (3) thrombocytopenic purpuras, (4) disorders of coagulation (liver disease, anticoagulation drug). If the hemorrhage from incision & drainage site is aggressive, the site must be packed with proper wet gauze and wound closure & drainage dressing are applied. The specific causes of bleeding may be associated with hypoxia, changes in the pH of blood & chemical changes affecting vascular contractility and blood clotting. This is a case report of bleeding control by the circumferential suture & drainage on active bleeding incision & drainage site of temporal space abscess due to advanced odontogenic infection in a multiple medically compromised disabled patient.

• Biomolecules & Therapeutics
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• 제11권2호
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• pp.119-125
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• 2003

The present study was conducted to investigate the effects of bornyl acetate on arterial blood pressure and vascular contractile responses in the normotensive rats and to establish the mechanism of action. Both phenylephrine (an adrenergi$\alpha$-receptor agonist) and high potassium (a membrane-depolarizing agent) caused greatly contractile responses in the isolated aortic strips. These phenylephrine (10$^{-5}$ M)-induced contractile responses were depressed in the presence of high concentrations of bornyl acetate (10∼20 $\mu\textrm{g}$/ml), but not affected in low concentrations of bornyl acetate (2.5∼5$\mu\textrm{g}$/ml). High potassium (5.6 ${\times}$ 10$^{-2}$ M)-induced contractile responses were also greatly inhibited in the presence of bornyl acetate (2.5∼20 $\mu\textrm{g}$/ml) in a dose-dependent fashion. Bornyl acetate (1∼10 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient (data not shown). Interestingly, the infusion of a moderate dose of bornyl acetate (3mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. Collectively, these results obtained from the present study demonstrate that intravenous bornyl acetate causes a dose-dependent depressor action in the anesthetized rat at least partly through the blockade of adrenergic $\alpha$$_1$-receptors. bornyl acetate also causes vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic $\alpha$$_1$-receptors, in addition to the unknown mechanism of direct vasorelaxation.

• Natural Product Sciences
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• 제10권5호
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• pp.228-236
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• 2004

The aim of the present study was to examine whether green tea extract (CUMC6335) affects the blood pressure and the isolated aortic contractility of the rabbit in comparison with one of the most powerful active catechins, epigallocatechin gallate (EGCG). The phenylephrine $(1-10\;{\mu}M)-induced$ contractile responses were greatly inhibited in the presence of CUMC6335 (0.3-1.2 mg/ml). Also, high potassium (56 mM)-induced contractile responses were depressed in high concentration (0.6-1.2 mg/ml), but not affected in low concentration CUMC6335 (0.3 mg/ml). However, epigallocatechin gallate $(EGCG,\;4-12\;{\mu}g/ml)$ did not affect the contractile responses evoked by phenylephrine and high $K^+$. The infusion of CUMC6335 with a rate of 20 mg/kg/30 min made a significant reduction in pressor responses induced by intravenous norepinephrine. However, EGCG (1 mg/kg/30 min) did not affect them. Collectively, these results obtained from the present study suggest that intravenous CUMC6335 causes depressor action in the anesthetized rat at least partly through the blockade of adrenergic ${\alpha}_1-receptors$. CUMC6335 also causes the relaxation in the isolated aortic strips of the rabbit partly via the blockade of adrenergic ${\alpha}_1-receptors$, in addition to the unknown direct mechanism. It seems that there is no species difference in the vascular effect between the rat and the rabbit.

• The Korean Journal of Physiology and Pharmacology
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• 제21권1호
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• pp.91-97
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• 2017

Hyperglycemia is associated with an increased risk of cardiovascular diseases. It has been demonstrated that chronic exposure to high glucose impaired endothelial functions. However, specific effects of short-term exposure to high glucose on vascular reactivity are controversial. Moreover, the combined effects of other metabolic substrates such as free fatty acids (FFA) on vascular reactivity remain poorly understood. Here we investigate the effects of short-term exposure to high glucose with or without other metabolic substrates including FFAs termed "nutrition full" (NF) solution, on mesenteric (MA) and deep femoral arteries (DFA) of rats. Arterial ring segments were mounted in a double-wire myograph. Contraction in response to phenylephrine (PhE) was determined in control (5 mM) and high glucose (23 mM, HG) environments over a 30 min period. In both arteries, PhE-inducedvasocontraction was enhanced by pre-incubation of HG solution. A combined incubation with HG and palmitic acid ($100{\mu}M$) induced similar sensitization of PhE-contractions in both arteries. In contrast, high $K^+$-induced contractions were not affected by HG. Interestingly, pre-incubation with NF solution decreased PhE-induced contraction in MA but increased the contraction in DFA. In NF solution, the HG-induced facilitation of PhE-contraction was not observed in MA. Furthermore, the PhE-induced contraction of DFA was attenuated by HG in NF solution. Our results demonstrate that the sensitization of PhE-induced arterial contraction by HG is differentially affected by other metabolic substrates. The conversation of skeletal arterial contractility by HG in NF solution requires careful interpretation of the previous in vitro studies where only glucose is included in physiological salt solutions. Further studies are required to elucidate the mechanism underlying the inconsistent effect of NF solution on MA and DFA.

• The Korean Journal of Physiology and Pharmacology
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• 제5권5호
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• pp.443-449
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• 2001

Previously we reported that THI 52 inhibits tumor necrosis factor $(TNF)-{\alpha}$ mRNA expression in mouse peritoneal macrophages exposed to LPS plus $IFN-{\gamma}.$ In the present study, the effects of THI 52 on vascular reactivity ex vivo, and iNOS protein expression (rat lung) were investigated in LPS-treated rats. Treatment of THI 52 concentration-dependently reduced not only serum nitrite production but also the expression of iNOS protein in rat lung tissues. Thoracic aorta taken from LPS injected rat for 8 h ex vivo resulted in suppression of vasoconstrictor effects to phenylephrine (PE), which was restored by THI 52 (20 mg/kg) 30 min prior to LPS. When measured iNOS activity, treatment of THI 52 concentration-dependently reduced the enzyme activity in RAW 264.7 cells activated with LPS plus $IFN-{\gamma}.$ Likewise, iNOS activity was significantly reduced in lung tissues taken those rats that were injected THI 52 prior to LPS injection compared with LPS injection alone. These results strongly suggest that THI 52 can suppress iNOS gene expression induced by LPS, and restore the vascular contractility to PE. Thus, THI 52, a new synthetic isoquinoline alkaloid, may be beneficial in inflammatory disorders where production of NO is excessed by iNOS expression.

• Toxicological Research
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• 제12권2호
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• pp.195-201
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• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.