• Title/Summary/Keyword: contractile effect

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Study on Relaxing Effect of Oxybutynin on the Contractile Response of Arterial Smooth Muscle (동맥근 수축에 대학 Oxybutynin의 이완효과에 관한 연구)

  • Ko, Jae-Ki;Baik, Yung-Hong
    • The Korean Journal of Pharmacology
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    • v.24 no.1
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    • pp.93-101
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    • 1988
  • Pharmacological actions of an antispasmodic agent, oxybutynin were investigated in the isolated procine coronary arteries. The coronary rings were contracted by acetylcholine (ACh) and KCl in a dose-dependent fashion. The ACh-induced contractions were signifcantly potentiated by removal of endothelium and $EC_{50}=0.52\;{\mu}M$ of intact endothelial rings was about 2 times greater than $EC_{50}=0.28\;{\mu}M$ of rings without the endothelium. These results suggest that the endothelium plays an inhibitory role in ACh-induced contraction. Oxybutynin and atropine inhibited dose-dependently $1.0\;{\mu}M$ ACh-induced contraction and atropine inhibited dose-dependently $1.0\;{\mu}M$ ACh-induced contraction and the $IC_{50s}$ were 11.0 nM and 0.47 nM, respectively. Atropine did not affect 35 mM KCl-induced contraction but oxybutynin inhibited the contraction to the basal tension in a dose-dependent manner. The $IC_{50}$ of oxybutynin on the KCl-induced contraction was $49.7\;{\mu}M$. The dose-response curve to ACh was parallelly shifted to the right by pretreating coronary rings with $IC_{50}$ of atropine (0.47 nM) or oxybutynin (11.0 nM) but the curve to KC1 was rightward shifted in a noncompetitive manner under pretreatment with $IC_{50}$ of oxybutynin $(49.7\;{\mu}M$). Oxybutynin inhibited $0.1\;{\mu}M$ Bay K 8644-induced contraction to the basal tension in a dose dependent manner, but $35\;{\mu}M$ histamine-induced contraction was inhibited to only 50e/e of the original level even in maximal concentration $(5{\times}10^{-4}M)$ of oxybutynin. These results suggest that oxybutynin causes antispasmodic action through sensitive blocking action on muscarinic receptors and inhibitory action on calcium influx in the procine coronary artery.

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Effects of Aqua-Acupuncture of Carthami Flos(GV15) on the Changes of Cerebral Hemodynamics in Rats (아문(瘂門)(GV15)의 홍화약침(紅花藥針)이 백서(白鼠)의 뇌혈류역학(腦血流力學) 변동(變動)에 미치는 영향(影響))

  • Ahn, Young-sun;Wei, Tung-shuen;Cho, Myung-rae;Chae, Woo-seok;Yun, Yeo-choong
    • Journal of Acupuncture Research
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    • v.19 no.5
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    • pp.92-111
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    • 2002
  • Objective : Carthami Flos has been used as a herb to promote blood circulation to remove blood stasis in oriental medicine for many centuries, and Amun(GV15) has been used as a meridian point to treat apoplexy etc. To investigate treatment of cerevral vascular disease(CVA) by promoting blood circulation and removing blood stasis(活血化瘀法), we observed the experimental effects and mechanism of auqa-acupunture of Carthami Flos(ACF) injected into GV15 on cerevral hemodynamics and cardiovascular system of rats. Method : Aqua-acupuncture of Carthami Flos(ACF) was injected into GV15, and then we investigated experimental effects and mechanism of ACF on the cerebral hemodynamics[regional cerebral blood flow(rCBF), pial arterial diameter(PAD), meal arterial blood pressure(MABP)] and cardiovascular system[cardiac muscle contractile force(CMF), heart rate(HR)I by pretreatment with methylene blue(MTB) and indomethacin(IDN). The changes in rCBF, MABP, CMF and HR were tested by Laser Doppler Flowmetry(LDF), and the changes in PAD was determinated by video microscopy methods and video analyzer. Results :The results were as follows in normal rats ; The changes of rCBF and PAD were significantly increased by ACF($120{\mu}{\ell}/kg$) in a injected time-dependent manner, but MABP was not changed by ACF. The changes of cardiovascular system were increased by ACF in a injected time-dependent manner. And pretreatment with MTB was significantly inhibited ACE induced increase of rCBF and PAD, and was decreased ACF induced increase of HR. And pretreatment with IDN was increased ACF induced MABP and CMF. And the results were as follows in cerebral ischemic rats ; The changes of rCBF was increased stabilizly by treatment with ACF($120{\mu}{\ell}/kg$) in during the period of cerebral reperfusion, but pretreatment with MTB was increased ACF induced increase of rCBF during the period of cerebral reperfusion. The results were as follows in normal rats ; The changes of rCBF and PAD were significantly increased by ACF($120{\mu}{\ell}/kg$) in a injected time-dependent manner, but MABP was not changed by ACF. The changes of cardiovascular system were increased by ACF in a injected time-dependent manner. And pretreatment with MTB was significantly inhibited ACF induced increase of rCBF and PAD, and was decreased ACF induced increase of HR. And pretreatment with IDN was increased ACF induced MABP and CMF. And the results were as follows in cerebral ischemic rats ; The changes of rCBF was increased stabilizly by treatment with ACF($120{\mu}{\ell}/kg$) in during the period of cerebral reperfusion, but pretreatment with MTB was increased ACF induced increase of rCBF during the period of cerebral reperfusion Conclusions : In conclusion, ACF causes a diverse response of rCBF, PAD an HR, and action of ACF is mediated by cyclic GMP. I suggested that ACF has an anti-ischemic effect through the improvement of crebral hemodynamics in a transient cerebral ischemia.

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Effect of Left Atrial Volume Reduction with Maze Operation on Sinus Conversion and Recovery of Left Atrial Transport Function (Maze 수술 후 동율동 및 좌심방 수축능 회복에 대한 좌심방 부피 감소 성형술의 영향)

  • Hong Seong-Beom;Ryu Sang-Wan;Jung Eun-Kyung;Jung In-Suk;Bum Min-Sun;Park Jung-Min;Lee Kyo-Sun;Kim Sang-Hyung;Ahn Byung-Hee
    • Journal of Chest Surgery
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    • v.38 no.11 s.256
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    • pp.739-745
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    • 2005
  • Background: The Maze procedure considered the most effective method of treatment for atrial fibrillation. However, the sinus conversion rates decreased due to several factors, especially enlarged left atrium. The purpose of this study was to investigate the effects of Maze procedure with aen atrial volume reduction plasty on rheumatic mitral valve disease, Material and Method: From December of 200f to July of 2004, 45 patients received mitral valve and Maze operation. The patients were placed in either group f or group 2, based on the left atrial volume reduction plasty. The presence and onset of sinus rhythm and the incidence of trans mitral A waves were monitored during the postoperative 7 days and throughout the follow up period of 3 and 6 months. Mean follow up periods were 15.8 10.1 months in group 1 and $6.1\pm2.7$ months in group 2. Result: The sinus onset were $9.88\pm12.2$ days in group 1, and $1\pm3.6$ days in group 2 (p<0.01). The sinus conversion rates in the group 1 and 2 were $65\%,\;75\%$ (p=0.07) in the postoperative 7 days, $70.5\%,\;100\%$ (p<0.01) at postoperative 3 months, and $93\%,\;100\%$ (p<0.01) at postoperative 6 months, respectively. The wave detection rates in the postoperative 7days were $31.2\%\;and\;63.6\%$, and continued to improve over time to $83.3\%\;and\;100\%$ by 6months, respectively. Conclusion: The results suggest that Maze procedure with left atrial volume reduction plasty is effective for inducing sinus rhythm and for restoring left atrial contractile function after concomitant rheumatic mitral valve surgery. However further follow up of this patients for long time is necessary.

Ischemic Preconditioning and Its Relation to Glycogen Depletion (허혈성 전처치와 당원 결핍과의 관계)

  • 장대영;김대중;원경준;조대윤;손동섭;양기민;라봉진;김호덕
    • Journal of Chest Surgery
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    • v.33 no.7
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    • pp.531-540
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    • 2000
  • Baclgrpimd; Recent studies have suggested that the cardioprotective effect of ischemic preconditioning(IP) is closely related to glycogen depletion and attenuation of intracellular acidosis. In the present study, the authors tested this hypothesis by perfusion isolated rabbit hearts with glucose(G) is closely related to glycogen depletion and attenuation of intracellular acidosis. In the present study, the authors tested this hypothesis by perfusion isolated rabbit hearts with glucose(G)-free perfusate. Material and Method; Hearts isolated from New Zealand white rabbits(1.5~2.0 kg body weight) were perfused with Tyrode solution by Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to 45 min global ischemia followed by 120 min reperfusion with IP(IP group, n=13) or without IP(ischemic control group, n=10). IP was induced by single episode of 5 min global ischemia and 10 min reperfusion. In the G-free preconditioned group(n=12), G depletion was induced by perfusionwith G-free Tyrode solution for 5 min and then perfused with G-containing Tyrode solution for 10 min; and 45 min ischemia and 120 min reperfusion. Left ventricular functionincluding developed pressure(LVDP), dP/dt, heart rate, left ventricular end-distolic pressure(LVEDP) and coronary flow (CF) were measured. Myocardial cytosolic and membrane PKC activities were measured by 32P-${\gamma}$-ATP incorporation into PKC-specific peptide and PKC isozymes were analyzed by Western blot with monoclonal antibodies. Infarct size was determined by staining with TTC(tetrazolium salt) and planimetry. Data were analyzed by one-way analysis of variance (ANOVA) and Turkey's post-hoc test. Result ; In comparison with the ischemic control group, IP significantly enhanced functional recovery of the left ventricle; in contrast, functional significantly enhanced functional recovery of the left ventricle; in contrast, functional recovery were not significantly different between the G-free preconditioned and the ischemic control groups. However, the infarct size was significantly reduced by IP or G-free preconditioning(39$\pm$2.7% in the ischemic control, 19$\pm$1.2% in the IP, and 15$\pm$3.9% in the G-free preconditioned, p<0.05). Membrane PKC activities were increased significantly after IP (119%), IP and 45 min ischemia(145%), G-free [recpmdotopmomg (150%), and G-free preconditioning and 45 min ischemia(127%); expression of membrane PKC isozymes, $\alpha$ and $\varepsilon$, tended to be increased after IP or G-free preconditioning. Conclusion; These results suggest that in isolated Langendorff-perfused rabbit heart model, G-free preconditioning (induced by single episode of 5 min G depletion and 10 min repletion) colud not improve post-ischemic contractile dysfunction(after 45-minute global ischemia); however, it has an infarct size-limiting effect.

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