• 대한수의학회지
• /
• 제37권3호
• /
• pp.533-540
• /
• 1997

To elucidate the effects of purinergic nerve on relaxation of pig coronary artery, the effects of ATP, 2-methylthio ATP and electrical perivascular nerve stimulation were investigated from physiograph on the isolated coronary artery of pig. The results btained were as follows; 1. The relaxative responses induced by perivascular nerve stimulation(20V, 0.5msec, 10sec) were the frequency(1~8Hz) dependent manner with phentolamine($10^{-5}M$) and atropine($10^{-6}M$) on isolated coronary artery of pig. 2. The relaxative responses induced. by adenosine($10^{-7}{\sim}5{\times}10^{-3}M$) or ATP($10^{-7}{\sim}5{\times}10^{-5}M$) on precontraction with histamine($10^{-5}M$) were the dose-dependent manner, but the contractile responses were often induced by ATP($10^{-4}M$ and $10^{-3}M$). 3. The relaxative responses induced by 2-methylthio ATP($2.5{\times}10^{-8}{\sim}2.5{\times}10^{-6}M$) on precontraction with histamine($10^{-5}M$) were the dose-dependent manner. 4. The relaxative response induced by 2-methylthio ATP($10^{-7}M$) on precontraction with histamine($10^{-5}M$) was completely blocked by the pretreatment with $P_{2Y}$-purinoceptor blocker, reactive blue 2($10^{-4}M$). 5. The neurogenic relaxative response induced by perivascular nerve stimulation(20V, 8Hz, 0.5msec, 10sec) was weakly inhibited by the pretreatment with ${\beta}$-adrenoceptor blocker, propranolol($10^{-5}M$) and blocked by the addition with $P_{2Y}$-purinoceptor blocker, reactive blue 2($10^{-4}M$). The results suggest that the purinergic nerve is innervated, and its relaxative response was mediated by $P_{2Y}$-purinoceptor on isolated coronary artery in pig.

• 대한수의학회지
• /
• 제35권2호
• /
• pp.237-243
• /
• 1995

The effects of various autonomic blocking agents to perivascular nerve stimulation were investigated on isolated coronary artery of pig. 1. The magnitude of contractile response to perivascular nerve stimulation increased with increasing frequency(280Hz) of stimulation. 2. The contractions to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) were increased by pretreatment of the cholinestrase inhibitor, physostigmine. 3. The contraction to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) was antagonised by the muscarinic antagonist, atropine. 4. The contraction to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) was blocked by the neural blocker, tetrodotoxin. 5. The contractions to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1min) were not significantly affected by the ${\alpha}$-adrenergic antagonist, phentolamine or ${\beta}$-adrenergic antagonist, propranolol. 6. The contractile response by the acetylcholine was increased by the pretreatment of cholinestrase inhibitor, physostigmine. This findings suggest that the powerful excitatory action by the perivascular nerve stimulation may be linked to muscarinic receptor by cholinergic nerve excitation in coronary artery of pig.

• Journal of Ginseng Research
• /
• 제18권2호
• /
• pp.95-101
• /
• 1994

Saponin of Panax ginseng (C.A. Meyer) is composed of Protopanaxatriol (PT) and Protopanaxa- diol (PD). We investigated the effects of PT and PD on the contractility and $^{45}Ca$ uptake in the pig coronary artery. Isometric tension in the helical strips and $^{45}Ca$ uptake in the ring strips were measured in the presence or absence of PT and PD. PT and PD did not affect the high K+ (40 mM)-induced contraction but relaxed the ACh-induced contraction in a dose4ependent manner (1~10 mg/dl). The vasorelaxing effect of PT on the ACh-induced contraction was more potent than that of PD. Those relaxations were partially suppressed by the rubbing of endothelium removal. ACh-induced contraction in the $Ca^{2+}$-free Tyrode's solution was suppressed by the pretreatment of PT or PD. Following the depletion of ACh-sensitive intracellular $Ca^{2+}$ pool, ACh-induced contraction was suppressed by the pratreatment of PT or PD. With the pretreatment of PT or PD, $^{45}Ca$ uptake by high K+ (43 mM) was not changed but that by ACh was suppressed in the pig coronary artery. From the above results, we suggested that the vasorelaxing effect of PT and PD of Panax ginseng was due to inhibition of intracellular $Ca^{2+}$ release, inhibition of $Ca^{2+}$ uptake via receptor-operated $Ca^{2+}$ channels and in part a release of vasorelaxing factor from endothelium in pig coronary artery.

• Journal of Mechanical Science and Technology
• /
• 제19권6호
• /
• pp.1313-1320
• /
• 2005

Stenosed coronary artery may play an important role in various coronary heart diseases. However, it has not been known how much stenosed coronary artery affects coronary circulation system, quantitatively. The present study developed a mathematical model for microcirculation in the left common coronary artery (LCCA) with adopting a previously measured morphological data and mechanical properties of the coronary vessels. We examine the effect of percent diameter stenosis on blood flow rate and shear stress for two cases. Case I comprised of one-stenosed element at $10^{th}$ order ($\%$ diameter stenosis are 10, 30, and 50, respectively). Case II consisted of completely occluded element at $10^{th}$ order (number of occluded elements are 0, 1, and 2 out of 8, respectively). As the level of stenosis becomes severe, the shear stress increases significantly but the flow rate reduction was relatively small. However, for the occluded case, there was linearly proportional reduction of flow rate according to number of occluded elements. Either such high shear stress associated with coronary artery stenosis or reduced flow rate due to occlusion may cause atherosclerosis and myocardial ischemia.

• 대한수의학회지
• /
• 제38권4호
• /
• pp.730-736
• /
• 1998

To elucidate whether or not innervation of purinergic nerve and functional action of $P_{2X}$-, $P_{2Y}$-purinoceptor, the neurogenic effects of perivascular nerve stimulation were investigated using by physiograph recording system in isolated coronary artery of pig. 1. The contractile responses induced by perivascular nerve stimulation (20V, 0.5msec, 20sec) were the frequency (2~64Hz) dependent manner. 2. The neurogenic contractile responses induced by perivascular nerve stimulation were inhibited by the pretreatment with either ATP or adenosine ($10^{-7}{\sim}10^{-4}M$). 3. The neurogenic contractile responses induced by perivascular nerve stimulation (20V, 16Hz, 0.5msec, 20sec) were increased by the pretreatment with reactive blue 2, but were not affected by the pretreatment with 8-phenyltheopylline ($10^{-5}M$). 4. The neurogenic contractile responses induced by perivascular nerve stimulation (20V, 16Hz, 0.5msec, 20sec) were inhibited by the desensitization of the P2X-purinoceptor using by treatment of $10^{-5}M$, -methylene ATP as 3 times over again. The accomplished present study on isolated coronary artery of pig suggest that purinergic nerve is innervated and that the neurogenic contractile response was mediated by activation of $P_{2X}$-purinoceptor and the neurogenic relaxative response was mediated by activation of both $P_1$ and $P_{2Y}$-purinoceptor.

• The Journal of Korean Physical Therapy
• /
• 제13권1호
• /
• pp.61-71
• /
• 2001

The purpose oi this study is to identify clearly the physiologic significance of autonomic nervous system. This study is to find the loose of endogenous neurotransmitter while using the neural response of the neural excitatory action which is distributed to the perivascular smooth muscle through the electrical stimulation of the smooth muscle of coronary artery of pig. The effects of perivascular nerve stimulation were investigated on isolated coronary artery of pig.1 . The magnitude of contractile response to perivascular nerve stimulation increased with increasing frequency (2-80 Hz) of stimulation. 2. The contractions to perivascular nerve stimulation(40V, 40Hz. 0.5msec, 1 min) were increased greatly by pretreatment of the cholinestrase inhibitor physostigmine. 3. The contraction to perivascular nerve stimulation(40V,40Hz, 0.5msec, 1min) was antagonised markedly by the muscarinic antagonist atropine. 4. The contraction to perivascular nerve stimulation(40V, 40Hz, 0.5msec, 1 min) was blocked by the neural blocker tetrodotoxin. 5. The contractions to perivascular nerve stimulation(40V. 40Hz, 0.5msec, 1 min) were not affected significantly by the -adrenergic antagonist phentolamine or - adrenergic antagonist propranolol. 6. The contractile response by the acetylcholine was increased by the pretreatment of cholinestrase inhibitor physostigmine. The finding suggest that it is powerful excitatory action linked to muscarinic receptor by cholinergic nerve in coronary artery of pig.

• Journal of Chest Surgery
• /
• 제24권7호
• /
• pp.637-646
• /
• 1991

Effect of noradrenaline and endothelium on the high K+ or Ach-induced contraction were investigated in the pig myocardial coronary artery. The helical strip of isolated pig myocardial coronary artery was immersed in the Tris-buffered Tyrode`s solution equilibrated with 100% O2 at 37oC and its isometric tension was measured. High K+ and Ach-induced contraction were dose-dependent. By denuding the endothelium, dose-contraction curve of K+ was not shifted significantly to the left and upward, but that of Ach was shifted significantly to same direction 25 mM K+ - and Ach-induced contraction were relaxed by norepinephrine[NE]. NE-induced relaxation was blocked by the pretreatment of propranolol, which was known as b-adrenoceptor blocker. And, phenylephrine known as a-adrenoceptor agonist, and clonidine known as a-adrenoceptor agonist increased the 25mM K+ - induced contraction respectively. Denuding of endothelium did not show any significant effects on NE-induced relaxation and contraction increased by phenylephrine and clonidine. Tyramine increased 25mM K+ - induced contraction further. The contractile response by tyramine on the 25mM K+ - induced contraction was not blocked by the pretreatment of phentolamine, but was partially blocked by the pretreatment of atropine. From the above results, it is suggested that activation of a1-and a2-adrenoceptors induce the contraction, activation of b-adrenoceptors induce the relaxation, and NE-induced relaxation is mainly due to activation of b-adrenoceptors. Also it is suggested that denudation of endothelium did not influence NE-induced relaxation, but influence Ach-induced contraction in the pig myocardial coronary artery.

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

• 대한기계학회:학술대회논문집
• /
• 대한기계학회 2003년도 춘계학술대회
• /
• pp.1923-1929
• /
• 2003

The present study investigated the microcirculation of blood in the left common artery (LCCA). In order to develop a mathematical model for microcirculation in LCCA, the present study adopted preexisted set of measured morphological data on anatomy, mechanical properties of the coronary vessels, viscosity of blood, the basic laws of physics, and the appropriate boundary conditions. In this study, the statistical distribution of blood pressure, blood flow, and blood volume in the LCCA were determined based on the anatomical branching pattern of the coronary arterial tree and the statistical data of blood vessel dimensions. Our calculations were in good agreement with the previous studies. The present results showed that the mean longitudinal pressure drop profile was function of the vessel order numbers. It was found that the normalized pressure drop was a logarithmic function of the compliance.

• The Korean Journal of Physiology
• /
• 제27권1호
• /
• pp.27-35
• /
• 1993

Effects of the endothelium on the contractile responses to norepinephrine (NE) were investigated in isolated helical strips of the proximal and distal coronaries artery of pigs. The helical strips were immersed in Tris-buffered Tyrode's solution equilibrated with 100% $O_2$ at $35^{\circ}C$ and its isometric tension was measured. NE relaxed the strips precontracted with acetylcholine from both the proximal and distal coronary artery. NE-induced relaxation, which might be induced mainly by $\beta$-adrenoceptor function was dominant in the distal coronary arteries. NE-induced relaxation was converted to a contraction after $\beta$-adrenoceptor blockade with propranolol $(3{\times}10^{-6}M)$. ${\alpha}$-adrenoceptor-mediated contraction by NE was greater in the proximal coronary artery than the distal coronary artery. Quantitatively, ${\alpha}_1$-adrenoceptor mediated contraction by NE was greater than ${\alpha}_2$-adrenoceptor mediated contraction by NE in both arteries. NE-induced relaxation was decreased by rubbing of endothelium in both arteries. ${\alpha}_1-and\;{\alpha}_2$-adrenoceptor mediated contraction by NE were potentiated by rubbing of endothelium in both arteries. Pretreatment with methylene blue, an inhibitor of soluble guanylate cyclase, increased ${\alpha}_1-\;and\;{\alpha}_2$-adrenoceptor mediated contraction by NE in both arteries with endothelium. From the above results, we suggest that the effect of activation of $\alpha$-adrenoceptors by NE may be modulated by endothelium in the proximal and distal coronary arteries of pigs. This effect may be mediated via endothelium derived relaxing factor.