Hypothermia is an essential preparatory procedure for cardiac surgery, which lows the metabolic rate and myocardial oxygen demand. However, hypothermia itself is a stress enough to change the tonus of sympathoadrenal system, especially the cardiovascular responses to the catecholamines. It is reported that the positive chronotropic and inotropic response of catecholamines is exaggerated during hypothermia because of decreased norepinephrine uptake at the junctional cleft or decreased catecholamine metabolism. On the other hand, there are evidences of diminished catecholamines responses in low temperature ana further, interconversion of adrenergic receptors is also suggested. Present investigation was planned to observe the cardiovascular changes and its responses to catecholamines during surface hypothermia in cat. Healthy mongrel cats, weighing $2{\sim}3\;kg$, anesthetized with secobarbital(30 mg/kg), were permitted to hypothermia by external cooling technic. Esophageal temperature, ECG (lead II), heart rate, left ventricular pressure with dP/dt, carotid artery pressure and left ventricular contractile force were monitored with Polygragh (Model 7, Grass), and the respiration was maintained with artificial respirator (V 5 KG, Narco). Followings are summarized results. 1) Surface cooling caused progressive decrease of body temperature and reached $l8.8{\pm}0.8^{\circ}C$ and $16.9{\pm}0.6^{\circ}C$ in 120 and 150 min respectively, after immersion into ice water, and ventricular fibrillation was developed at $20.4{\pm}0.65^{\circ}C$. 2) Heart rate, blood pressure and myocardial contractility were decreased after initial increase as the body temperature falls. 3) Systolic and diastolicdd P/dt of left ventricular pressure were decreased and that the decrement of diastolic dP/dt was more marked. 4) On ECG, ST depression, Twave inversion and prolongation of PR interval were prominent in hypothermia, and moreover, the prolongation of PR interval was marked just prior to the development of ventricular fibrillation. 5) The cardiovascular responses to catecholamines, especially to isoproterenol, were suppressed under hypothermia.
Chronic hypertension is associated with impaired endothelial function such as reduced synthesis/release of endothelium-derived relaxing factor(EDRF, nitric oxide) and increased synthesis/release of endothelium-derived contracting factor(EDCF) including prostaglandin endoperoxide($PGH_2$) , superoxide anion both in animals and in humans. We have previously shown that ginsenosides lower the blood pressure and enhance the release of nitric oxide(NO) from endothelial cells in the rat aorta of the normotensive rats. The aim of the present study is to examine whether in vivo treatment of spontaneously hypertensive rats(SHRs) with protopanaxatriol ginsenosides(PPT) reduces the blood pressure and improves endothelial function in the isolated thoracic aorta of SHR. In addition, the contractile response to $PGH_2$ and superoxide anion in the aorta treated with PPT was assessed. SHRs at the age of 16 weeks were savaged with PPT(30 mg/kg/ day) for 2 weeks and systolic blood pressure was measured by the tail-cuff method. Whereas blood pressure was significantly increased in SHRs by 5.4 mmHg during this period of treatment, treatment of SHRs with PPT blocked the elevation of blood pressure. Endothelium-dependent relaxation to acetylcholine was significantly increased in the PPT-treated animals. $PGH_2$- and oxygen-derived free radical-induced contractions were significantly suppressed in aortic rings without endothelium from PPT-treated SHR. These findings indicate that PPT reduces the blood pressure of SHR, which may be associated with either increase of NO release or by antagonizing superoxide anion and PGH2 in the aortic smooth muscle.
The muscarinic antagonist 1-[benzilic 4, 4'-$[^3H]$ QUINUCLIDINYL BENZILATE $([^3H]$ QNB) bound to a single class of muscarinic receptors with high affinity in rabbit ileal membranes. The $K_D\;and\;B_{ max}$ values for $([^3H]$ QNB calculated from analysis of saturation isotherms were 52.5 pM AND 154 fmol/mg, respectively. Chlopheniramine (CHP), histamine $H_1$ blocker, increased $K_D$ vlue for $([^3H]$QNB without affecting the binding site concentrations and Hill coefficient. The $K_i$ value of CHP for inhibition of $([^3H]$QNB binding in ileal membranes was 1.44\mu{M}$ and the pseudo-Hill coefficient for CHP was close to unit. In the functional assay carbachol, muscarinic agonist, increased the contractile force of ileum with $ED_{50}$ value of $0.11\mu{M}$. CHP caused the rightward shift of the dose-response curve to carbachol. The $pA_2$ value of CHP determined from Schild analysis of carbacholinduced contraction was 5.77 and the slope was unity indicating competitive antagonism with carbachol. The dissociation constant $(K_i)$ of CHP obtained in competitive experiments with $([^3H]$ QNB was similar to the $K_A$ value (1.69 \mu{M)}$ of CHP as inhibitor of carbachol induced contraction in rabbit ileum. This result suggest that the binding of $H_i$ blocker. CHP, vs $([^3H]$QNB to muscarinic receptors in ileal membranes represents an interaction with a receptor of physiological relevance.
Journal of Physiology & Pathology in Korean Medicine
/
v.19
no.6
/
pp.1573-1579
/
2005
This study was undertaken to define the effect of DaeSiHo-Tang extract on the hypertension in spontaneous hypertensive rat and norepinephrine-induced arterial contraction in rabbit. Systolic blood pressure and blood velocity were significantly attenuated by administration of DaeSiHo-Tang extract. but blood flow and renin-angiotensin-aldosterone system unaffected by DaeSiHo-Tang extract. The relaxation effect of DaeSiHo-Tang extract was dependent on the presence of endothelium, showing that DaeSiHo-Tang extract-induced relaxation was not observed in the strips without endothelium. The endothelium-dependent relaxation induced by DaeSiHo-Tang extract was decreased by the pretreatment of $N{\omega}$-nitro-L-arginine or methylene blue, but it was not observed in the strips pretreated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of DaeSiHo-Tang extract inhibited contractile response to $Ca^{2+}$. These results indicate that antihypertensive effect of DaeSiHo-Tang extract is due to descend arterial resistance by the arterial relaxation through the formation of nitric oxide in the vascular endothelial cells.
Journal of Physiology & Pathology in Korean Medicine
/
v.19
no.6
/
pp.1622-1628
/
2005
This study was undertaken to define the effect of SoPung-Tang extract on hypertension in spontaneous hypertensive rat and norepinephrine- induced arterial contraction in rabbit. In order to investigate the effect of SoPung-Tang extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of SoPung-Tang extract-induced relaxation, SoPung-Tang extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, Nu-nitro-L-arginine, methylene blue or tetraethylammonium chloride. Blood pressure was significantly decreased five days after administration of SoPung-Tang extract. SoPung-Tang extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, SoPung-Tang extract- induced relaxation was significantly inhibited. SoPung-Tang relax arterial strip contracted by norepinephrine, but in the strips contracted by high $K^+$, SoPung-Tang extract-induced relaxation was significantly inhibited. The endothelium-dependent relaxation induced by SoPung-Tang extract was decreased by the pre-treatment of $N{\omega}$-nitro-L-arginine or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of SoPung-Tang extract inhibited contractile response to $Ca^{2+}$. We suggest that SoPung-Tang could be applied effectively for hypertension and may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide in the vascular endothelial cells.
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.
Objectives : This experiments were performed to determine the effect of Linderae Radix extract on norepinephrine-induced arterial contraction in rabbit. Methods : In order to investigate the effect of Linderae Radix extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of Linderae Radix extract-induced relaxation, Linderae Radix extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, tetraethylammonium chloride, $N{\omega}-nitro-L-arginine$ or methylene blue. Results : Linderae Radix extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, Linderae Radix extract-induced relaxation was significantly inhibited. Linderae Radix extract-induced relaxation was decreased by the pre-treatment of $N{\omega}-nitro-L-arginine$ or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of Linderae Radix extract inhibited contractile response to norepinephrine and $Ca^{2+}$. Conclusions : We suggest that Linderae Radix may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide, and release of intra-cellular $Ca^{2+}$.
Objectives : This experiments were performed to determine the effect of OYakSoonGi-San extract on hypertension in spontaneous hypertensive rat and norepinephrine-induced arterial contraction in rabbit. Methods : In order to define the effect of OYakSoonGi-San extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of OYakSoonGi-San extract-induced relaxation, OYakSoonGi-San extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, $N{\omega}-nitro-L-arginine$, methylene blue or tetraethylammonium chloride. Results : Blood pressure was significantly decreased five days after administration of OYakSoonGi-San extract. The relaxation effect of OYakSoonGi-San extract was dependent on the presence of endothelium, showing that OYakSoonGi-San extract-induced relaxation was not observed in the strips without endothelium. Also OYakSoonGi-San extract-induced relaxation was significantly inhibited in arterial strips which were contracted by high $K^+$. OYakSoonGi-San extract-indeced relaxation was significantly inhibited by the pre-treatment of $N{\omega}-nitro-L-arginine$ or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When additive application of $Ca^{2+}$ in arterial strips which were pre-contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But contractile response to $Ca^{2+}$ was attenuated by pre-treatment of OYakSoonGi-San extract. Conclusions : These results demonstrated that OYakSoonGi-San could be applied effectively to hypertension and may inhibit agonist-induced contraction through an decrease influx of extra-cellular $Ca^{2+}$ by the formation of nitric oxide in the vascular endothelial cells.
To learn how maximal locomotory speed of animals is defined in terms of hindlimb structure and muscle contractile function, take-off speed, hindlimb length, thigh muscle mass, shortening velocity and power of the sastrocnemius muscle were measured with one fast species, Rono nigromaculota and one relatively slowresponding species, Bombina orientalis. Take-off speed (m.sec-1) was greater in R. nigromoculata $(2.4\pm0.2SD, $ n: 14) than in the Bombino $(1.6\pm0.1SD, $ n=8). Stvle of the take-off response was a long-iump type in the Rano and a short-ranged hopping in the Bombing. Faster take-off capacity of the ranid frogs was supported by the longer hindlimb length (relative to body length) and the more massive thigh muscles (relative to body mass), compared to the Bombina. Further, the ranids exhibited faster maximal shortening velocity and Breater maximal power generateion than the Bombina [Vmax $(ML.sec-1)=11.79\pm1.69SD$ for the Runa and $9.74\pm1.27SD$ for the Bombina; Pmax $nW.kg-1)=222.42\pm42.42SD$ for the Rono and $169.03\pm34.52SD$ for the Bombinal. With more massive thigh muscles and greater mechanical power, the ranids would generate greater total power and thus higher energy release per unit time to muscle tissues for the burst take-off. As a consequence, biomechanical properties seen in the ranids seem to be more effective for frost take-off than in the Bombina.
Force development of smooth muscle cells is directly regulated by the concentration of free calcium ions in the sarcoplasm, and the sarcoplasmic concentration of calcium ion can be modulated by electrogenic Na-K pump. The role of Na-K pump on vascular tone was studied in isolated rabbit renal artery. Helical strips of arterial muscle were prepared from left renal arteries. All experiments were performed in $HCO_3^--buffered$ Tyrode solution which was aerated with $3%CO_2-97%\;O_2$ mixed gas and kept at $35^{\circ}C$. In some experiments, rabbit was injected intraperitoneally $18{\sim}24$ hours prior to the experiments, with a large dose(5 mg/kg body wt) of reserpine, in order to eliminate the catecholamines present in intrinsic adrenergic nerve terminate. Treatment used in this experiment that inhibits Na-K pump was the exposure of strips to K-free Tyrode solution. Contractile response to K free Tyrode solution developed slowly and the time required for maximum contracture was $20{\sim}30$ minutes. This K-free contracture was rapidly relaxed by the addition of potassium to the bathing solution. No K-free contracture occurred in a Ca-free Tyrode solution. But contraction developed rapidly when calcium ion was added to the bathing solution after 30 minute exposure of the strip to Ca-free Tyrode solution. This contracture was completely inhibited by Ca-antagonist, verapamil. The K-free contracture was abolished by ${\alpha}-adrenergic$ blocker, phentolamine, as well as by the catecholamine depletion from adrenergic nerve terminals. Even in reserpinized strip, the exogenous norepinephrine-induced contraction in K-free Tyrode solution was rapidly suppressed by the addition of potassium ion. The results of this experiment suggest that K free contracture develops by norepinephrine release from adrenergic nerve terminals, while the relaxation of K-free contracture is induced by the activation of electrogenic Na-K pump.
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