• Title/Summary/Keyword: 혈관압

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Effect of Glycopyrrolate on Cardiovascular System in Dogs Sedated with Medetomidine-Midazolam Combination (개에서 Medetomidine과 Midazolam 병용 투여 시 Glycopyrrolate가 심맥관계에 미치는 영향)

  • Han, Dae-Kyung;Shin, Beom-Jun;Lee, Jae-Yeon;Jee, Hyun-Chul;Park, Ji-Young;Kim, Myung-Cheol;Jeong, Seong-Mok
    • Journal of Veterinary Clinics
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    • v.26 no.4
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    • pp.317-323
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    • 2009
  • This study was performed to evaluate the effect of intravenous administration of glycopyrrolate on cardiovascular and respiratory system in dogs given intravenous medetomidine (20 ${\mu}g$/kg) and intramuscular midazolam (0.3 mg/kg) (MM). Prior to administration of MM, glycopyrrolate was administered intravenously at doses of 5 ${\mu}g$/kg (Gly-5), 10 ${\mu}g$/kg (Gly-10) or 20 ${\mu}g$/kg (Gly-20), respectively. For the control group saline was administered intravenously. In the cardiovascular system, HR, BP, RAP, PAWP, CI, SI, SVR, and PVR were measured. RR, $V_T$, $P_{ETCO2}$, and arterial blood gas analysis were measured for respiratory system. Although rapid and satisfied depth of sedation was obtained by MM, life-threatening bradycardia, the outstanding side-effect on cardiovascular system in dogs were observed. This combination also decreased CO and increased SVR, RAP, and PAWP significantly. The bradycardia could be prevented in all the glycopyrrolate treated groups, but tachycardia was observed in Gly-10 and Gly-20 groups. Significant increases in blood pressure were shown in glycopyrrolate treated groups. Also, tachycardia depends on dose of glycopyrrolate, compensating the CO. However, these were not fully reserved. In conclusion, MM combination could induce rapid and satisfied depth of sedation but was not the suitable method for the deep sedation of dogs with cardiovascular or circulatory problems.

Altered Functions of Adrenoceptors in Splanchnic Vascular Beds in Portal Hypertensive Rat Model: Effect of Propranolol (문맥 고혈압 흰쥐에 있어서 내장혈관의 아드레나린성 수용체의 기능변동과 이에 대한 Propranolol의 효과)

  • Kim, Chi-Dae;Hong, Ki-Whan
    • The Korean Journal of Pharmacology
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    • v.24 no.1
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    • pp.63-70
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    • 1988
  • Alterations in splanchnic circulatory hemodynamics along with reactivities to the alpha adrenoceptor agonists were assessed in association with the preventive effects of propranolol 10 days after portal ligation. Decreases in precapillary resistance (Ra) and postcapillary resistance (Rv) along with increases in mesenteric blood flow (MBF) and capillary pressure (CP) were observed in conjunction with an increment of splenic pulp pressure (SPP). Dose-dependent increase in Rv in response to noradrenaline, increases in Ra and RV to adrenaline, and increases in superior mesenteric arterial pressure (SMAP), Ra and Rv to phenylephrine observed in sham group were significantly attenuated by portal vein stenosis. In PPL-3 group (propranolol 3 mg/kg, i.p. three times daily for 10 days), MBF was significantly decreased in association with decrease in mesenteric venous pressure (MVP) when compared with those of protal ligated (PL) group, and decreased Ra and Rv in PL group were recovered toward the values of sham group. Likewise, in PPL-1 group (propranolol 5 mg/kg, i.p. once daily for 10 days), the pressor response of Rv to adrenaline was recovered up to the level of sham group. Thus, it is suggested that decreases in Ra and Rv in association with increases in MBF and CP may have a close relevance to the increased SPP, and the changes in circulatory hemodynamics and vascular reactivities were effectively reversed by longterm propranolol treatment. Based on these results, it is concluded that these changes observed in portal hypertension are closely related with the altered functions of the adrenoceptors in the splanchnic vascular beds.

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Change of Pulmonary Artery Hemodynamics and Pulmonary Vascular Resistance in Experimental Pulmonary Embolism (실험적 급성 폐색전증에서 폐동맥혈역학 및 폐혈관저항의 변화)

  • Chung, Hee-Soon;Lee, Jae-Ho;Kim, Cheol-Ho
    • Tuberculosis and Respiratory Diseases
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    • v.42 no.6
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    • pp.913-922
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    • 1995
  • Background: When we define the pressure of pulmonary vasculature in which a recruitment of blood flow occurs as $P_I$ and the proportion of change in pulmonary artery to that in cardiac output as IR and then we compare PI and IR with pulmonary vascular resistance, we would find some problems in pulmonary vascular resistance. In other words, it is the theory that, IR should be increased mainly in pulmonary embolism in which decreases the cross sectional area of pulmonary vasculature. But there are many contradictory reports resulted from various researches and the fact is known widely that any difference exists between PVR and PI, IR. For this reason, the purpose of this study is to observe how PI and IR change at the time of the outbreak and during treatment of the pulmonary embolism, and to find out the meaning of these new indicators and the difference from the pulmonary vascular resistance used generally when we subdivide the pulmonary vascular resistance into PI and IR. Method: After making AV fistula in experimental dog, we controlled cardiac output at the intervals of 15 minute in case of three kinds(all AV fistula are obstructed, only one of fistula is open and all of fistula is open), and after evoking massive pulmonary embolism with radioactive autologous blood clots, we measured the mean pulmonary artery pressure, and calculated PI and IR. We observed the pattern of change in PI and IR, without giving the control group any specific treatment and with injecting intravenously rtPA in the Group 1 and Group 2 at the dose of 1mg per kg, for 15 minutes fot the former and 3 hours for the latter. Result: 1) Pulmonary vascular resistance showed a change similar to that of pulmonary artery pressure and in all three group, PVR increased significantly, but group 1 and group 2 showed tendency that PVR keeps on decreasing after treatment, and the rate of decrease in group 1 is more rapid than group 2 significantly. 2) Both intersection(PI) and degree(IR) are proved statistically significant, in view of the straight line relationship between cardiac output and pulmonary artery pressure, calculated by minimal regression method. 3) PI changed similarly to pulmonary vascular resistance, while in the IR which is theoretically more similar to PVR, there was no significant difference or change after rtPA infusion. Conclusion: In the pulmonary embolism, Both change in IR which means real resistance of pulmonary vasculature and PI which was developed due to secondary vasoconstriction by pulmonary embolism are reflected same time.

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The Effect of Lidocaine Dose and Pretreated Diazepam on Cardiovascular System and Plasma Concentration of Lidocaine in Dogs Ansthetized with Halothane-Nitrous Oxide (Diazepam 전투여와 Lidocaine 투여용량이 혈중농도 및 심혈역학적 변화에 미치는 영향)

  • Lee, Kyeong-Sook;Kim, Sae-Yeon;Park, Dae-Pal;Kim, Jin-Mo;Chung, Chung-Gil
    • Journal of Yeungnam Medical Science
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    • v.10 no.2
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    • pp.451-474
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    • 1993
  • Lidocaline if frequently administered as a component of an anesthetic : for local or regional nerve blocks, to mitigate the autonomic response to laryngoscopy and tracheal intubation, to suppress the cough reflex, and for antiarrythmic therapy. Diazepam dectease the potential central nervous system (CNS) toxicity of local anesthetic agents but may modify the sitmulant action of lidocaine in addition to their own cardiovascular depressant. The potential cardiovascular toxicity of local anesthetics may be enhanced by the concomitant administration of diazepam. This study was designed to investigate the effects of lidocaine dose and pretreated diazepam to cardiovascular system and plasma concentration of lidocaine. Lidocaine in 100 mcg/kg/min, 200 mcg/kg/min, and 300 mcg/kg/min was given by sequential infusion to dogs anesthetized with halothane-nitrous oxide (Group I). And in group II, after diazepam pretreatment, lidocaine was infused by same way when lidocaine was administered in 100 mcg/kg/min, the low plasma levels ($3.97{\pm}0.22-4.48{\pm}0.36$ mcg/ml) caused a little reduction in cardiovascular hemodynamics. As administered in 200 mcg/kg/min, 300 mcg/kg/min, the higher plasma levels ($7.50{\pm}0.66-11.83{\pm}0.59$ mcg/ml) reduced mean arterial pressure (MAP), cardiac index (CI), stroke index (SI), left ventricular stroke work index (LVSWI), and right ventricular stroke work index (PVSWI) and increased pulmonary artery wedge pressure (PAWP), central venous pressure (CVP), systemic vascular resistance index (SVRI), but was associated with little changes of heart rate (HR), mean pulmonary artery pressure (MPAP), and pulmonary vascular resistance index (PVRI). When lidocaine with pretreated diazepam was administered in 100 mcg/kg/min, the low plasma level, the lower level than when only lidocaine administered, reduced MAP, but was not changed other cardiovascular hemodynamics. While lidocaine was infused in 200 mcg/kg/min, 300 mcg/kg/min in dogs pretreated diazepam, the higher plasma level ($7.64{\pm}0.79-13.79{\pm}0.82$ mcg/ml) was maintained and was associated with reduced CI, SI, LVSWI and incresed PAWP, CVP, SVRI but was a little changes of HR, MPAP, PVRI. After $CaCl_2$ administeration, CI, SI, SVRI, LVSWI was recovered but PAWP, CVP was rather increased than recovered. The foregoing results demonstrate that pretreated diazepam imposes no additional burden on cardiovascular system when a infusion of large dose of lidocaine is given to dogs anesthetized with halothanenitrous oxide. But caution may be advised if the addition of lidocaine is indicated in subjects who have impared autonomic nervous system and who are in hypercarbic, hypoxic, or acidotic states.

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The Effects of Nitric Oxide Inhibitor on Hyperdynamic Circulation in Portal Hypertensive Rats (산화 질소 억제제가 문맥 고혈압 쥐의 혈역학 변화에 미치는 영향)

  • Kim, Pill-Young;Jang, Byeong-Ik;Kim, Tae-Nyeun;Chung, Moon-Kwan
    • Journal of Yeungnam Medical Science
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    • v.16 no.2
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    • pp.181-192
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    • 1999
  • Background: Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells, accounts for the biological activity of endothelium derived relaxing factor. Previous studies demonstrated that nitric oxide inhibitor, $N^{\omega}$-Nitro-L-Arginine(NNA) diminished the hyperdynamic splanchnic and systemic circulation in portal hypertensive rats The present study was done to determine the role of nitric oxide in the development of hyperdynamic circulations in the prehepatic portal hypertensive rat model produced by partial portal vein ligation. Methods: The portal hypertensive rats were divided into water ingestion group and NNA ingestion group. After partial portal vein ligation, NNA ingestion group and water ingestion group received NNA 1mg/kg/day and plain water through the mouth for 14 days, respectively. Cardiac output, mean arterial pressure, organ blood flow and porto-systemic shunting were measured by radioisotope labeled microsphere methods. Vascular resistances were calculated by standard equation. Results: There were significant decreases in mean arterial pressure, increases in cardiac output and cardiac index, and decreases in total systemic and splanchnic vascular resistance in portal hypertensive rats compared to normal control group (p<0.01). Compared to the water ingestion group, significantly increased mean arterial pressure with decreased cardiac output and cardiac index were developed in the NNA ingestion group. Total systemic and splanchnic vascular resistance were significantly increased in the NNA ingestion group compared to water ingestion group (p<0.05). But, there was no significant difference in portal pressure between the two groups. Conclusion: The hemodynamic results of this study indicate that hyperdynamic circulation in prehepatic portal hypertensive rat mode1 was attenuated by ingestion of NNA. Nitric oxide may play an important role in the development of hyperdynamic circulation with splanchnic vasodilation in chronic portal hypertension.

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숙성 어간장으로부터 Fibrin 용해활성과 Protein 분해활성을 가지는 Baillius sp.의 최적성장조건 및 동정에 관한 연구

  • 신일식;이상수;김상무;박욱연
    • Proceedings of the Korean Society of Fisheries Technology Conference
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    • 2001.05a
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    • pp.112-113
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    • 2001
  • 최근 전 세계적으로 혈관내 장애에 의한 사망률이 증가하고 있으며 그 중 뇌졸증은 현재 우리 국민들의 사망원인 중에서 높은 수위를 차지하고 있는 질환 중의 하나이다. 이러한 뇌졸중이 발생하는 경우는 여러 가지 원인이 있으나, 혈액 내에 존재하는 혈전(Fibrin)들이 혈관 벽에 침착하게 되어 혈액의 흐름을 방해함으로서 각 조직으로의 원활한 영양분 및 산소의 공급을 차단하게 되고, 이로 인하여 동맥벽이 변성을 일으켜 동맥압을 이겨내지 못하고 파열되어서 직접적인 사망의 원인으로 작용하게 된다. (중략)

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Arginine Vasopressin Therapy of Vasodilatory Shock after Cardiac Surgery (심장 수술 후 혈관 확장성 쇼크가 발생한 환자에서 바소프레신 투여 요법)

  • Ahn, Young-Chan;Park, Chul-Hyun;Kim, Gun-Woo;Lee, Jae-Ik;Jun, Yang-Bin;Choi, Chang-Hyu;Hyun, Sung-Youl;Park, Kook-Yang
    • Journal of Chest Surgery
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    • v.39 no.12 s.269
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    • pp.913-919
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    • 2006
  • Background: Vasodilatory shock has been implicated in life-threatening complications after open heart surgery, where the systemic inflammatory reaction is attributed to the cardiopulmonary bypass(CPB). The secretion of arginine vasopressin(AVP) has been found to be defective in a variety of vasodilatory shock states and administration of AVP markedly improves vasomotor tone and blood pressure. So we reviewed our experience of AVP therapy in patients with vasodilatory shock following heart surgery using CPB. Material and Method: From January 2004 to July 2006, we reviewed the records of patients who received AVP therapy for vasodilatory shock following heart surgery using CPB. Vasodilatory shock was defined as a mean arterial pressure lower(MAP) than 70 mmHg, a cardiac index greater than 2.5 $L/min/m^2$, peripheral vascular resistance lower than 800 $dyn/s/cm^5$, and vasopressor requirements. The hemodynamic responses of patients who received AVP therapy for vasodilatory shock after cardiac surgery were analyzed retrospectively. Result: One hundred ninety nine open cardiac surgery patients were consecutively included in this study. Twenty two patients(11.1%) met criteria for vasodilatory shock. Despite the administration of high dose catecholamine vasopressor, all patients were hypotensive with a mean arterial pressure less than 70 mmHg. AVP therapy increased MAP from $53.3{\pm}7.4\;to\;82.0{\pm}12.0$ mmHg at 1 hour (p<0.001) and decreased other vasopressor requirements from $25{\pm}7\;to\;18{\pm}6$ at 1 hour(p<0.001) and individually maintained it for 12 hours. Conclusion: Our date suggest that AVP may be a safe and an effective vasopressor in patients with vasodilatory shock. In patients exhibiting vasodilatory shock after heart surgery, replacement of AVP increases blood pressure and reduces catecholamine vasopressor requirements.

Study on Myocardial Protective Effect of L-arginine (L-Arginine의 흰쥐 적출심근보호 효과에 관한 연구)

  • 이인성;이헌재
    • Journal of Chest Surgery
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    • v.29 no.10
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    • pp.1076-1080
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    • 1996
  • The results about the myocardial protection of recta of the nitric oxide precursor L-arginine upon reperrusion injury after ischemia are diverse. These diversities may be model dependent. Experiments were designed and performed to investigate myocardial protection effects according to the concentration of L-arginine. The Isolated rat hearts were subjected in a 30 minutes oi normothermic ischemia and reperfused for 30 minutes with reperfusate containing 0, 1, 2, 3, 4 moil L-arginine. After 30 minutes of reperfusion, group with 1 and 2 mM/L L-arginine showed a trend of better recovery in left ventricular systolic function(left ventricular developed pressure, positive maximum dpfdt), diastolic function(negative maximum dpfdt) and coronary flow compared to control group(reperfusate no L-arginine). Recovery was impaired with a higher concentration, and at 4 moil L-arginine r covery was worse than control(p (0, 05). These results suggest that optimal concentration of L-arginine Is Important or the recovery of myocardial and endothelial function after ischemia and reperfusion.

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학술 1 - 개와 고양이의 비심인성 폐부종

  • Lee, Hyeon-Un;Han, Dong-Hyeon
    • Journal of the korean veterinary medical association
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    • v.53 no.3
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    • pp.192-197
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    • 2017
  • 폐부종은 심인성, 혹은 비심인성 요인에 의해 발생한다. 심인성폐부종(Cardiogenic Pulmonary Edema, CPE)은 심질환, 좌심방 압력의 증가, 폐정맥과 폐모세혈관의 압력 증가와 관련있다. 이와는 대조적으로 비심인성 폐부종(Noncardiogenic Pulmonary Edema, NCPE)은 좌심방의 압력증가에 의해서 혹은 기저질환인 심장 질환과 관련없이 발생한 국소적인 정수압의 증가하여 발생하거나, 폐포나 모세혈관내 피표면의 투과도의 변화에 의해서 발생한다. 혹은 국소적인 정수압 및 투과도의 복합적인 변화 모두에 의하여 발생한다. NCPE의 환축을 적절하게 치료하기 위하여 CPE와 반드시 감별되어야 한다. 또한, 심인성 및 NCPE의 감별 및 적절한 처치를 위하여는 철저한 환축의 병력, 신체검사, 흉부방사선 촬영 등의 검사를 실시하여야 한다. NCPE는 원발요인과 치료반응에 따라 예후가 달라질 수 있다.

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