ELISA法测定人血管加压素血药浓度的方法及意义

目的 建立测定人血管加压素血药浓度含量的ELISA检测方法,探讨其临床意义.方法 用ELISA法对30例正常人体血样和8例定量配制加压素的血样进行血管加压素含量测定.结果 ELISA法检测血管加压素的回归方程为Y=102.7X+3.4959,R2=0.9758,回收率为101.7％,经检测健康人体的血管加压素水平为(40±20) pg/ml.结论 ELISA法可适用于人血管加压素血药浓度的测定.     

血管加压素对脑复苏的研究

目的探讨血管加压素对脑复苏成功率的研究.方法对53例心脏骤停的患者随机分组;①A组40例为治疗组应用血管加压素 肾上腺素,血管加压素40单位,肾上腺素为1mg,.依此类推增加剂量;②B组13例为对照组:应用肾上腺素1mg,肾上腺素可用1mg、3mg、5mg,依此类推增加剂量;③观察复苏成功指标,应用心脏监护观察心脏电活动波形,心脏复跳,血压回升,瞳孔缩小,昏迷程度变浅,彩色经颅多普勒观察大脑电活动情况.结果40例患者脑复苏成功37例,3例合并严重肺部感染而死亡,无1例发生脑死亡.结论应用血管加压素使脑复苏成功率提高,可以防止脑组织的病理性损害,降低脑死亡的发生率.血管加压素是个安全,有效的药物,可望在心肺脑复苏中有着突破性的进展.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素在心肺复苏中的应用观察

目的 研究大剂量血管加压素在心肺复苏中的疗效.方法 47例心跳停搏患者随机分为3组,肾上腺素标准剂量组(A组)17例,血管加压素40u+标准剂量肾上腺素组(B组)14例,大剂量血管加压素80U+标准剂量.肾上腺素组(C组)16例.各组分别观察自主循环恢复率、存活率、自主循环恢复时间.结果 A组、B组、C组自主循环恢复率分别为17.6%、50%、56.3%,B组、C组明显高于A组,C组存活率(31.3%)显著高于A组(5.9%)、B组(14.3%);B组、C组的自主循环恢复时间明显短于A组.结论 心肺复苏期间,联合应用大剂量血管加压素和肾上腺素比单独应用标准剂量肾上腺素、血管加压素40U+标准剂量肾上腺素能显著缩短自主循环恢复时间,提高自主循环恢复率和存活率.     

大剂量血管加压素治疗静脉曲张性上消化道出血

目的：探讨血管加压素不同剂量对静脉曲张性上消化道出血疗效。方法：收集46例确诊的肝硬化失代偿期并食道、胃底静脉曲张破裂出血的病人，以不同剂量血管加压素进行疗效对比。结果：大剂量血管加压素治疗有效率高，止血时间快，复发率低。结论：大剂量血管加压素治疗明显优于常规剂量血管加压素。     

Characterization of acute hemodynamic effects of antidiuretic agonists in conscious dogs

Conscious dogs instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter) received intravenous injections of 4-valine-8-D-arginine vasopressin (VDAVP) and 1-deamino-8-D-arginine vasopressin (dDAVP), two specific antidiuretic agonists. Both agents led within minutes to dose-dependent increases in cardiac output and heart rate, as well as to decreases of total peripheral resistance and mean arterial pressure. Indomethacin did not affect the hemodynamic responses to VDAVP administration. The analog 8-arginine-9-desglycinamide vasopressin, which retains behavioral effects of vasopressin but is a weak antidiuretic agonist, showed only weak hemodynamic effects that were similar in nature to those of VDAVP and dDAVP. Thus, the capability to increase cardiac output and decrease peripheral resistance appeared to correlate best with the antidiuretic activity of the three vasopressin analogs tested. We also observed that pretreatment of dogs with a combined vasopressor (V1) and antidiuretic (V2) vasopressin antagonist completely prevented the increase in cardiac output that is normally associated with the infusion of arginine-vasopressin, 10 ng kg-1 min-1, after V1 blockade. Our results confirm the existence of powerful, dose-related hemodynamic effects of various antidiuretic agonists in conscious dogs; these effects being opposite to those normally elicited by arginine-vasopressin.     

Vasopressin During Cardiopulmonary Resuscitation and Different Shock States

Vasopressin administration may be a promising therapy in the management of various shock states. In laboratory models of cardiac arrest, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the rate of return of spontaneous circulation, and neurological recovery compared with epinephrine (adrenaline). In a study of 1219 adult patients with cardiac arrest, the effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity; however, vasopressin was superior to epinephrine in patients with asystole. Furthermore, vasopressin followed by epinephrine resulted in significantly higher rates of survival to hospital admission and hospital discharge. The current cardiopulmonary resuscitation guidelines recommend intravenous vasopressin 40 IU or epinephrine 1mg in adult patients refractory to electrical countershock. Several investigations have demonstrated that vasopressin can successfully stabilize hemodynamic variables in advanced vasodilatory shock. Use of vasopressin in vasodilatory shock should be guided by strict hemodynamic indications, such as hypotension despite norepinephrine (noradrenaline) dosages >0.5 mug/kg/min. Vasopressin must never be used as the sole vasopressor agent. In our institutional routine, a fixed vasopressin dosage of 0.067 IU/min (i.e. 100 IU/50 mL at 2 mL/h) is administered and mean arterial pressure is regulated by adjusting norepinephrine infusion. When norepinephrine dosages decrease to 0.2 microg/kg/min, vasopressin is withdrawn in small steps according to the response in mean arterial pressure. Vasopressin also improved short- and long-term survival in various porcine models of uncontrolled hemorrhagic shock. In the clinical setting, we observed positive effects of vasopressin in some patients with life-threatening hemorrhagic shock, which had no longer responded to adrenergic catecholamines and fluid resuscitation. Clinical employment of vasopressin during hemorrhagic shock is experimental at this point in time.     

Chronic vasopressin V(1A) but not V(2) receptor antagonism prevents heart failure in chronically infarcted rats

Evidence is increasing that therapeutic modulation of neurohormonal activation with vasopressin receptor antagonists via V(1A) and V(2) receptors may favourably affect prognosis of heart failure. This study was designed to compare in vivo hemodynamic effects of early treatment (1-21 days after infarction) with a V(1A) (SR-49059 or ((2S)1-[(2R3S)-5-chloro-3-(2-chlorophenyl)-1-(3,4-dimethoxybenzene-sulfonyl)-3-hydroxy-2,3-dihydro-1H-indole-2-carbonyl]-pyrrolidine-2-carboxamide); 0.3 mg/kg/day) and a V(2) (SR-121463B or (1-[4-(N-tert-Butylcarbamoyl)-2-methoxybenzene sulfonyl]-5-ethoxy-3-spiro-[4-(2-morpholinoethyoxy)-cyclo-hexane]indol-2one,furmate; 0.5 mg/kg/day) receptor antagonist in myocardial infarcted rats, chronically instrumented for hemodynamic measurements. Left ventricular dysfunction in conscious myocardial infarcted rats, which was evidenced by a significantly decreased cardiac output (myocardial infarction: 70+/-3 vs. sham: 81 +/- 3 ml/min) and stroke volume (myocardial infarction: 190 +/- 10 vs. sham: 221 +/- 7 microl), was restored by the vasopressin V(1A) (81+/-2 ml and 224 +/- 5 microl, respectively) but not V(2) receptor antagonist. Improved cardiac output with the vasopressin V(1A) receptor antagonist resulted from an increased stroke volume at a reduced myocardial infarction induced tachycardia. In addition to the hemodynamic measurements, left ventricular hypertrophy and capillary density were determined, histologically measured as the cross-sectional area of Gomori-stained myocytes and Lectin-stained capillaries per tissue area, respectively. The observed left ventricular concentric hypertrophy (myocardial infarction: 525 +/- 38 vs. sham: 347 +/- 28 microm(2); P < 0.05) and reduced capillary density (myocardial infarction: 2068 +/- 162 vs. sham: 2800 +/- 250 number/mm(2); P<0.05) in the spared myocardium of myocardial infarcted rats, remained unaffected by the vasopressin V(1A) or V(2) receptor antagonist. Thus, chronic vasopressin V(1A) but not V(2) receptor blockade prevents heart failure in 3-week-old infarcted rats. Moreover, the improved cardiac function could not attributed to changes in left ventricular hypertrophy and/or capillary density.     

Lack of an effect of body mass on the hemodynamic response to arginine vasopressin during septic shock

STUDY OBJECTIVE: To determine whether body mass alters the effectiveness of a fixed-dose infusion of arginine vasopressin. DESIGN: Retrospective medical record review. SETTING: All intensive care units of a tertiary medical center. PATIENTS: Sixty-six mechanically ventilated patients who received a fixed-dose intravenous infusion of arginine vasopressin at 0.04 U/minute as the sole agent for hemodynamic support during septic shock. MEASUREMENTS AND MAIN RESULTS: Patients were divided into four groups on the basis of body mass index. Effectiveness was measured as hemodynamic stability, which was defined as the proportion of patients achieving a mean arterial pressure (MAP) of 65 mm Hg or higher, the magnitude of the change in MAP at 1 hour, and the need for additional rescue vasopressors. Secondary outcomes included mortality and length of stay. Baseline characteristics of all four groups were comparable for age, sex, and severity of illness determined by using Acute Physiology and Chronic Health Evaluation II (APACHE II), Simplified Acute Physiology II (SAPS II), and Sequential Organ Failure Assessment (SOFA) scores. The only significant differences in baseline characteristics among the groups were in their central venous pressures. The four groups similarly achieved hemodynamic stability at 1 hour after the administration of arginine vasopressin (p=0.41). We observed no significant differences among groups in the magnitude of MAP change (p=0.62), need for rescue catecholamine vasopressors (p=0.17), 28-day mortality rates (p=0.31), or length of stay in the intensive care unit (p=0.43). CONCLUSION: Body mass index did not alter the effects of arginine vasopressin on hemodynamic stability or changes in MAP when the drug was administered as a fixed-dose infusion of 0.04 U/minute. Our results do not support weight-based dosing of vasopressin, unlike the dosing for catecholamine vasopressors.     

Increase in sensitivity of the baroreceptor reflex following microinjection of carbachol into the posterior hypothalamic nucleus of awake rats

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Vasopressin and renin in high output heart failure of rats: hemodynamic effects of elevated plasma hormone levels

We studied the hemodynamic effects of vasopressin and the renin-angiotensin system in an animal model of high output heart failure in conscious rats (aorto-caval fistula). We found significantly elevated levels of plasma renin concentration (p less than 0.025), norepinephrine (p less than 0.02), and up to 4 to 5 times higher values of vasopressin (p less than 0.002) in the rats with heart failure as compared with control animals. In contrast to the control rats that had a normally functioning osmoreceptor system, we found an inverse relationship between plasma osmolality and arginine vasopressin in the rats with heart failure in association with edema. Using a specific antagonist of the pressor activity of vasopressin, we found no significant effect on heart rate, mean arterial pressure, cardiac output (thermodilution), and peripheral vascular resistance in the control animals and in the rats with aorto-caval fistula. Captopril resulted in a significant fall of mean arterial pressure in the rats with shunt (p less than 0.001). The coincidence of high values of vasopressin and, in a number of animals, low plasma osmolalities and edema suggests a role of vasopressin in the formation of edema and in the development of "dilutional hypo-osmolality."     

Blood pressure and heart rate responses to microinjection of vasopressin into the nucleus tractus solitarius region of the rat

The nucleus tractus solitarius (NTS) region in the rat has been shown to receive arginine vasopressin (AVP) and oxytocin (OT) neurophysin-containing neuronal projections from the suprachiasmatic (SCN) and paraventricular nucleus (PVN). Thus, vasopressin and oxytocin might have central influences on the circulation. This was investigated by measuring arterial blood pressure and heart rate (HR) responses following microinjection of vasopressin and oxytocin (0.1, 1.0 and 10.0 ng) into the right nucleus tractus solitarius region of rats anesthetized with urethane. Injections of vasopressin into nucleus tractus solitarius produced dose-related increases in blood pressure and heart rate. The effect of oxytocin on the blood pressure and heart rate was of a lesser magnitude without showing a dose-response relationship. Equivolumetric injections of vehicle and luteinizing hormone-releasing hormone (LH-RH) peptide had no detectable effect on blood pressure and minimal effect on heart rate. Injections of vasopressin into three different sites in the brain stem (1 mm anterior, posterior, and lateral to the tractus solitarius) did not produce significant hemodynamic changes. Intravenously injected vasopressin produced increments in blood pressure only at the highest dose level (10.0 ng) and a decrease rather than an increase in heart rate. Ganglionic blockade significantly reduced pressor responses to vasopressin injected into the nucleus tractus solitarius region and completely eliminated HR responses. Pretreatment of the nucleus tractus solitarius with a vasopressin antagonist abolished the blood pressure and heart rate responses produced by injection of vasopressin. These results suggest that vasopressin acts in the region of the nucleus tractus solitarius to exert a central action on the circulation.     

Effects of parathyroid hormone or haloperidol-induced catalepsy and nigral GAD activity

The blood pressure and heart rate effects of the specific pressor antagonist of vasopressin d(CH₂)₅Tyr(Me)AVP, 5 μg i.v. was evaluated in conscious normotensive rats. Our results suggest that a baroreceptor reflex mediated decrease in sympathetic nerve activity, as reflected by a slowing in heart rate, returns blood pressure to baseline levels shortly after injections of exogenous vasopressin. This has to be taken into account when interpreting the hemodynamic response to vasopressin antagonists in rats pretreated with this vasopressive hormone.     

Massive caffeine overdose requiring vasopressin infusion and hemodialysis

INTRODUCTION: Massive caffeine overdose is associated with life-threatening hemodynamic complications that present challenges for clinicians. We describe the highest-reported serum concentration of caffeine in a patient who survived and discuss the first-reported use of vasopressin and hemodialysis in a caffeine-poisoned patient. CASE REPORT: A 41-yr-old woman presented 3 h after ingesting approximately 50 g of caffeine. She subsequently underwent cardiopulmonary resuscitation and received multiple medications in an attempt to raise her blood pressure and control her heart rate without success. Vasopressin infusion increased her blood pressure to the point where hemodialysis could be performed. Despite ensuing multisystem organ failure, she survived and has made a complete recovery. CONCLUSION: Hemodialysis and vasopressin infusions may be of benefit in the management of caffeine-intoxicated patients who fail to respond to standard therapies.     

伴有低钠血症的心力衰竭治疗新药——托伐普坦

心力衰竭时常伴随低钠血症。心力衰竭的一般治疗方法对低钠血症疗效不佳。托伐普坦是精氨酸加压素V_2受体的拮抗药。托伐普坦通过抑制肾脏集合管水的重吸收,使肾脏对水的排泄增加,起到纠正低钠血症、增加尿量、改善心力衰竭症状等作用。临床研究表明托伐普坦在伴有低钠血症的心力衰竭治疗中发挥重要作用。