Comparison of epinephrine and vasopressin in a pediatric porcine model of asphyxial cardiac arrest

OBJECTIVE: This study was designed to compare the effects of vasopressin vs. epinephrine vs. the combination of epinephrine with vasopressin on vital organ blood flow and return of spontaneous circulation in a pediatric porcine model of asphyxial arrest. DESIGN: Prospective, randomized laboratory investigation using an established porcine model for measurement of hemodynamic variables, organ blood flow, blood gases, and return of spontaneous circulation. SETTING: University hospital laboratory. SUBJECTS: Eighteen piglets weighing 8-11 kg. INTERVENTIONS: Asphyxial cardiac arrest was induced by clamping the endotracheal tube. After 8 mins of cardiac arrest and 8 mins of cardiopulmonary resuscitation, a bolus dose of either 0.8 units/kg vasopressin (n = 6), 200 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered in a randomized manner. Defibrillation was attempted 6 mins after drug administration. MEASUREMENTS AND MAIN RESULTS: Mean +/- SEM coronary perfusion pressure, before and 2 mins after drug administration, was 13 +/- 2 and 23 +/- 6 mm Hg in the vasopressin group; 14 +/- 2 and 31 +/- 4 mm Hg in the epinephrine group; and 13 +/- 1 and 33 +/- 6 mm Hg in the epinephrine-vasopressin group, respectively (p = NS). At the same time points, mean +/- SEM left ventricular myocardial blood flow was 44 +/- 31 and 44 +/- 25 mL x min-(1) x 100 g(-1) in the vasopressin group; 30 +/- 18 and 233 +/- 61 mL x min(-1) x 100 g(-1) in the epinephrine group; and 36 +/- 10 and 142 +/- 57 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p < .01 epinephrine vs. vasopressin; p < .02 epinephrine-vasopressin vs. vasopressin). Total cerebral blood flow trended toward higher values after epinephrine-vasopressin (60 +/- 19 mL x min(-1) x 100 g(-1)) than after vasopressin (36 +/- 17 mL x min(-1) x 100 g(-1)) or epinephrine alone (31 +/- 7 mL x min(-1) x 100 g(-1); p = .07, respectively). One of six vasopressin, six of six epinephrine, and four of six epinephrine-vasopressin-treated animals had return of spontaneous circulation (p < .01, vasopressin vs. epinephrine). CONCLUSIONS: Administration of epinephrine, either alone or in combination with vasopressin, significantly improved left ventricular myocardial blood flow during cardiopulmonary resuscitation. Return of spontaneous circulation was significantly more likely in epinephrine-treated pigs than in animals resuscitated with vasopressin alone.     

氨茶碱和肾上腺素在大鼠窒息心脏停搏模型中的疗效比较

虽然肾上腺素是公认的一线心肺复苏药物 ,但其疗效尚不理想 ,心肺复苏的成功率仍很低 ( 0～ 10 %) 〔1〕。临床和实验研究发现 ,心肌缺血和缺氧时存在大量的腺苷释放 ,后者可拮抗儿茶酚胺的兴奋作用 ,降低起搏细胞的功能 ,减慢心率 ,抑制房室传导 〔2〕;扩张血管 ,增加电除颤的阈值 ,故推测拮抗腺苷的药物氨茶碱可能有助于心搏骤停的治疗 〔3〕。国内外报道的氨茶碱应用于心肺复苏中的初步结果都是在肾上腺素等药物无效时的使用 ,尚无单独早期使用氨茶碱的研究。本实验中试图比较单用氨茶碱和肾上腺素在心肺复苏中的疗效。1　材料与方法表 1…     

肾上腺素与血管加压素对窒息性心脏骤停大鼠早期心肺复苏的影响

目的：比较肾上腺素与血管加压素对室息性心脏骤停大鼠早期心肺复苏的影响。方法：健康SI）夫鼠48只,体重200～250g,雌雄产拘,将大鼠随机分成4组（n=12）：正常对照组（C组）、模型组（M组）、肾上腺素组（E组）和血管加雎素组（V组）。M组、E组及V绀大鼠均经气管夹闭1min,建立窒息性心脏骤停模型。肖窒息时间达1min时,分别在常规心肺复苏前：c组和M组大鼠经股静脉注射生理盐水1m1。E组及V纰大鼠经股静脉分别注射肾上腺素0．04mg／kg及血管加压素0．4u／kg,H时开始胸外心脏按压及机械通气,观察自主循环恢复情况,5min无效则放弃复苏。自主循环恢复的大鼠连续监测心电和血压30min。记录在CPR30min内自主循环恢复情况及血流动力学;记录CPR30rain后,采用免疫组织化学法检测各组实验大鼠血清中肿瘤坏死因子-水平、白细胞介素6及白细胞介素10水平。结果：E、V组大鼠自主循环恢复率均显著高于M组（分别为73．4％．74．6％,和15．3％,P〈0．05）．E组大鼠自主循环恢复牢与V组比较差异无统计学意义（P〉0．05）;E、V组大鼠平均动脉压明显高于M绀大鼠（P〈0．05）,V组大鼠MAP高于E组大鼠。差异有统计学意义（P〈0．05）。M组大鼠血清中自细胞介素6及肿瘤坏死因子-水平与E、V组差异有统计学意义（P〈0．05）;E组大鼠m清中肿瘤坏死阔子-及白细胞介素-6水平高于V组（P〈0．05）。E组大鼠血清中白细胞介素-10水平低于V组（P〈0．05）。结论：肾卜腺素与血管加压素在窒息性心脏骤停大鼠早期心肺复苏过程中复苏成功牢无明显差异,但血管加乐素町维持大鼠复苏后平均动脉搓在相对较高水平;同时血管加压素可提高复苏后大鼠血清中抗炎因子水平。     

心肺复苏中单用肾上腺素或联合血管加压素治疗的Meta分析

目的 在心搏骤停实施心肺复苏过程中,联合应用血管紧张素和肾上腺素的效果是否优于单用肾上腺素目前尚无统一的结论,本研究拟针对现有临床资料进行荟萃分析.方法 在NED-LINE及EMBASE数据库中检索关于比较成人心肺复苏时单用肾上腺素或联合应用血管紧张素的所有临床研究,首要观察指标为复苏后自主循环恢复率(ROSC).结果 在检索到的485篇文章中,6篇为随机对照临床研究.荟萃分析结果显示,除复苏后24 h生存率联合用药优于单用肾上腺素(OR值为2.99,95%CI 1.43～6.28)外,其余各项指标比较差异均无统计学意义.结论 荟萃分析中仅有包含122例患者的24 h生存率组联合用药优于单用肾上腺素,因此尚不支持复苏中应用血管加压素联合肾上腺素.     

Comparison of normal saline, hypertonic saline and hypertonic saline colloid resuscitation fluids in an infant animal model of hypovolemic shock

PurposeIncorrect resuscitation after hypovolemic shock is a major contributor to preventable pediatric death. Several studies have demonstrated that small volumes of hypertonic or hypertonic–hyperoncotic saline can be an effective initial resuscitation solution. However, there are no pediatric studies to recommend their use. The aim of this study is to determine if in an infant animal model of hemorrhagic shock, the use of hypertonic fluids, as opposed to isotonic crystalloids, would improve global hemodynamic and perfusion parameters.MethodsExperimental, randomized animal study including thirty-four 2-to-3-month-old piglets. 30 min after controlled 30 mL kg^?1 bleed, pigs were randomized to receive either normal saline (NS) 30 mL kg^?1 (n = 11), 3% hypertonic saline (HS) 15 mL kg^?1 (n = 12), or 5% albumin plus 3% hypertonic saline (AHS) 15 mL kg^?1 (n = 11).ResultsHigh baseline heart rate (HR) and low mean arterial pressure (MAP), cardiac index (CI), brain tissue oxygenation index (bTOI), and lactate were recorded 30 min after volume withdrawal, with no significant differences between groups. Thirty minutes after volume replacement there were no significant differences between groups for HR (NS, 188 ± 14; HS, 184 ± 14; AHS, 151 ± 14 bpm); MAP (NS, 80 ± 7; HS, 86 ± 7; AHS, 87 ± 7 mmHg); CI (NS, 4.1 ± 0.4; HS, 3.9 ± 0.4; AHS, 5.1 ± 0.4 mL min^?1 m^?2); lactate (NS, 2.8 ± 0.7; HS, 2.3 ± 0.6; AHS, 2.4 ± 0.6 mmol L^?1); bTOI (NS, 43.9 ± 2.2; HS, 40.1 ± 2.5; AHS, 46.1 ± 2.3%).ConclusionsIn this model of hypovolemic shock, hypertonic fluids achieved similar end-points as twice the volume of NS. Animals treated with albumin plus hypertonic saline presented prolonged increase in blood volume parameters and recovery of the oxygen debt.     

Splanchnic and renal blood flow after cardiopulmonary resuscitation with epinephrine and vasopressin in pigs

In laboratory investigations, vasopressin given during CPR resulted in improved vital organ blood flow when compared with epinephrine. Given the profound and long lasting vasopressor effects of vasopressin, we tested the hypothesis that vasopressin given during CPR would result in renal and splanchnic hypoperfusion in the post-resuscitation period when compared with epinephrine. After 4 min of ventricular fibrillation, 16 pigs were randomly assigned to receive either 0.045 mg·kg⁻¹ epinephrine or 0.4 U·kg⁻¹ vasopressin before defibrillation. Splanchnic and renal blood flow were measured 30, 90, and 240 min after restoration of spontaneous circulation (ROSC) in the epinephrine and vasopressin groups and in a control group of eight pigs using radiolabeled microspheres. Hepatic blood flow was measured before arrest and 30, 90, and 240 min after ROSC by means of indocyanine green infusion. Thirty minutes after ROSC, renal and adrenal blood flow were significantly lower in the vasopressin group (300 [273–334] and 256 [170–284] ml·min⁻¹·100 g⁻¹) (median and 25th and 75th percentile) as compared with the epinephrine group (370 [346–429] and 360 [326–420] ml·min⁻¹·100 g⁻¹; P<0.05). Pancreatic, intestinal, and hepatic blood flow were not significantly different in animals after receiving epinephrine or vasopressin. In comparison to epinephrine, vasopressin given during cardiac arrest impairs renal and adrenal perfusion temporarily but does not lead to intestinal or hepatic hypoperfusion in the post-resuscitation phase.     

Comparison of high-dose epinephrine versus standard-dose epinephrine in adult cardiac arrest in the prehospital setting

OBJECTIVE: To compare the efficacy of high-dose epinephrine (HDE) with standard-dose epinephrine (SDE) in the management of cardiac arrest in adults in the prehospital setting. HYPOTHESIS: The use of HDE will improve the outcome of adult patients in cardiac arrest. METHODS: In a general population of 700,000 persons, in a mixed geographical area of 2,200 square miles, a 12-month retrospective study of SDE and a 12-month prospective trial of HDE were conducted involving adult patients in cardiac arrest in the prehospital setting. Treatment was provided by paramedic-level clinicians. In the control group, patients were treated according to existing American Heart Association cardiac resuscitation guidelines using SDE (defined as 1.0 mg boluses to a maximum dose of 4 mg). In the test group, the same guidelines were revised to use HDE (defined as a rapid sequence of 5, 10, and 15 mg boluses to a total dose of 30 mg). RESULTS: The control group included 594 patients; the test group consisted of 580 patients. The overall survival rate to hospital admission in the control group was 14.5% (84 patients) and in the test group 15.3% (89 patients). The survival rate to hospital discharge in the control group was 4.9% (29 patients) versus 4.8% (28 patients) in the test group. For patients whose initial rhythms were ventricular fibrillation, survival to admission in the control group was 20.4% (39 patients) versus 24.4% (43 patients) in the test group. Survival to discharge for patients with ventricular fibrillation in the control group was 8.9% (17 patients) versus 10.8% (19 patients) in the test group. CONCLUSION: There was no statistically significant difference in overall rate of survival to hospital admission or discharge between patients treated with SDE and those treated with HDE, regardless of the initial rhythm.     

Terlipressin versus adrenaline in an infant animal model of asphyxial cardiac arrest

Purpose  

The objective of this study was to compare the efficacy of terlipressin versus adrenaline in an experimental infant animal model of asphyxial cardiac arrest (ACA).     

Comparison of epinephrine and norepinephrine in the treatment of asphyxial or fibrillatory cardiac arrest in a porcine model

Many animal experiments have shown that alpha-receptor stimulation is a prerequisite for the improvement of myocardial perfusion during CPR. As there are no recent reports on the effectiveness of norepinephrine in the treatment of cardiac arrest, we investigated the effectiveness of epinephrine and norepinephrine after asphyxial or ventricular fibrillation cardiac arrest using a porcine model. After 3 min of asphyxial cardiac arrest, seven animals each received either 45 micrograms/kg epinephrine, 45 micrograms/kg norepinephrine, or placebo (controls). All drugs were given blind. All seven animals given epinephrine could be resuscitated after 174 +/- 53 sec, whereas six of seven given norepinephrine could be resuscitated after 473 +/- 116 sec. None of the seven given the placebo could be resuscitated. After 4 min of ventricular fibrillation cardiac arrest, none of the seven animals that received defibrillating countershocks at 4 min without either mechanical measures or drug therapy, and none of the seven that received CPR and countershocks but no drugs, could be resuscitated. In the group that received CPR plus 45 micrograms/kg epinephrine, defibrillation and restoration of spontaneous circulation were achieved in six of seven animals in 667 +/- 216 sec. In the group that received CPR plus 45 micrograms/kg norepinephrine, defibrillation and restoration of spontaneous circulation were achieved in all seven animals in the significantly shorter time of 86 +/- 18 sec. In this porcine model, norepinephrine appeared superior to the same dose of epinephrine in the treatment of ventricular fibrillation, with respect to resuscitation time.     

Effect of cardiac arrest time on cortical cerebral blood flow during subsequent standard external cardiopulmonary resuscitation in rabbits

Standard external cardiopulmonary resuscitation (SECPR) produces high cerebral venous and intracranial pressure peaks, low cerebral perfusion pressure, and low cerebral blood flow (CBF). Cerebral viability seems to require 20% of normal CBF, which SECPR cannot reliably generate. We tested the hypothesis that SECPR can produce adequate CBF if started immediately, but not if started after a long period of cardiac arrest (no flow, stasis). Cardiac arrest times of 1, 3, 5, 7 and 9 min were studied in rabbits. We measured unifocal cortical CBF with H2 clearance curves after saturation with H2 10%, O2 50% and N2O 40% by intermittent positive-pressure ventilation (IPPV). Measurements were made during spontaneous circulation (control condition), and then after resaturation immediately before induction of asystole by KCl i.v., and H2 clearance starting at end of arrest time during SECPR-basic life support with IPPV 100% and manual chest compressions (120/min) during asystole. Control cortical CBF was 30-40 ml/100 g brain per min. During asystole and SECPR, CBF greater than 20% normal was achieved only after no-flow of 1 min. After longer arrest (no-flow) times, CBF was less than 20% normal. Values were near zero after 7 and 9 min of cardiac arrest. Decrease in mean arterial pressures (MAP) produced by SECPR during asystole paralleled CBF values. Thus, the longer the preceding period of stasis, the lower the MAP and CBF generated by SECPR without epinephrine. This effect may be the result of anoxia-induced vasoparalysis and stasis-induced increased blood viscosity.     

Dose-response of vasopressin in a rat model of asphyxial cardiac arrest

The advantage of vasopressin over epinephrine in the treatment of cardiac arrest (CA) is still being debated, and it is not clear whether a high dose of vasopressin is beneficial or detrimental during or after cardiopulmonary resuscitation (CPR) in a rat model of CA. In this study, asphyxial CA was induced in 40 male Sprague-Dawley rats. After 10 minutes of asphyxia, CPR was initiated; and the effects of different doses of vasopressin (low dose, 0.4 U/kg; medium dose, 0.8 U/kg; and high dose, 2.4 U/kg; intravenous; n = 10 in each group) and a saline control (isotonic sodium chloride solution, 1 mL, intravenous) were compared. Outcome measures included the rate of restoration of spontaneous circulation (ROSC) and changes of hemodynamic and respiratory variables after ROSC. The rates of ROSC were 1 of 10 in the saline group and 8 of 10 in each of the 3 vasopressin groups. There were no differences in mean aortic pressure or changes of respiratory function after CPR among the vasopressin groups. However, the heart rate was lower in the high-dose vasopressin group than in the low- and medium-dose groups. These findings indicate that different doses of vasopressin result in a similar outcome of CPR, with no additional benefits afforded by a high dose of vasopressin during or after CPR, in a rat model of asphyxial CA. The mechanism and physiologic significance of the relative bradycardia that occurred in the high-dose vasopressin group are currently unknown and require further investigation.     

Effects of N-methyl-L-arginine on cardiac and regional blood flow in a dog endotoxin shock model

PURPOSE: Indirect evidence suggests a decrease in organ perfusion as a result of nitric oxide (NO) inhibition in endotoxic shock. Cardiac and regional hemodynamic responses to N-methyl-L-arginine (L-NMA), a nonspecific inhibitor of constitutive and inducible nitric oxide synthase (NOS), were assessed in nine conscious dogs subjected to endotoxin. MATERIALS AND METHODS: Lipopolysaccharide (LPS) was titrated to a maximum of 200 microg/kg, IV, over 45 minutes. L-NMA was given in a dose of 20 mg/kg, IV. Hemodynamic parameters were recorded for 6 hours following L-NMA administration. RESULTS: LPS induced significant decreases in mean arterial blood pressure (MAP), cardiac output (CO), first derivative of left ventricular pressure (dP/dt), coronary blood flow, carotid blood flow, mesenteric blood flow, renal blood flow, and a significant hepatic vasodilation. L-NMA fully reversed the effects of LPS on MAP, heart rate, dP/dt, coronary and carotid blood flow, and reversed mesenteric blood flow and hepatic blood flow at 1 and 3 hours, respectively. L-NMA partially overcame the LPS-induced decrease in renal blood flow at 30 minutes and 1 hour. Except for mesenteric and carotid circulation, L-NMA did not change regional vascular resistance. CONCLUSIONS: It is likely that constitutive NOS is implicated in immediate cardiac, carotid, mesenteric, and renal vascular changes, whereas inducible NOS accounted for delayed responses in hepatic and coronary circulation.     

Arterial blood gases during cardiac arrest: markers of blood flow in a canine model.

Measures of CO2 have been shown to correlate with coronary perfusion pressure and cardiac output during cardiac arrest. We evaluated arterial pH (pHa) relative to blood flow during cardiac arrest in a canine electromechanical dissociation (EMD) model of cardiac arrest using different resuscitation techniques. Following 15 min of cardiac arrest, 24 mongrel dogs received epinephrine with continued CPR or closed-chest cardiopulmonary bypass. Central arterial blood gases, end-tidal carbon dioxide (PetCO2), coronary perfusion pressure and cardiac output were measured. During CPR, prior to epinephrine or bypass, there was no correlation of pHa, PACO2 and PetCO2, with cardiac output or coronary perfusion pressure. Immediately after instituting the resuscitation techniques, both pHa and PaCO2 showed a significant correlation with cardiac output (pHa; R = -0.78, P less than 0.001 and PaCO2; R = 0.87, P less than 0.001) and with coronary perfusion pressure (pHa; R = -0.75, P less than 0.001 and PaCO2; R = 0.75, P less than 0.001). Eventual survivors (n = 15) had an early significant decrease in pHa, base excess and a significant increase in PaCO2 which was not present in non-survivors (n = 9). Neither pHa nor PaCO2 correlate with blood flow under low flow conditions of CPR. However, with effective circulatory assistance, pHa and PaCO2 reflect systemic blood flow and reperfusion washout.     

Vasopressin and epinephrine in the treatment of cardiac arrest: an experimental study

Background

Epinephrine remains the drug of choice for cardiopulmonary resuscitation. The aim of the present study is to assess whether the combination of vasopressin and epinephrine, given their different mechanisms of action, provides better results than epinephrine alone in cardiopulmonary resuscitation.

Methods

Ventricular fibrillation was induced in 22 Landrace/Large-White piglets, which were left untreated for 8 minutes before attempted resuscitation with precordial compression, mechanical ventilation and electrical defibrillation. Animals were randomized into 2 groups during cardiopulmonary resuscitation: 11 animals who received saline as placebo (20 ml dilution, bolus) + epinephrine (0.02 mg/kg) (Epi group); and 11 animals who received vasopressin (0.4 IU/kg/20 ml dilution, bolus) + epinephrine (0.02 mg/kg) (Vaso-Epi group). Electrical defibrillation was attempted after 10 minutes of ventricular fibrillation.

Results

Ten of 11 animals in the Vaso-Epi group restored spontaneous circulation in comparison to only 4 of 11 in the Epi group (p = 0.02). Aortic diastolic pressure, as well as, coronary perfusion pressure were significantly increased (p < 0.05) during cardiopulmonary resuscitation in the Vaso-Epi group.

Conclusion

The administration of vasopressin in combination with epinephrine during cardiopulmonary resuscitation results in a drastic improvement in the hemodynamic parameters necessary for the return of spontaneous circulation.     

Effects of hypertonic saline on myocardial blood flow in a porcine model of prolonged cardiac arrest

OBJECTIVE: To evaluate the effects of hypertonic saline (HS) on myocardial reperfusion pressure (MPP) and blood flow (MBF), and cardiac index (CI) during and after cardiopulmonary resuscitation (CPR). METHODS: In 21 domestic swine (16-23 kg) open chest cardiac massage was initiated after 10 min of ventricular fibrillation. With the onset of CPR animals randomly received HS (7.2%; 2 ml/kg per 10 min or 4 ml/kg per 20 min) or normal saline ((NS); 2 ml/kg per 10 min). Haemodynamic variables were monitored continuously, and coloured microspheres were used to measure MBF and CI before cardiac arrest (CA), during CPR and 5, 30 and 120 min after the return of spontaneous circulation. RESULTS: During CPR HS significantly increased MPP, MBF, and CI in comparison to NS (P<0.05, resp., MANOVA). Doubling the volume of HS did not improve the haemodynamic effects seen after application of 2 ml/kg per 10 min. HS-infusion significantly increased the survival rate at 120 min, 6/7 and 5/7 animals receiving 2 ml/kg per 10 min or 4 ml/kg per 20 min versus 2/7 after NS-infusion (P<0.05, chi(2)-test). CONCLUSIONS: HS applied during open chest cardiac massage enhanced MBF and CI, and significantly increased resuscitation success and survival rate. The positive effects of this promising new approach need to be confirmed in clinical studies.     

加压素与肾上腺素在小鼠心肺复苏中的疗效比较

目的 比较加压素与肾上腺素在小鼠心肺复苏中的疗效.方法 30只雄性昆明小鼠经食道快速起搏心窒诱发室颤、建立心搏骤停模型,起搏开始后4 min将小鼠随机分成3组(n=10/组):对照组(Sal-gro)、加压素组(Vas-gro)、肾上腺素组(Epi-gro),分别经动脉注射药物(生理盐水、加压素0.4 U/kg和肾上腺素0.04mg/kg)1次,开始胸外心脏按压及机械通气,观察自主循环恢复情况,10min无效则放弃复苏.自主循环恢复的小鼠连续监测心电和血压60 min,观察血压、心率、呼吸恢复情况及生存时间.结果 加压素与肾上腺素组小鼠的自主循环恢复率均显著高于对照组(9/10,10/10和3/10,P＜0.05,P＜0.01).加压素与肾上腺素组组间比较差异无统计学意义(P＞0.05).肾上腺素组小鼠在自主循环恢复后全部出现自主呼吸,而加压素组小鼠只有4只出现自主呼吸(P＜0.05).肾上腺素组小鼠的生存时间明显长于加压素组和对照组小鼠(P＜0.05,P＜0.05).结论 加压素和肾上腺素均可显著提高心搏骤停小鼠的自主循环恢复率,但0.04 mg/kg的肾上腺素对自主循环恢复后小鼠呼吸功能及生存时间的影响明显优于0.4 U/k的加压素,其机制尚不清楚,还有待进一步研究.     

氨茶碱与肾上腺素对窒息致心脏停搏大鼠心脏硬度影响的研究

目的探讨氨茶碱与肾上腺素在大鼠窒息致心脏停搏模型中对心脏硬度的影响。方法采用呼气末夹闭气管方法建立起大鼠心脏停搏模型。48只大鼠随机分为生理盐水对照组(对照组)、氨茶碱组、肾上腺素组、氨茶碱与肾上腺素合用组(合用组),心肺复苏后1h处死动物尸检观察心脏硬度。结果①氨茶碱组心肌硬度记分(2．92±0．79)和肾上腺组(3．92±1．00)均高于对照组(2．17±0．83,P均＜0．05);②合用组心肌硬度记分(2．50±1．09)低于肾上腺组,差异具统计学意义(P=0．003);③氨茶碱组、肾上腺素组和合用组自主循环恢复动物的心脏硬度记分均值均明显低于未恢复者,且差异均具统计学意义(P均＜0．05);④复苏后1h处死动物心脏硬度记分与复苏过程中最高收缩压、舒张压和平均压之间均存在中度正相关(P均＜0．05)。结论在窒息致心脏停搏大鼠模型中肾上腺素与氨茶碱均可导致心脏硬度的增加,这种心脏过度收缩致舒张障碍,即石头心现象,可能是其复苏失败的原因之一。