多次活性炭灌胃对大鼠血浆敌敌畏浓度的影响

目的 探讨活性炭灌胃对急性有机磷农药中毒的治疗作用.方法 30只雄性清洁级Wistar大鼠随机(随机数字法)分成3组:对照组(A组)、单次活性炭番泻叶组(B组)和多次活性炭番泻叶组(C组),每组10只.A组按35 mg/kg剂量经口敌敌畏染毒,不给予活性炭和番泻叶.B组按35 mg/kg剂量经口敌敌畏染毒,染毒后立即给予活性炭175 mg/kg,半小时后再予番泻叶35 mg/kg经口灌服.C组按35 mg/kg剂量经口敌敌畏染毒,染毒后立即给予活件炭175 mg/kg、番泻叶35 mg/kg每4 h经口灌服.每组均于染毒后不同时间分别采血,检测血中敌敌畏浓度和全血胆碱酯酶活性.对3组各时间点血中敌敌畏质最浓度、峰浓度(Cmax)、曲线下面积(AUC)0→∞、平均保留时间(MRT)值、胆碱酯酶活性数据进行单因素方差分析.结果 染毒后单次灌胃组及多次灌胃组血液中敌敌畏浓度水平显著低于对照组(P<0.05);染毒4 h后多次灌胃组血中敌敌畏浓度水平与单次灌胃组间差异具有统计学意义(P<0.05);活性炭灌胃两组的AUC,Cmax与对照组比较差异具有统计学意义(P<0.05).MRT三组比较差异无统计学意义(P>0.05).全血胆碱酯酶抑制水平于染毒后4 h内,B组、C组与A组比较差异具有统计学意义(P<0.05),B组与C组比较差异无统计学意义(P>0.05);4 h后,三组之间两两比较差异具有统计学意义(P<0.05).结论 染毒后多次灌胃组及单次灌胃组的峰浓度降低,进入血液的敌敌畏量减少,全血胆碱酯酶抑制水平得到改善,并且多次灌胃组疗效优于单次灌胃组.     

神经性N受体拮抗剂对犬有机磷杀虫剂中毒所致的循环衰竭的治疗作用

目的　在有机磷杀虫剂中毒诱发犬循环衰竭的模型上 ,研究中枢N受体拮抗剂的实验治疗学作用。方法　健康成年雄性杂种犬 ,体重 1 2～ 1 6kg。随机分为 4组 ,对照组 (A组 )、美加明组 (B组 )、阿托品组 (C组 )、阿托品和美加明 (剂量比 1 0∶1 )联用组 (D组 )。肌肉注射敌敌畏诱发循环衰竭模型 ,观察药物对其血流动力学参数的影响。结果　敌敌畏诱发犬循环衰竭时 ,平均动脉压 (MAP)由 (1 2 3 0±1 0 3)mmHg降至染毒后 (4 3 2± 1 2 )mmHg,下降了 6 6 2 % ,心率 (HR)、心室内压最大上升速率 (+dp/dtmax)、心室内压最大下降速率 (-dp/dtmax)、心肌纤维缩短速度 (Vpm)、心肌纤维缩短速率 (Vmax)、左心室收缩压 (LVSP)等与染毒前相比分别下降了 6 8 7%、 5 1 0 %、 5 0 7%、 6 7 2 %、 94 3%、 7 4 %。而B组、C组、D组在循环衰竭治疗后 1 0min左右开始与循环衰竭时相比 ,+dp/dtmax、 -dp/dtmax等心功能指标均开始明显改善 ,其中D组在循环衰竭治疗的 1 0～ 2 0min左右与其它 3组组间同时相相比 ,△MAP、△+dp/dtmax、△ -dp/dtmax、△Vpm均有显著增高。结论　神经性N受体拮抗剂美加明对有机磷杀虫剂中毒诱发的循环衰竭有明确的治疗作用 ,并与M受体拮抗剂阿托品之间存在协同增强作用     

急性完全性颈髓损伤患者循环系统异常的观察与护理

观察97例急性完全性颈髓损伤患者循环系统异常情况及其对组织器官血液灌注的影响,发现患者伤后2周内血压下降(占67.01%)、心率减慢(占75.26%)的发生率较高;但当血压下降、心率减慢在一定范围内(收缩压≥75mmHg、心率≥40次/min)时,不会对人体组织器官的血液灌注产生不良影响.认为护士在患者伤后应严密观察其血压、心率及意识状态、心电图变化等;高热、缺氧的患者因心率代偿性增加不明显,要及时予以处理.     

兔急性草乌中毒血液灌流治疗实验方法的建立

目的 探讨建立血液灌流(HP)治疗兔急性草乌中毒的实验方法.方法 将24只实验兔随机分成中毒模型组、HP组和假HP组,每组8只.中毒模型组及HP组用草乌酒灌胃制作急性中毒模型;假HP组及HP组经颈内动脉、颈外静脉插管,建立HP装置后进行HP 2 h,假HP组吸附柱内无吸附剂.用液相-质谱联用仪检测中毒模型组与HP组灌流前后相同时间点血中乌头碱的浓度;检测假HP组灌流前后血液有形成分及电解质、血浆蛋白浓度的变化.结果 HP组灌流2 h后血中乌头碱浓度为(2.02±1.46)μg/L,明显低于中毒模型组(36.97±8.30)μg/L(P<0.05);假HP组灌流前、后血细胞计数和血红蛋白、血浆蛋白质及电解质数值变化差异无统计学意义(P均>0.05).结论 HP可明显降低血中乌头碱浓度,HP实验装置对兔血液系统无不良影响,是一项安全有效的实验方法与治疗技术.     

胆碱酯酶抑制剂类神经性毒剂中毒诱发犬循环衰竭时心电图的变化

目的在胆碱酯酶抑制剂(cholinesterase inhibitor,ChEI)类神经性毒剂沙林、梭曼、塔崩和维埃克斯(VX)所致犬循环衰竭模型上,观察循环衰竭前后动物心电图变化的特征。方法健康成年雄性杂种犬40只,体重11～16 kg,随机分为4组：梭曼、沙林、塔崩和VX组,每组10只。观察犬循环衰竭过程中的心电图变化。结果ChEI类神经性毒剂诱发循环衰竭时可出现Ⅰ度、Ⅱ度、Ⅲ度房室传导阻滞,房性和室性早搏,室性心动过速,心室扑动,心室颤动,心房扑动,心房颤动,窦性心动过缓,窦性心动过速,窦性停搏等各种心律失常。在导致休克的缓慢性心律失常中,Ⅱ度Ⅱ型及Ⅲ度房室传导阻滞(AVB)占91．6%,窦性心动过缓及窦性停搏占8．4%。心电图发生T波高耸和P波增幅的特征性变化。结论ChEI类神经性毒剂中毒诱发循环衰竭时,可出现各种心律失常,其中以房室传导阻滞最常见,心电图常发生T波高耸和P波增幅的特征性变化。     

血液灌流对急性草乌中毒兔血浆毒性成分及组织病理学的影响

目的 探讨血液灌流对急性草乌中毒兔血浆毒性成分和组织病理学的影响.方法 雄性日本大耳白兔16只,随机分成中毒组(AP组,n=8)和血液灌流治疗组(AH组,n=8).两组用草乌酒1 mL/kg灌胃,制作急性中毒模型(以1 h内出现心律失常为制模成功标准),AH组用活性碳血液灌流2 h.光镜下观察两组兔脑、心肌、肝组织病理改变.分别比较两组相同时间点血浆中乌头碱、新乌头碱、次乌头碱浓度.两样本均数比较采用成纽t检验.结果 AP组兔脑组织、心肌组织、肝组织充血水肿明显,AH组兔的肝脏组织轻度允血,脑组织、心肌组织未见明显改变;两组染毒后1 h内血浆乌头碱、新乌头碱、次乌头碱浓度比较,差异无统计学意义(P＞0.05).AH组染毒后2 h,3 h血浆乌头碱、新乌头碱、次乌头碱浓度分别为[(2.11±1.08),(2.02±1.46)],[(39.70±9.31),(19.71±16.06)],[(1.70±0.71),(2.12±1.33)]ng/mL,均明显低于AP组,差异有统计学意义(P＜0.05).结论 急性草乌中毒兔血液灌流治疗后血浆中草乌成分浓度明显降低,器官组织病理改变减轻,血液灌流是兔急性草乌中毒的有效治疗手段.     

大鼠急性甲醇中毒视神经损伤实验研究

目的探讨大鼠急性甲醇中毒视神经损伤时间窗及程度。方法用SD大鼠经口灌注甲醇,灌注后分不同时段处死大鼠取血测甲醇浓度、取视神经做病理检查。结果LD50从2h开始出现较为明显的损伤,4h后程度最重。LD0损伤最重的时间段在8h后。不论是LD0、LD50在损伤程度达到最严重之后,连续观察24h、48h、72h随着血液中甲醇浓度的降低,视神经的损伤仍然明显地持续存在。结论急性甲醇中毒对视神经早期（0.5h）就有损伤,损伤程度和剂量浓度有关,视神经的损伤最严重出现在血液中甲醇浓度高峰值的4h后,随时间推移甲醇在大鼠体内的继续弥散,致使损害迁延。     

连续静静脉血液滤过(CVVH)在儿童危重症中的应用(附5例报告)

目的评价连续性血液净化(CBP)在儿童危重症救治中的疗效及安全性。方法采用CBP治疗儿童危重症患者5例,观察治疗前后的血压、心率、血尿素氮(BUN)、血肌酐(Cr)、电解质和血气变化,对临床资料作回顾分析。结果5例危重儿治疗前有多脏器功能障碍、严重电解质紊乱、代谢性酸中毒同时合并少尿无尿。治疗后患儿生命体征平稳,血压、心率变化无显著差异,BUN、Cr、电解质和血气变化明显好转。结论CBP治疗过程中,血流动力学稳定,循环衰竭患儿也能进行CBP治疗。CBP能有效纠正氮质血症和水电解质酸碱平衡紊乱,是治疗儿童危重症的一种有效和安全的方法。     

连续性血液净化治疗儿童多脏器功能障碍综合征

目的评价连续性血液净化(CBP)在救治儿童多脏器功能障碍综合征(MODS)时的疗效及安全性。方法采用CBP治疗儿童MODS患者10例,观察治疗前后的血压、心率、血BUN、Cr、电解质和血气变化,对临床资料作回顾分析。结果10例患儿年龄2~10岁,治疗前存在2个以上脏器功能障碍、严重电解质紊乱、代谢性酸中毒同时合并少尿无尿。治疗后患儿生命体征平稳,血压、心率变化无显著差异,血BUN、Cr、电解质和血气变化明显好转。结论CBP治疗过程中,血流动力学稳定,循环衰竭患儿也能进行CBP治疗。CBP能有效纠正氮质血症和水电解质酸碱紊乱,是治疗儿童MODS合并少尿无尿者一种有效和安全的方法。     

连续性血液净化救治伴有低钠血症的难治性心力衰竭患者的疗效

目的:探讨连续性血液净化在伴有低钠血症的难治性心力衰竭患者中的应用价值.方法:常规治疗效果不佳的伴低钠血症难治性心力衰竭患者23例,分为A、B两组.A组12例血压顽固性升高(收缩压＞140mmHg),B组11例血压降低(收缩压＜100mmHg).行持续床边血液净化治疗,分别监测A、B两组平均动脉压、心率、动脉血氧饱和度、B型钠尿肽(BNP)、血钠浓度以及恢复正常时间、脱机时间、抢救成功率.结果:A、B组平均动脉压、心率、氧饱和度均较治疗前好转.差异有统计学意义(P＜0.05);BNP随病情变化,逐渐改善(P＜0.05).治疗后血钠均恢复正常,血钠平均恢复时间(213±1.4)d,A、B组无明显区别.A、B组脱机时间差异有显著性[(4.5±1.2)d vs(6.0±2.3)d,P＜0.05],平均(5.5±2.1)d.A组抢救成功率91.7%(11/12),B组成功率63.6%(7/11),P＜O.05.死亡病例均为B组血压降低组患者,血钠(105.3±2.5)mmol/L,与平均值(110.3±12.0)mmol/L比较差异有显著性(P＜0.05).结论:持续性床边血液净化对于伴有低钠血症的难治性心力衰竭患者疗效明显,特别对于此类血压降低合并严重低钠患者,应尽早行血液净化治疗.     

Pharmacokinetics, hemodynamic, renal, and neurohormonal effects of atrial natriuretic factor in experimental heart failure

The hemodynamic, renal, neurohormonal effects and pharmacokinetics of synthetic atrial natriuretic factor (ANF) were studied in six conscious dogs with severe heart failure induced by right ventricular pacing at 250 beats/min for 5.0 +/- 0.6 weeks. Severe heart failure was characterized by a low cardiac output (2.1 +/- 0.1 L/min, elevated pulmonary capillary wedge pressure (26.8 +/- 2.8 mmHg) and right atrial pressure (14.5 +/- 2.2 mmHg). Synthetic ANF (human 99ser-126tyr ANF) was administered intravenously as 2 consecutive 30 min infusions (0.02 and 0.10 microgram/kg.min respectively); and each infusion was preceded by a priming dose of 1 microgram/kg. In contrast to the potent vasorelaxant, natriuretic and renin-lowering effects previously reported in normal dogs, these effects were not observed in the dogs with heart failure with either dose of ANF. The plasma half-life was 10.0 +/- 2.6 min, significantly longer than that reported previously in normal dogs. These data suggest that in this model of heart failure, the pharmacokinetics of ANF are altered and there is generalized target organ resistance to the actions of ANF.     

Spontaneous, Electrically, and Cesium Chloride Induced Arrhythmia and Afterdepolarizations in the Rapidly Paced Dog Heart

JONES, D.L., et al. : Spontaneous, Electrically, and Cesium Chloride Induced Arrhythmia and Afterdepolarizations in the Rapidly Paced Dog Heart. Despite frequent arrhythmia and sudden death in heart failure, attempts to study arrhythmia mechanisms in patients are difficult. The dog heart, paced for several weeks at a fast rate to induce heart failure is prone to arrhythmia. The aim of this study was to determine the activation patterns of spontaneous and electrically induced arrhythmia and the susceptibility of the failing dog heart to arrhythmia and early afterdepolarization (EAD) induced triggered activity elicited by exogenous administration of cesium chloride (CsCl). The hearts of 56 mongrel dogs were paced at 240 beats/min for 3–5 weeks (heart failure group). Twenty‐one similarly operated, but not paced dogs served as the control group. At baseline, all dogs were healthy as assessed electrophysiologically and hemodynamically. Spontaneous (bradycardia, tachycardia, and arrhythmic deaths) and electrically induced arrhythmia was frequent in dogs with heart failure. Also, the minimal dose of CsCl that produced ventricular tachycardia was significantly lower in the heart failure than the control dogs (1.02 ± 0.02 vs 1.21 ± 0.07 mMol/kg, P < 0.05 ). Epicardial mapping during spontaneous and electrically induced arrhythmia in the heart failure dogs showed initiation patterns with focal origin, often from multiple sites. This pattern was consistent with the patterns observed with CsCl induced ventricular tachycardia. In in vitro microelectrode studies, CsCl superfusion (2.5–5 mMol/L ) induced triggered activity due to EADs within 30 minutes, in seven of the eight Purkinje fibers from four heart failure dogs. EADs were also found in ventricular myocytes of papillary muscle from two heart failure dogs. In contrast, 5 mMol/L CsCl induced EADs in only one of eight Purkinje fibers from the hearts of four control dogs and no papillary myocytes even with continuous superfusion for up to 60 minutes (P < 0.01 ). These results demonstrate that pacing induced heart failure in the dog has an increased tendency to develop ventricular tachycardia and triggered activity unmasked by CsCl.     

Systemic activation of the transient receptor potential vanilloid subtype 4 channel causes endothelial failure and circulatory collapse: Part 2

The transient receptor potential (TRP) vanilloid subtype 4 (V4) is a nonselective cation channel that exhibits polymodal activation and is expressed in the endothelium, where it contributes to intracellular Ca2+ homeostasis and regulation of cell volume. The purpose of the present study was to evaluate the systemic cardiovascular effects of GSK1016790A, a novel TRPV4 activator, and to examine its mechanism of action. In three species (mouse, rat, and dog), the i.v. administration of GSK1016790A induced a dose-dependent reduction in blood pressure, followed by profound circulatory collapse. In contrast, GSK1016790A had no acute cardiovascular effects in the TRPV4-/- null mouse. Hemodynamic analyses in the dog and rat demonstrate a profound reduction in cardiac output. However, GSK1016790A had no effect on rate or contractility in the isolated, buffer-perfused rat heart, and it produced potent endothelial-dependent relaxation of rodent-isolated vascular ring segments that were abolished by nitric-oxide synthase (NOS) inhibition (N-nitro-L-arginine methyl ester; L-NAME), ruthenium red, and endothelial NOS (eNOS) gene deletion. However, the in vivo circulatory collapse was not altered by NOS inhibition (L-NAME) or eNOS gene deletion but was associated with (concentration and time appropriate) profound vascular leakage and tissue hemorrhage in the lung, intestine, and kidney. TRPV4 immunoreactivity was localized in the endothelium and epithelium in the affected organs. GSK1016790A potently induced rapid electrophysiological and morphological changes (retraction/condensation) in cultured endothelial cells. In summary, inappropriate activation of TRPV4 produces acute circulatory collapse associated with endothelial activation/injury and failure of the pulmonary microvascular permeability barrier. It will be important to determine the role of TRPV4 in disorders associated with edema and microvascular congestion.     

Substantial effect of acute hydration on blood pressure in patients with autonomic failure

Summary. The effect of acute hydration on arterial blood pressure levels was investigated in ten patients with severe postural hypotension due to autonomic failure. Blood pressure and heart rate were determined in the supine and 60-degree head-up tilted position. Plasma volume and left ventricular ejection fraction were measured in the supine position. Measurements were repeated after rapid infusion of 11 of isotonic saline. Acute hydration resulted in increased supine mean blood pressure levels (P<0·01) despite normal plasma volumes in all patients. The postural reductions in mean blood pressure were reduced from 40 mmHg before to 20 mmHg after saline (median values, P<0·01). The results indicate that normal plasma volumes do not ensure optimal circulatory status in patients with autonomic failure. Acute hydration with isotonic saline may be used for immediate corrections of blood pressure levels in patients with autonomic failure and the response to acute hydration may be used as an indicator of the circulatory status in these patients.     

Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia

Introduction

Arginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.

Methods

Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs using transit-time flow probes. Left ventricular pressure-volume catheter and central arterial and venous catheters were used for haemodynamic recordings and blood sampling. Transient left ventricular ischemia was induced by intermittent left coronary occlusions resulting in a 17% reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg (p < 0.001). A low-dose therapeutic level of AVP (0.005 U/kg/min) was used to restore MAP to pre-ischemic values (93 ± 4 mmHg).

Results

AVP further impaired systemic perfusion (CO and brain, heart and kidney blood flow reduced by 29, 18, 23 and 34%, respectively) due to a 2.0-, 2.2-, 1.9- and 2.1-fold increase in systemic, brain, heart and kidney specific vascular resistances. The hypoperfusion induced by AVP was associated with an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 29 ± 1 to 21 ± 3% (p = 0.01). Finally, these effects were reversed 40 min after AVP was withdrawn.

Conclusion

Low dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.     

Effects of yohimbine, an α2-adrenoceptor antagonist, on experimental neurogenic orthostatic hypotension

Summary— Yohimbine has been proposed for the treatment of neurogenic orthostatic hypotension; however, no controlled trial has been performed in experimental models of orthostatic hypotension or in patients with autonomic failure. The aim of the present study was to compare the effects of yohimbine (0.05 mg/kg, intravenously [iv]) and placebo (saline) in a new model of neurogenic orthostatic hypotension obtained by sinoaortic denervation (SAD) in chloralose-anaesthetized dogs. Blood pressure, heart rate, noradrenaline plasma levels and systolic blood pressure and heart rate short-term variabilities (calculated on low frequency [40–50 MHz] and high frequency [390–490 MHz] bands) were measured in supine position and after a 10 min 80° head-up tilting. The drugs were administered in a double-blind cross-over randomized fashion. The head-up tilting performed in normal animals increased diastolic blood pressure (+12 ± 4 mmHg), heart rate (+39 ± 12 beats per minute [bpm]), the low frequency band of systolic blood pressure and noradrenaline plasma level, without changing systolic blood pressure or heart rate variability. In SAD dogs, a marked fall in systolic (-80 ± 11 mmHg) and diastolic (-43 ± 4 mmHg) blood pressures was observed within 1 min after placebo, without modification in heart rate, systolic blood pressure and heart rate short-term variabilities and noradrenaline plasma levels. In SAD dogs, yohimbine (0.05 mg/kg, iv) delayed the blood pressure fall elicited by head-up tilting, but failed to modify its magnitude. These results show that, in the model of orthostatic hypotension obtained by SAD, yohimbine, at an α₂-adrenoceptor selective dose (0.05 mg/kg), delays the fall in blood pressure elicited by head-up tilting. The effect of yohimbine can be explained by an increase in sympathetic tone.     

Soman-induced hypertension in conscious rats is mediated by prolonged central muscarinic stimulation

The acetylcholinesterase inhibitor, soman, induces marked and sustained hypertension and tachycardia associated with a convulsive syndrome in rats. The aims of the present study were to distinguish between the cardiovascular and convulsant effects of soman and to determine whether the maintenance of the soman-induced hypertension and tachycardia depends solely on a central muscarinic effect. To this end, using a computerised analysis of blood pressure (BP) in conscious freely moving rats, we examined the consequences on the increase in mean BP (MBP) and heart rate (HR) induced by soman (60 micrograms/kg, i.v.) of 1) a pre-treatment with the anticonvulsant drug diazepam (3 mg/kg, i.v.) and 2) atropine sulphate (10 mg/kg, i.v.) administered 10 or 60 min after the intoxication. Pretreatment with diazepam prevented the convulsions, assessed by electroencephalogram (EEG) recording, but modified neither the magnitude nor the kinetics of the pressor and tachycardic effects of soman (delta MBP = 74 +/- 2 and 73 +/- 5 mmHg, delta HR = 69 +/- 10 and 79 +/- 7 bpm, maximum MBP = 186 +/- 3 and 182 +/- 6 mmHg, maximum HR = 545 +/- 9 and 522 +/- 16 bpm in solvent- (n = 8) and diazepam- (n = 8) pre-treated rats, respectively). Whatever its time of administration, atropine sulphate fully and immediately reversed the rise in BP induced by soman. The soman-induced tachycardia was also suppressed by atropine administered 10 min after soman whereas it persisted when atropine was injected 60 min after the intoxication. These results show that the cardiovascular effects of soman can occur independently of the convulsive syndrome and that the maintenance of the soman-induced hypertension depends entirely on a permanent central muscarinic stimulation.     

生脉注射液静注对麻醉犬血流动力学影响的实验研究

目的探讨静注生脉注射液对麻醉犬血流动力学的影响。方法10只健康杂种犬麻醉后,静注生脉注射液5～10ml。于用药前和用药后连续监测主动脉内收缩压、舒张压、平均动脉压和心率等变化。并测定用药前后心输出量变化。结果生脉注射液静注后5分钟内血压开始下降,20分钟时主动脉平均动脉压降至(9.5±2.2)kPa(1kPa=7.5mmHg),与用药前〔（14.9±7.0)kPa〕相比有显著性差异(P<0.05)。但此时心率与用药前相比无显著变化(P>0.05)。且不同注射剂量的生脉注射液产生的降压幅度存在差异,提示生脉注射液存在一定的量效关系。同时发现静注生脉注射液对心输出量无影响。结论生脉注射液静注对麻醉犬正常血压有明显的降压作用,对心率和心输出量无明显影响。     

Alterations in the Baroreceptor Reflex in Conscious Dogs with Heart Failure

The effectiveness of the baroreceptor reflex in conscious dogs with experimental cardiac hypertrophy and heart failure was compared with that in a group of normal conscious dogs. Cardiac hypertrophy and heart failure were produced by tricuspid avulsion and progressive pulmonary stenosis. The sensitivity of the baroreceptor reflex to transient hypertension was assessed by determining the slope of the regression line relating the prolongation of the R-R interval to the rise in systolic arterial pressure during the transient elevation of arterial pressure induced by an intravenous injection of 1-phenylephrine. The mean slope averaged 22.4+/-2.3 msec/nm Hg in 16 normal animals. 23.1 +/-1.5 in five sham-operated animals, and was significantly reduced to 8.3 +/-0.8 in 10 dogs with hypertrophy alone (P < 0.001), and to 3.3+/-0.5 in nine dogs with heart failure (P < 0.001). The response to baroreceptor hypotension was compared during bilateral carotid artery occlusion (BCO) in six normal and six heart failure dogs previously instrumented with Doppler flow transducers on the superior mesenteric and renal arteries. During BCO, in normal dogs arterial pressure increased 52+/-4 mm Hg, heart rate 33+/-2 beats/min, mesenteric resistance 0.17+/-0.03 mm Hg/ml per min, and renal resistance 0.37+/-0.10 mm Hg/ml per min. In the heart failure group all of these variables increased significantly less (P < 0.01); arterial pressure rose 25 +/-3 mm Hg, heart rate 13 +/-4 beats/min, mesenteric resistance 0.04+/-0.007 mm Hg/ml per min, and renal resistance 0.18+/-0.09 mm Hg/ml per min.Thus, in heart failure, all measured systemic and regional circulatory adjustments consequent to baroreceptor hypo- and hypertension are markedly attenuated. This study demonstrates a profound derangement of a major cardiovascular control mechanism in experimental heart failure.     

无创正压通气治疗心脏术后并发急性呼吸功能衰竭的护理

目的 探讨无创双水平呼吸道正压通气（bi-level positive airway pressure,BIPAP）模式对体外循环心脏手术后并发急性呼吸功能衰竭的疗效。方法对20例心脏术后并发急性呼吸功能衰竭患者采用BIPAP呼吸机进行通气,准确记录通气前及通气后2、6、24h心率、血压、呼吸频率及动脉血气的变化。结果除2例患者因排痰不畅,导致二氧化碳潴留需重新置管行机械通气外,其余18例患者治疗期间至撤机后pH值变化不明显,呼吸及循环功能等指标均明显改善,和治疗前比较有统计学意义（P〈0．05或P〈0．01）,患者病情明显好转。结论合理应用无创双水平呼吸道正压通气可以迅速改善心脏术后并发急性呼吸功能衰竭患者的通气功能,有利于纠正呼吸功能衰竭,且对循环功能影响小,可作为再次插管前的补救措施之一。