保留与消除自主呼吸行双相气道正压通气对犬呼吸循环的影响

本研究比较保留与消除自主呼吸行双相气道正压通气（ＢＩＰＡＰ）对犬呼吸、循环的影响以进一步探讨两种方式的利弊，供临床参考。材料和方法１２只健康杂种犬，体重（１１．７±２．３）ｋｇ，静注戊巴比妥钠２００·ｍｇ·ｋｇ－１，继以１．２ｍｇ·ｋｇ－１·ｈ－１静滴维持麻醉。经口插入ＤＩ７．５的气管导管，用德国ＤｒａｇｅｒＥｖｉｔａⅡ型呼吸机进行机械通气，并监测ＰＥＴＣＯ２，左股动脉插管监测ＭＡＰ和采血样以测定血气，经右股静脉插入带温度探头的Ｓｗａｎ－Ｇａｎｚ三腔漂浮导管（Ｆ７）至肺动脉，并连接至血液动力学监…     

异丙酚对大鼠心肌收缩力的影响

目的：判定异丙酚对大鼠心脏心肌收缩力的影响及其程度。方法：２０只大鼠随机分为两组，Ⅰ组静注异丙酚２．５ｍｇ．ｋｇ＾－１，Ⅱ组静注硫喷妥钠４ｍｇ．ｋｇ＾－１，测量经后３０秒、１、２、５、１０分钟时ｄｐ／ｄｔｍａｘ、ＬＶＳＰ和ＬＶＤＰ、ＣＶＰ、ＨＲ的变化。结果：静注异酚后ｄｐ／ｄｔｍａｘ无显著变化，而静注硫喷妥钠后１分钟ｄｐ／ｄｔｍａｘ明显明显下降。结论：异丙酚对心肌缩力影响较小，与等效剂量的硫喷妥钠     

异丙酚诱异对心瓣膜手术病人血流动力学的影响

目的和方法：采用Ｓｗａｎ－Ｇａｎｚ导管及热稀释法检测心搏量技术,观测心瓣膜手术病人异丙酚（１．５ｍｇ／ｋｇ）诱导时的血流动力学（血动学）变化。结果：两组病人麻醉前血动学紊乱主要表现为右心后负荷及作功增加;给予异丙酚１．５ｍｇ／ｋｇ后２ｍｉｎ,ＨＲ、ＣＩ、ＭＰＡＰ、ＭＡＰ、ＭＣＷＰ、ＬＶＷＩ、ＲＶＷＩ较麻醉前明显降低,在无气管插管操作刺激的Ａ组中可一直持续,并超近１０ｍｉｎ;Ｂ组病人麻醉后３ｍｉｎ行     

咪唑安定硬膜外注射时患者血流动力学及通气功能变化

咪唑安定（ＭＩＤ）硬膜外注射的节段性镇痛效应及其对患者血流动力学（ＭＡＰ、ＨＲ、ＳＩ、ＣＩ、ＴＦＩ、ＶＥＴ、ＥＶＩ、ＳＶＲＩ、ＩＣ、ＰＥＩ、ＬＶＷＩ、ＲＰＰ）与通气功能（ＶＴ、ＲＲ、ＶＥ、ＦＥＶ１、Ｉ－ＥｔＯ２、ＰＥＴＣＯ２、ＳｐＯ２）的影响。４４例患者随机分成四组：Ｅ１组硬外注ＭＩＤ０．０５ｍｇ／ｋｇ，Ｅ２组硬外注ＭＩＤ０．１ｍｇ／ｋｇ，Ｖ１、Ｖ２组为静脉组，剂量与Ｅ１、Ｅ２组相同。结果：（１）     

静吸复合麻醉中不同小剂量芬太尼对脑电边缘频率和双波谱指数的影响

目的 研究静吸复合麻醉中不同小剂量芬太尼对脑电边缘频率（ＳＥＦ）和双小的指数（ＢＩＳ的影响。方法 随机将ＡＳＡⅠ～Ⅱ级病人３０例分为Ⅰ、Ⅱ、Ⅲ组地全麻诱导吸入安氟醚达０．８ＭＡＣ后三组分别静注芬太尼３μｇ．ｋｇ＾０－１、５μｇ．ｋｇ＾－１,于给药后６ｍｉｎ记录每组病人的ＭＡＰ、ＨＲ、ＳＥＦ及ＢＩＳ。结果 三组 内、组间ＭＡＰ、ＨＲ相比均无显著差异（Ｐ〈０．０５）,ＢＩＳ无显著性差异（Ｐ〉０．０５）     

异丙酚对血压、心率及内皮依赖性血管调节的影响

目的;观察异丙酚麻醉诱导对血压,心率及内皮依赖性血管调节的影响。方法：心肺功能正常的择期非心脏手术病人１８例,用异丙酚２．０ｍｇ／ｋｇ,芬太尼４μｇ／ｋｇ,潘库溴铵０．０８ｍｇ／ｋｇ和琥珀胆碱１．５ｍｇ／ｋｇ麻醉诱导。记录诱导前,插管前和插管后１,３和５分钟时ＳＢＰ,ＤＢＰ,ＭＡＰ和ＨＲ,同时测定血浆内皮素－１,前列环素和血栓素２变化。结果：插管前ＳＢＰ,ＤＢＰ和ＭＡＰ均较诱导前明显降低,降幅分别     

静脉复合诱导对肺高压心脏瓣膜病人体肺循环血液动力学的影响

目的 研究安定－芬太尼－羟丁酸钠复合诱导对不同程度肺动脉高压心脏瓣膜手术病人体、肺循环血液动力学的影响。方法 ７０例择期手术病人,根据麻醉前肺动脉平均压（ＭＰＡＰ）分为三组。组１,ＭＰＡＰ≤２．６７ｋＰａ;组,２〉２．６７ｋＰａ≤５．３３ｋＰａ;组３,〉５．３３ｋＰａ。麻醉诱导均采用安定０．２ｍｇ／ｋｇ、芬太尼２μｇ／ｋｇ及羟丁酸钠５０ｍｇ／ｋｇ。以Ｓｗａｎ－Ｇａｎｚ导管技术监测血液动力学。结果：     

异丙酚及咪唑安定诱导对心脏瓣膜轩换术患者血液动力学的影响

目的：比较异丙酚和咪唑安定对心脏瓣膜置换术患者在诱导前后对血液动力学的影响。方法：２０例ＡＳＡⅡ－Ⅲ级，成年患者随机分成２组，分别静注异丙酚２ｍｇ／ｋｇ（Ｐ组）或咪唑安定０．２ｍｇ／ｋｇ（Ｍ组）诱导。局麻下插Ｓｗａｎ－Ｇａｎｚ导管到肺动脉，分别在诱导前，注药后２、５、１０分钟时测血液动力学变化。结果，Ｐ组ＳＰ、ＤＰ、ＭＡＰ、ＣＯ在诱导后２分钟即显著下降（Ｐ〈０．０５），Ｍ组ＳＰ、ＤＰ、ＭＡＰ和ＣＯ     

环孢素A及硫唑嘌呤对大鼠肝毒性的对比研究

给Ｗｉｓｔａｒ大鼠分别胃饲环孢素Ａ（ＣｓＡ）５０ｍｇ·ｋｇ~（－１）·ｄ~（－１），硫唑嘌呤（Ａｚａ）１０ｍｇ·ｋｇ~（－１）·ｄ~（－１），ＣｓＡ３０ｍｇ·ｋｇ~（－１）·ｄ~（－１）加Ａｚａ５ｍｇ·ｋｇ~（－１）·ｄ~（－１）及橄榄油２周，检测肝功能指标，血清丙二醛（ＭＤＡ），全血谷胱甘肽（ＧＳＨ）含量及肝组织病理学变化。结果Ａｚａ组血清ＡＬＴ、ＴＢｉｌ、ＭＤＡ升高以及肝组织损害最明显，ＣｓＡ组血清ＴＰ、ＡＬｂ降低、ＡＫＰ升高较Ａｚａ组及合并用药组更明显。结果表明ＣｓＡ与Ａｚａ导致肝损害的机理不同，Ａｚａ肝毒性大于ＣｓＡ，且为剂量依赖性。     

气管插管应激时血浆血栓素A2和前列环素含量变化

为比较气管插管应激时血浆血栓素Ａ２（以ＴｘＢ２表示）和前列环素（以６－ｋｅｔｏ－ＰＧＦ１ａ表示）的变化，２２例患者随机分为芬太尼组和对照组，两组患者均给予硫喷妥钠４ｍｇ／ｋｇ和琥珀胆碱１。５ｍｇ／ｋｇ诱导后插管，结果显示诱导后５分内，对照组ＳＢＰ、ＤＢＰ、ＭＡＰ、ＨＲ、ＰＡＷＰ、ＴＰＲ及血浆ＴＸＢ２含量较芬太尼组明显升高（Ｐ＜０。０５），对照组ＴＸＢ２的升高与ＭＡＰ及ＴＰＲ的升高呈高度正相关系，对     

Narcotic reversal in hypercapnic dogs: comparison of naloxone and nalbuphine

Reversal of opioid effects by naloxone (NX) can lead to significant cardiovascular problems. We have reported previously that hypercapnic dogs develop greater increases in blood pressure and plasma catecholamine (CA) levels than hypocapnic ones when reversed with naloxone. We have also demonstrated differences between NX and nalbuphine (NBPH) in producing excitatory adrenergic responses when administered during normocapnia. The present study was designed to investigate possible dissimilarities in cardiovascular and sympathetic events after administration of either NX or NBPH in dogs made hypercapnic following fentanyl administration. After induction of anaesthesia with thiopentone and intubation, two groups of dogs were maintained with controlled ventilation on enflurane in oxygen anaesthesia and given 50 micrograms.kg-1 fentanyl IV. This caused a significant decrease in heart rate (HR) (P less than 0.001), mean arterial blood pressure (MAP) (P less than 0.001), and plasma concentrations of norepinephrine (NE) (P less than 0.002). Then, ventilation was decreased to produce a PaCO2 of 60 mmHg; this was accompanied by a significant elevation in plasma level of both epinephrine (EPI) (P less than 0.02) and NE (P less than 0.001). Administration of 20 micrograms.kg-1 NX to six dogs resulted in immediate increases in HR (P less than 0.01) and MAP (P less than 0.01), and a further rise in CA levels to greater than pre-fentanyl baseline values. In six other dogs, NBPH (0.3 mg.kg-1) caused increases in HR (P less than 0.001) and MAP (P less than 0.001) only, and the MAP rise was significantly less than that seen in the NX group (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

芬太尼复合诱导气管插管对神经外科病人大脑中动脉血流速率的影响

目的应用经颅多普勒(TCD)研究不同剂量芬太尼和依托咪酯复合诱导气管插管对神经外科病人脑血流动力学的影响。方法20例病人随机分成两组(每组10例)F5组,芬太尼5μg／kg;F10组,芬太尼10μg／kg。余诱导用药相同安定0．1mg／kg、依托咪酯0．3mg／kg、维库溴铵0．1mg／kg。采用TCD监测双侧大脑中动脉血流速率(V-MCA),同时监测BP、HR、记录麻醉诱导前、插管前和插管后3分钟的变化。结果与麻醉前比,插管前和插管后3分钟,两组V-MCA均明显降低(P＜0．01);血压在插管前降低(P＜0．01),插管后恢复麻醉前水平。但两组间的变化差异无显著意义。结论芬太尼和依托咪酯复合诱导能抑制插管刺激引起的脑血流量增加和心血管反应,减少脑血流量。     

High-Dose Analgesic Anesthesia with Morphine or Sufentanil in Propranolol-Treated Dogs

In propranolol-pretreated dogs (2 mg . kg -1) the immediate cardiovascular effects of sufentanil (0.01 mg . kg -1) or morphine (4 mg . kg -1) were compared. Besides a 40% decrease in cardiac index (CI), sufentanil and morphine initiated quite different hemodynamic changes. Sufentanil did not significantly change mean arterial pressure (MAP), central venous pressure (CVP) and mean pulmonary artery pressure (MPAP), while the pulmonary capillary wedge pressure (PCWP) increased by 50%. After morphine, MAP declined significantly by about 65%, and significant decreases in MPAP (14%) and PCWP (33%) were also observed. Propranolol reduced heart rate by 16%, and morphine caused no further reduction in HR. A significant decrease of about 30% was seen in HR after sufentanil. Sufentanil significantly raised systemic vascular resistance index (SVRI) by 15%, whereas morphine decreased it by 32%. Pulmonary vascular resistance index (PVRI) was unchanged after sufentanil, but significantly increased after morphine. Right ventricular stroke work index (RVSWI) was unaffected by both analgesics, and morphine decreased left ventricular work index (LVSWI) significantly by 80%. Oxygen transport index declined significantly after both analgesics. Sufentanil reduced oxygen consumption by 20%, while morphine left this parameter unaffected. We conclude that the administration of high-dose sufentanil leads to a stable circulation, even when a total beta-blockade exists.     

Effects of continuous nitroglycerin infusion on acute myocardial ischemia in dogs

The effects of a continuous infusion of nitroglycerin (NTG) were evaluated by hemodynamic measurements and measurements of regional myocardial blood flow (RMBF) in dogs on right heart bypass with left anterior descending coronary artery ligation. NTG infusion which decreased afterload, mean aortic pressure (MAP) decreased from 100 to 85 mm Hg, thus also decreasing coronary perfusion pressure) resulted in an 11.8% increase in total coronary blood flow (CBF), a 19.1% decrease in coronary vascular resistance index (CVRI), and a 21.7% decrease in myocardial oxygen consumption (MV?O₂). When MAP was returned to the control level (100 mm Hg) with continuing infusion of NTG, CBF increased 49.1%, and CVRI decreased by 23.4% compared to the pre-NTG ischemic state. Regional myocardial blood flow (microsphere technique) to ischemic tissue at the border of the infarct remained stable with NTG infusion despite decreased MAP, in contrast to the significant fall in RMBF in this region with decreased MAP in the control group without NTG. When MAP was elevated back to pre-NTG levels, an 18.6% increase in RMBF to the border of the infarct was seen compared to an insignificant change in RMBF in untreated (control) animals. These data are consistent with the concept that under conditions of regional myocardial ischemia, coronary blood flow to the “border zone” (ischemic myocardium) is maintained or enhanced by NTG, even when coronary perfusion pressure is modestly reduced.     

Cerebral blood flow and cerebral blood flow velocity during angiotensin-induced arterial hypertension in dogs

Pressure-passive perfusion beyond the upper limit of cerebral blood flow (CBF) autoregulation may be deleterious in patients with intracranial pathology. Therefore, monitoring of changes in CBF would be of clinical relevance in situations where clinical evaluation of adequate cerebral perfusion is impossible. Noninvasive monitoring of cerebral blood flow velocity using transcranial Doppler sonography (TCD) may reflect relative changes in CBF. This study correlates the effects of angiotensininduced arterial hypertension on CBF and cerebral blood flow velocity in dogs. Heart rate (HR) was recorded using standard ECG. Catheters were placed in both femoral arteries and veins for measurements of mean arterial blood pressure (MAP), blood sampling and drug administration. A left ventricular catheter was placed for injection of microspheres. Cerebral blood flow velocity was measured in the basilar artery through a cranial window using a pulsed 8 MHz transcranial Doppler ultrasound system. CBF was measured using colour-labelled microspheres. Intracranial pressure (ICP) was measured using an epidural probe. Arterial blood gases, arterial pH and body temperature were maintained constant over time. Two baseline measures of HR, MAP, CBF, cerebral blood flow velocity and ICP were made in all dogs (n = 10) using etomidate infusion (1.5 mg · kg^?1 · hr^?1) and 70% N₂O in O₂ as background anaesthesia. Following baseline measurements, a bolus of 1.25 mg angiotensin was injected iv and all variables were recorded five minutes after the injection. Mean arterial blood pressure was increased by 76%. Heart rate and ICP did not change. Changes in MAP were associated with increases in cortical CBF (78%), brainstem CBF (87%) and cerebellum CBF(64%). Systolic flow velocity increased by 27% and Vmean increased by 31% during hypertension (P < 0.05). Relative changes in CBF and blood flow velocity were correlated (CBF cortex — Vsyst: r = 0.94, CBF cortex — Vmean: r = 0.77; P < 0.001; CBF brainstem — Vsyst: r = 0.82, CBF brainstem — Vmean: r = 0.69; P < 0.05). Our results show that increases in arterial blood pressure beyond the upper limit of cerebral autoregulation increase CBF in dogs during etomidate and N₂O anaesthesia. The changes in CBF are correlated with increases in basilar artery blood flow velocity. These data suggest that TCD indicates the upper limit of the cerebral autoregulatory response during arterial hypertension. However, the amount of CBF change may be underestimated with the TCD technique.     

Effects of Morphine and Halothane Anesthesia on Coronary Blood Flow

This study was undertaken to determine the relative effects of morphine and halothane anesthesia on coronary blood flow. Right heart bypass was instituted in 20 dogs by draining the vena cava blood into a cardiotomy reservoir and returning it to the main pulmonary artery. Coronary sinus drainage was measured by a right ventricular cannula. Group I (10 dogs) was sequentially given 0.5, 1, 1.5, 2.0, and 2.5% halothane. Group II (10 dogs) was given 1, 2, 3, 4, and 5 mg per kilogram of morphine intravenously. Arterial pressure, coronary sinus blood flow, cardiac output, arterial pH, Pco₂, and Po₂ were determined and repeated at each dose level of anesthesia and compared to the control values.Morphine significantly increased coronary flow at 3, 4, and 5 mg/kg without pressure adjustment and at 2 mg/kg after pressure adjustment. Coronary flow with halothane was unchanged from control values except for a decrease at 2.5%. Coronary flow was significantly greater with 3, 4, and 5 mg/kg of morphine than with 1.0 and 1.5% halothane.     

Opiate receptors and endorphins in the pathophysiology of hemorrhagic shock

We investigated the hypothesis that endorphins released by stress act on opiate receptors to depress cardiovascular function during hemorrhagic shock. Anesthetized adult mongrel dogs were bled into a heparinized reservoir to achieve a mean arterial pressure (MAP) of 45 mm Hg. The reservoir was adjusted to maintain MAP for 1 hour and then clamped for 1 hour, at the end of which time the shed blood was reinfused. While the reservoir was clamped we treated the animals with an intravenous bolus followed by 3-hour infusion of either 0.9% NaCl (as control) or the specific opiate receptor antagonist naloxone at three dose regimens (0.5, 1, or 2 mg/kg plus 0.5, 1, or 2 mg/kg . hr). Naloxone produced dose-dependent increases in MAP, cardiac output, stroke volume, and left ventricular contractility. Survival at 72 hours was related to the dose of naloxone used. None of six dogs treated at 0 mg/kg . hr survived, one of six survived at 0.5 mg/kg . hr, four of five at 1 mg/kg . hr, and five of five at 2 mg/kg . hr. Since naloxone has minimal effect on cardiovascular function in nonshocked dogs, these results implicate opiate receptors and perhaps endorphins in the cardiovascular pathophysiology of hemorrhagic shock.     

Cardiovascular effects of fentanyl reversal by naloxone at varying arterial carbon dioxide tensions in dogs

Clinical reports, as well as animal studies, have described cardiovascular and sympathetic stimulation after the administration of naloxone (NX) to reverse opioid-induced respiratory depression. This investigation examines the effect of PaCO2 on hemodynamic and adrenergic responses to NX, by means of 24 experiments carried out in six dogs. Each dog underwent NX reversal of fentanyl (FEN) at three different PaCO2 levels: 20, 35, and 60 mm Hg. In a final series of six experiments, the dogs were exposed to increasing PaCO2 after autonomic block by total spinal anesthesia and vagotomy. During enflurane anesthesia, 50 micrograms/kg FEN decreased mean arterial blood pressure (MAP), heart rate (HR), and plasma concentrations of norepinephrine (NE) and epinephrine (EPI) significantly. NX 0.4 mg promptly returned HR and MAP to baseline or above in all experiments; catecholamine (CA) levels increased only in hypercapnic dogs. Increases in HR were the same in all series. MAP, EPI, and NE levels were significantly greater than pre-FEN baseline values only in hypercapnic dogs 1 minute after NX and were also significantly higher in hypercapnic than in hypocapnic dogs at this time. NE levels were greater in hypercapnic dogs at all time periods after NX. In blocked dogs, neither F nor NX had any effects on hemodynamic functions or plasma CA levels; the institution of hypercapnia caused significant decreases in HR, MAP, and systemic vascular resistance. This direct circulatory depressant action of an elevated PCO2 may have attenuated the indirectly mediated excitatory hemodynamic effects of NX in intact dogs, thus explaining the relatively greater effect of hypercapnia on adrenergic than on hemodynamic responses to reversal.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial metabolism and haemodynamic responses during high-dose fentanyl anaesthesia for coronary patients

Fentanyl (mean dose 109 micrograms X kg-1) and oxygen were given to ten patients having coronary vein grafts. Serial studies were done before, during and after operation, of central and mean arterial pressures (MAP), cardiac index (CI) and coronary sinus flow (CBF) by thermodilution, myocardial oxygen consumption (MVO2) and lactate extraction (MLE). On induction CI and stroke work index decreased, but heart rate and MAP were unchanged as systemic resistance increased. Mean MAP and heart rate remained at the awake levels. Mean CBF remained unchanged along with stable MAP and coronary resistance. Oxygen content of CS blood increased on induction and remained elevated until the incision; it was above the awake level early postoperatively. MVO2 was low normal when the patients were awake and remained so. Normal MLE continued with a few exceptions. High-dose fentanyl did not uniformly abolish autonomic reflexes. Heavy premedication, complete beta adrenergic blockade and a high initial doses of fentanyl plus its continued infusion, aided in retaining a hypodynamic circulation and myocardial oxygenation.     

Hemodynamic interactions of propofol and dantrolene in chronically instrumented dogs

The hemodynamic interaction of dantrolene, a specific drug for malignant hyperthermia, and propofol which appears to be safe in malignant hyperthermia-susceptible patients, has not been investigated. We performed this study to examine the hemodynamic actions of dantrolene at a therapeutic dose during propofol anesthesia. Ten dogs were chronically instrumented for the measurements of systemic and coronary hemodynamics. The dogs were assigned to receive propofol with vehicle or dantrolene in a random manner on separate experimental days. Propofol significantly decreased mean arterial blood pressure, left ventricular systolic and end-diastolic pressure, the maximal rate of increase in left ventricular pressure, and left ventricular regional segment shortening. Coronary blood flow (CBF) was unchanged but coronary vascular resistance (CVR) decreased. Dantrolene reversed the decrease in mean arterial blood pressure and left ventricular systolic pressure caused by propofol, and significantly increased heart rate. However, left ventricular end-diastolic pressure, cardiac output, maximal rate of increase in left ventricular pressure, and segment shortening were unchanged. CBF was significantly increased with a decrease in CVR. These results suggest that dantrolene reverses the hypotensive action produced by propofol and causes an increase in CBF with a decrease in CVR, but does not significantly change the negative inotropic effects. Thus, dantrolene exerts favorable hemodynamic effects during propofol anesthesia. IMPLICATIONS: Our study suggests that dantrolene reverses the hypotensive action produced by propofol and causes an increase in coronary blood flow with a decrease in coronary vascular resistance, but does not significantly change the negative inotropic effects.