静脉普鲁卡因对失血性休克犬血流动力学影响

静脉普鲁卡因复合麻醉在正常血容量下对血流动力学的影响已有报道。但在失血性休克情况下,应用静脉普鲁卡因复合全麻是否适合尚无统一看法。本实验是探讨在失血性休克情况下,静脉普鲁卡因对血流动力学的影响,以便为临床麻醉提供参考。材料和方法 (一)杂种犬7只,雌雄兼有,体重13～20kg。先以戊巴比妥钠25～30mg/kg静脉麻醉,气管     

心内分流病人术中用肝素对血流动力学和心肌氧耗的影响

用ＨＭＵ－Ⅱ型心功能仪观察了心内分流病人术中用肝素对血流动力学和心肌氧耗的影响。４１例心内分流病人，按左向右分流和右向左分流分为两组。结果：两组病人术中用肝素后（３ｍｇ／ｋｇ），ＥＦ、ＳＶ、ＣＯ、ＳＶＲ、ＥＤＶ、ＭＡＰ、ＨＲ和ＣＭＯ均有不同程度的下降，其中ＭＡＰ、ＳＶＲ和ＣＭＯ下降与用肝素前比较有显著差异，ＶＤＰ略有升高。结果提示，肝素影响血流动力学和心肌氧耗的机理是肝素有抑制心脏功能和扩张外周血管的作用，其中以扩张外周血管作用为主，心内分流方向与肝素影响血流动力学和心肌氧耗无关。     

神经安定镇痛普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠…

实验研究神经安定镇痛、普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠脉循环血流动力学及心肌代谢的影响。结果表明，神经安定镇痛、普鲁卡因静脉复合麻醉抑制失血性休克状态下的心血管功能，降低心肌血流量，使得心肌氧供需失衡，心肌缺血缺氧。     

普鲁卡因静脉复合麻醉对左心功能的影响

作者曾对异氟酸和芬太尼对左心功能影响进行研究，发现大剂量芬太尼（４０μｇ／ｋｇ）抑制作用大于异氟醚。本文对普普卡因静脉复合麻醉对左心功能的影响进行研究，并与异氟醚吸入麻醉对照比较。资料与方法健康杂种犬旧只，体重１２．９±１．９ｋｇ。随机分为二组：对照组为异氟醚吸入麻醉（简称１组），犬８只，吸入１．５～１．６％（１．２ＭＡＣ）异氟醚。实验组为普鲁卡因静脉复合麻醉（简称Ｐ组），大１０只，静滴２％普鲁卡因复合液（１０％葡萄糖２００ｍｌ，１０％普鲁卡因５０ｍｌ，芬太尼０．２ｍｇ和琥珀胆碱２００ｍｇ），按…     

普鲁卡因在静脉复合麻醉中对颅内压的影响

２０例垂体瘤病人，均分两组。以硫喷妥钠和琥珀胆碱快速诱导，氟哌啶、芬太尼和潘库溴铵维持麻醉。在轻过度换气（维持ＥＴＣＯ２在４．０ｋＰａ）的条件下，观察组以０．７５ｍｇ·ｋｇ－１·ｍｉｎ－１的速度静脉滴注１％的普鲁卡因。１０例病人中，有４例脑脊液压力呈轻度降低，３例轻度升高，但皆在０．２７ｋＰａ（２ｍｍＨｇ）以内。平均脑脊液压保持稳定，未出现有统计学意义的变化（Ｐ＞０．０５）。结果表明，在此模式的麻醉条件下，静脉滴注普鲁卡因对于颅内压井无显著影响。合理使用，不失为一好的神经外科麻醉用药。     

普鲁卡因静脉复合麻醉对血高铁血红蛋白含量的影响

本文研究了普鲁卡因静脉复合麻醉对血高铁血红蛋白含量的影响。选择病人15例,气管插管后静滴2％普鲁卡因加0.04％哌替啶加0.08％琥珀胆碱维持麻醉,第1h静滴普鲁卡因150ml,第2h静滴100ml,分别于静滴前、静滴后1h、2h抽血查高铁血红蛋白含量,结果表明静滴普鲁卡因后1h、2h血中高铁血红蛋白显著增高。     

神经安定镇痛普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠脉循环血流动力学及心肌代谢的影响

实验研究神经安定镇痛、普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠脉循环血流动力学及心肌代谢的影响。结果表明，神经安定镇痛、普鲁卡因静脉复合麻醉抑制失血性休克状态下的心血管功能，降低心肌血流量，使得心肌氧供需失衡，心肌缺血缺氧。     

Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs

We investigated the relative effects of 0.5, 1.0, 1.5, 2.0 MAC halothane and enflurane, and concurrent noxious stimulus on hepatic blood flow and oxygen consumption in 14 mongrel dogs randomly divided into groups of seven each. Hepatic arterial and portal venous blood flow (HABF and PVBF, respectively) were measured continuously using ultrasonic transit time flow meter. Mean arterial blood pressure (MAP), cardiac index (CI), hepatic oxygen supply, and hepatic oxygen consumption (H _{O 2}) were measured. Halothane significantly deceased HABF, but not PVBF in a dose dependent manner. Enflurane did not affect HABF and PVBF significantly. MAP and CI decreased in both groups, with halothane producing more marked decreases than enflurane. H _{O 2} did not change with enflurane, but did with halothane, producing significant differences, with halothane being greater at 1.5, 2.0 MAC. A noxious stimulus only caused minor change in blood flow. The results suggest that liver blood flow and oxygen consumption are affected differently by halothane and enflurane and that halothane has a stronger tendency to cause an imbalance between liver oxygen supply and consumption than dose enflurane.(Masaki E, Yasuda N, Tanifuji Y et al.: Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs. J Anesth 3: 118–122, 1989)     

Effects of ketamine on liver blood flow and hepatic oxygen consumption. Studies in the anaesthetised greyhound

The effects of three increasing doses of ketamine on the blood flow to, and oxygen consumption of, the liver, were studied in seven anaesthetised greyhounds. Hepatic arterial and portal venous blood flows were measured continuously using electromagnetic flow probes, and mean arterial pressure and cardiac output monitored as appropriate. Ketamine, even at the highest dose, had little effect on the blood flow to the liver: hepatic arterial blood flow and portal venous blood flow did not differ significantly from their baseline values. However, the oxygen delivery to the liver decreased due, probably, to an increase in oxygen consumption by the pre-portal organs.     

地氟醚、七氟醚和异氟醚对猪肝血流及肝氧供需平衡的影响

目的 观察不同浓度地氟醚、七氟醚和异氟醚对肝脏氧供需平衡和肝脏血供的影响。方法 杂种猪１５只，随机分为３组：Ａ为地氟醚组（ｎ＝５），Ｂ为七氟醚组（ｎ＝５），Ｃ为异氟醚组（ｎ＝５）。采用连续温度稀释法心排血量监测仪和超声多普勒血流量测定仪观察不同浓度地氟醚、七氟醚和异氟醚对猪全身及肝脏的血流和氧供需平衡的影响。结果 （１）３组药物均使总肝血流剂量依赖性下降；地氟醚和异氟醚对总肝血流的影响与心排血量（     

尼莫地平、别嘌呤醇对完全性脑缺血后脑血流和氧耗影响的实验研究

２４只健康杂种犬随机平分为四组，单纯缺血组，尼莫地平组，别嘌呤醇组和复合治疗组。各治疗组在完全性脑缺血２０分钟后即刻，静注２０ｕｇ／ｋｇ尼莫地平或别嘌呤醇 ２０ｍｇ／ｋｇ，观察再灌注期间脑血流及氧耗的变化。研究结果显示，各治疗组脑血流量在再灌注期间明显增加，５～３０分钟时达最大值。随时间延长，脑血流量逐渐减少。再灌注初期，脑血管阻力明显降低。随后，脑血管阻力逐渐增加。脑组织可供氧量、矢状窦氧分压与脑血流量变化一致，脑组织氧耗变化不显著。本研究表明，尼莫地平。别嘌呤醇可以改善完全性脑缺血后微循环障碍，增加脑血流和可供氧量。两种药物可部分地发挥协同治疗作用。     

The effects of intravenously infused catecholamines on hepatic blood flow in conscious dogs with experimental obstructive jaundice

This study was conducted to examine how the effects of dopamine and dobutamine on hepatic blood flow were influenced by obstructive jaundice in a conscious canine model. Prior to biliary obstruction, portal venous blood flow (PVF) increased in response to the infusion of either dopamine or dobutamine: dopamine infused at 8 g/kg per min produced an increase of 19±0% in PVF, while dobutamine infused at 16 g/kg per min produced an increase of 30±2%. Although hepatic arterial blood flow (HAF) decreased dose-dependently in response to the infusion of dopamine, no significant change was observed in HAF in response to any dose of dobutamine. Obstructive jaundice attenuated or completely abolished the PVF-increasing effect of dopamine, whereas it did not significantly alter the effect of dobutamine on hepatic blood flow. In dogs with obstructive jaundice, dopamine at 16 g/kg per min produced a decrease of 17±3% in PVF. These findings suggest that dobutamine is more effective than dopamine for increasing hepatic blood flow in patients with obstructive jaundice.     

The effect of ketanserin on cerebral blood flow and oxygen metabolism in healthy volunteers

Summary The effect of the anti-hypertensive agent ketanserin on average global cerebral blood flow (CBF) and average global cerebral oxygen metabolism (CMRO₂) was examined in 8 healthy volunteers. CBF and CMRO₂ were measured with the Kety-Schmidt technique before ketanserin administration (baseline) and after administration of 2 different doses of ketanserin intravenously (dose I: 10 mg bolus and an infusion of 6 mg/h; dose II: 20 mg bolus and an ifusion of 20 mg/ h). Baseline CBF and CMRO₂ were 60 and 3.6 ml/100 g/min, respectively, and were not changed by administration of ketanserin dose I. During administration of dose II, however, CBF fell to 52 ml/ 100 g/min (p=0.05) and CMRO₂ was reduced to 3.2 ml/100 g/min (p < 0.05).We conclude that when administered in a high dose, ketanserin has the ability to depress cerebral oxygen metabolism, but when administered in a clinically relevant dose ketanserin does not influence average global CBF or average global CMRO₂. Ketanserin could be a safe antihypertensive drug in neuroanaesthesia or in the neuro-intesive care unit.     

The effects of midazolam on cerebral blood flow and oxygen consumption Interaction with nitrous oxide in patients undergoing craniotomy for supratentorial cerebral tumours

Cerebral blood flow and the cerebral metabolic rate of oxygen were measured in 30 patients during craniotomy for supratentorial cerebral tumours by a modification of the Kety-Schmidt technique using Xenon 133 intravenously. Anaesthesia was induced with midazolam 0.3 mg/kg, fentanyl and pancuronium, and maintained with midazolam as a continuous infusion, fentanyl, pancuronium and nitrous oxide in oxygen or oxygen in air. The concentration of midazolam in the blood of 10 patients was about 300 ng/litre during two measurements; the patients' lungs were ventilated with N2O in oxygen. The concentration of midazolam in the blood of another 10 patients was doubled to about 600 ng/litre during the second flow measurement; the patients' lungs were ventilated with N2O/O2. The concentration of midazolam in the blood of the third group of 10 patients was doubled to 600 ng/litre during the second flow measurement; the patients' lungs were ventilated with oxygen in air. No relationship was found between the dose of midazolam and cerebral blood flow or oxygen consumption. Nitrous oxide in combination with midazolam also had no effect on these variables.     

Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man

In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (PaCO2 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n = 7). CBF was measured after intravenous administration of 133xenon and CMRO2 was calculated from the arterial venous differences of oxygen content (AVDO2) determined in arterial and jugular venous bulb blood. CBF and CMRO2 (means +/- s.e. mean) determined prior to administration of volatile agents were 28 +/- 5 ml x 100(-1) x min-1 and 2.0 +/- 0.3 ml x 100 g-1 x min-1, respectively, in the isoflurane group. In the halothane group, CBF was 25 +/- 0.4 ml x 100 g-1 x min-1 and CMRO2 was 2.0 +/- 0.4 ml x 100 g-1 x ml-1. There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P less than 0.05) compared to values obtained during fentanyl/N2O anesthesia. In addition, isoflurane caused a further decrease in CMRO2 of 12% (P less than 0.01) as compared to a 20% increase (P less than 0.05) with halothane. The cerebral metabolic depression caused by the short-acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMRO2 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.     

Sevoflurane reduced but isoflurane maintained hepatic blood flow during anesthesia in man

The indocyanine green (ICG) clearance rate (K) and estimated total hepatic blood flow (THBF) were studied by the single injection technique. The THBF was estimated from the calculated circulating blood volume and the fixed extraction rate. The blood concentration of ICG was determined by the finger piece technique. Twenty-seven patients were randomly divided into three groups of nine and received 67% nitrous oxide, 33% oxygen, and the following volatile anesthetics: 0.8% halothane, 1.2% isoflurane, or 1.7% sevoflurane. ICG (0.5 mg·kg⁻¹) was administered intravenously and K was determined three times following the injection. The K value in the halothane and sevoflurane groups decreased significantly 1 h after induction of anesthesia: from 0.188±0.048 to 0.142±0.029 in the halothane group and from 0.178±0.027 to 0.155±0.021 in the sevoflurane group. There was no significant change in the K value in the isoflurane group throughout the study.