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（     

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)     

普鲁卡因静脉复合麻醉对肝脏血流和氧耗影响的实验研究

采用电磁血流仪和血气分析等技术，研究普鲁卡因静脉复合麻醉对犬体循环血流动力学及肝脏血流和氧耗影响。 １％普鲁卡因复合液以 １．０ｍｇ· ｋｇ－１／ｍｉｎ速度静滴时，随麻醉时间延长，血浆普鲁卡因浓度逐渐升高，６０分钟达５６．９±８．７ｍｇ／Ｌ。体循环各项血流动力学参数趋于稳定，仅在６０分钟产生明显的体循环抑制效应。心率和平均动脉压分别降低２７％、２５％，心指数由３．５２±０．２１Ｌ·ｍｉｎ－１／ｍ２降至 ３． ０８±０．１２Ｌ· ｍｉｎ－１／ｍ２。肝总血流量和氧耗与体循环动力学呈一致性变化。因此，肝脏疾患及肝手术的患者，只要控制血中普鲁卡因浓度不过高，仍可安全实施普鲁卡因静脉复合麻醉。     

The effects of triazolam on cerebral blood flow and metabolism in the dog

The new benzodiazepine triazolam was given to six initially awake dogs maintained with spinal anaesthesia and mechanical ventilation. Both cerebral blood flow (CBF) and cerebral metabolic rate for O2 (CMRO2) were significantly reduced after the initial dose of 0.1 mg X kg-1 triazolam, and the EEG changed from an awake to a sleep pattern in less than 20 s. CMRO2 was gradually reduced with increasing doses of triazolam (0.3, 1.0, 10.0 and 30.0 mg X kg-1) to 76% of control after the final 30 mg X kg-1 dose. CBF did not decrease further after the initial dose, and the addition of N2O after the final dose did not cause any significant change in CBF or CMRO2. The dogs were hemodynamically stable during the study. Small increases in brain lactate and pyruvate levels, but not in the L/P ratio were the only significant changes in brain metabolite levels. Triazolam appears to be a safe and rapidly acting induction agent in the dog.     

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.     

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 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.     

The relationship of systemic hemodynamics and oxygen consumption to early allograft failure after liver transplantation

The early postoperative hemodynamic data of 88 patients who underwent primary liver transplantation between July 1989 and October 1990 at the University Health Center of Pittsburgh were analyzed to establish the relationship of systemic hemodynamics and oxygen consumption to perioperative allograft function. The 15 patients whose allografts failed within the 1 st month following transplantation were designated as group 1, while 73 patients who retained adequate graft function constituted group 2. Although the cardiac index and oxygen delivery did not differ significantly between the groups, group 1 consistently demonstrated a lower mean arterial pressure, oxygen consumption, arteriovenous oxygen content difference, and arterial ketone body ratio. The etiology of reduced oxygen consumption in group 1 patients is speculative, but the data support the notion that oxygen consumption is a useful, predictive indicator for liver allograft function after transplantation.     

Effects of propofol on cerebral blood flow and the metabolic rate of oxygen in humans

BACKGROUND: Effects of propofol on human cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and blood flow-metabolism coupling have not been fully evaluated. We therefore assessed the effects of propofol on total-CBF and CMRO2 in patients without noxious stimuli and neurologic disorders. METHODS: General anesthesia was induced with midazolam (0.2 mg/kg) and fentanyl (5 microg/kg) in 10 patients (ASA physical status I) undergoing knee joint endoscopic surgery. Epidural anesthesia was also performed to avoid noxious stimuli during surgery. Cerebral blood flow (CBF) and cerebral arteriovenous oxygen content difference (a-vDO2) was measured using the Kety-Schmidt method with 15% N2O as a tracer before and after propofol infusion (6 mg/kg/h for 40 min), and the CMRO2 was also calculated. RESULTS: CBF decreased following propofol infusion from 34.4 ml/100 g/min (range 28.4-52.0) to 30.0 ml/100 g/min (range 20.2-42.4) (P=0.04). Although there was no significant change in a-vDO2, CMRO2 decreased following propofol infusion from 2.7 ml/100 g/min (range 2.2-4.3) to 2.2 ml/100 g/min (range 1.4-3.0) (P=0.04). There was a strong linear correlation between CBF and CMRO2 (r=0.90). CONCLUSION: Propofol proportionally decreased CBF and CMRO2 without affecting a-vDO2 in humans, suggesting that normal cerebral circulation and metabolism are maintained.     

The effects of prolonged isoflurane anaesthesia on cerebral blood flow and metabolism in the dog

To determine whether cerebral blood flow (CBF) changed with time under isoflurane anaesthesia, as has been reported for halothane, CBF and cerebral metabolic rate for oxygen (CMRO2) were studied in five dogs under prolonged isoflurane anaesthesia. CBF was measured with a modified sagittal sinus technique and CMRO2 was calculated as the product of CBF and the arteriovenous O2 difference. Maintaining this experimental dog model with 1% isoflurane in oxygen and nitrogen for 3 h in five dogs and for 4 h in three dogs did not cause any significant changes in CMRO2 or CBF. Cerebral metabolite levels were consistent with earlier reports from short-time studies and the EEG recordings showed a continuous sleep pattern with no pathological changes. It is concluded that there is no change in CBF or CMRO2 in our modified sagittal outflow model during 3-4 h of 1% isoflurane anaesthesia.     

Cerebral pharmacodynamics of anaesthetic and subanaesthetic doses of ketamine in the normoventilated pig

There are still divergent opinions regarding the pharmacodynamic effects of ketamine on the brain. In this study, the cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo₂) and electroencephalogra-phic (EEG) activity were sequentially assessed over 80 min in 17 normoventilated pigs following rapid i.v. infusions of anaesthetic (10.0 mg-kg^-1; n = 7) or subanaesthetic (2.0 mg-kg^-1; n = 7) doses of ketamine or of its major metabolite norketamine (10.0 mg-kg^-1; n = 3). The animals were continuously anaesthetized with fentanyl, nitrous oxide and pancuronium. CBF was determined by the intra-arterial mXe technique. Ketamine (10.0 mg-kg^-1) induced an instant, gradually reverting decrease in CBF, amounting to -26% (P<0.01) at 1 min and -13% (P<0.05) at 10 min, a delayed increase in CMRo₂ by 42% (P<0.01) at 10 min and a sustained rise in low- and intermediate-frequency EEG voltage by 87% at 1 and 97% at 10 min (P<0.0001). It is concluded that metabolically formed norketamine does not contribute to these effects. Considering the dissociation of CBF from CMRo₂ found 10–20 min after ketamine (10.0 mg-kg^-1) administration, it is suggested that ketamine should be used with caution for anaesthesia in patients with suspected cerebral ischaemia in order not to increase the vulnerability of brain tissue to hypoxic injury. Ketamine (2.0 mg-kg^-1) had no significant effects on CBF, CMRo₂ or EEG. It therefore seems that up to one fifth of the minimal anaesthetic i.v. dose can be used safely for analgesia, provided that normocapnaemia is preserved.     

Effects of hypoxia and isoflurane on liver blood flow: the role of adenosine

We investigated the role of endogenous adenosine in mediatingthe effects of hypoxia and isoflurane on portal tributary bloodflow (PTBF) and hepatic arterial blood flow (HABF) in rats.Liver blood flows were determined using radiolabelled microspheres.Hypoxia resulting from the exposure of rats to an atmospherecontaining 15% oxygen for 30 min decreased PTBF (23%) (P<0.05)and cardiac index (15%) (P<0.05), and increased HABF (78%)(P<0.05). Isoflurane (1.4 vol%) increased HABF in both normoxicand hypoxic conditions but did not affect PTBF. The adenosinereceptor antagonist 8-phenyltheophylline attenuated the hypoxia-inducedincrease in HABF but did not affect that resulting from theadministration of isoflurane. In conclusion, in contrast tothe increase in HABF induced by hypoxia, that induced by isofluraneappears to be independent of endogenous adenosine. Br J Anaesth 2000; 86: 425–7     

Low-dose midazolam antagonizes cerebral metabolic stimulation by ketamine in the pig

In order to test the hypothesis that low-dose midazolam reduces excitatory cerebral symptoms by attenuating ketamine-induced increases in the cerebral metabolic rate for oxygen (CMRo₂), we compared the cerebral effects of a combination of an anaesthetic dose of ketamine hydrochloride (10.0 mg-kg¹ i.v.) and a subanaesthetic dose of midazolam maleate (0.25 mg- kg^-1 i.v., n = 6; or 0.10 mg-kg^-1 i.v., n = 6) with results recently obtained with ketamine (10.0 mg-kg^-1 i.v.) in normoventilated pigs anaesthetized with fentanyl, nitrous oxide and pancuronium. Cerebral blood flow (CBF) was measured with the intra-arterial ¹³³Xe clearance technique, and CMRo₂ was calculated from CBF and the cerebral arteriovenous oxygen content difference (Cavo₂). The CMRo₂ did not increase significantly. In contrast, the maximal increase in cerebral Cavo₂ (by 56–59% at 10 min; P < 0.01) was similar to that induced by ketamine, since CBF was more depressed (by 35–45% at 1 min: P < 0.001) by ketamine-midazolam than by ketamine only. Midazolam was found to increase CVR (P < 0.01) and further depress CBF (P < 0.01), and to antagonize the ketamineinduced increase in CMRo₂ (P < 0.05). Ketamine-induced effects on mean arterial pressure (MAP) and spectral electroencephalographic (EEG) voltage were not significantly altered by midazolam. The pharmacokinetics of ketamine, as measured during an 80-min period, were not affected by the concomitant administration of midazolam. We propose that a ketamine-midazolam combination comprising a low-dose fraction (1/ 100-1/40) of midazolam is superior to ketamine alone for anaesthetic use.     

Splanchnic blood flow and oxygen consumption: effects of enteral nutrition and dopexamine in the elderly cardiac surgery patient

BACKGROUND: After cardiac surgery, patients are at risk of organ dysfunction because of decreased perfusion. Different measures have been used to increase the splanchnic blood flow. We compared the effects of enteral nutrition and dopexamine on the cardiac output, splanchnic blood flow and oxygen consumption. METHODS: Sixteen patients undergoing cardiac surgery were included. Indocyanine green extraction and thermodilution were used for repeated measurements of the splanchnic blood flow and cardiac output. On the first post-operative day, indocyanine green infusion was started. Patients were randomized to start with dopexamine (Dpx group) or enteral nutrition (EN group). After 180 min, both groups received a combination of dopexamine and enteral nutrition. Blood gases from the hepatic vein and pulmonary and radial arteries were analysed repeatedly. RESULTS: In the Dpx group, the cardiac index increased with dopexamine infusion, but not when enteral nutrition was added. In the EN group, enteral nutrition alone did not increase the cardiac index, but dopexamine addition increased the cardiac index in this group. The splanchnic blood flow increased initially in the Dpx group, but then returned to baseline and remained constant on addition of enteral nutrition. In the EN group, the splanchnic blood flow initially remained at baseline, but increased after dopexamine addition. There was no difference between the groups with regard to systemic or splanchnic oxygen consumption or the oxygen extraction ratio. In the Dpx group, lactate increased from baseline with no further increase on addition of enteral nutrition. Lactate was unchanged in the EN group. CONCLUSIONS: Dopexamine and enteral nutrition caused no adverse effects on oxygen consumption or the oxygen extraction ratio. Enteral nutrition did not increase the splanchnic blood flow or cardiac index. Dopexamine increased the systemic blood flow with only a transient effect on the splanchnic blood flow. Dopexamine increased the lactate concentration, possibly indicating a more ischaemic condition.     

Effects of sevoflurane and isoflurane on the ratio of cerebral blood flow/metabolic rate for oxygen in neurosurgery

Purpose. To examine the changes in cerebral blood flow (CBF) equivalent (CBF divided by cerebral metabolic rate for oxygen) during craniotomy under isoflurane and sevoflurane anesthesia in patients with intracranial disorders. Method. In 16 neurosurgical patients (8 anesthetized with isoflurane and 8 with sevoflurane), the CBF equivalent was measured while the end-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 minimum alveolar concentration (MAC) before surgery, and then 1.0 MAC during surgery, which lasted more than 4 h. Results. There was no significant difference in CBF equivalent at 0.5 MAC between the isoflurane (20 ± 4 ml blood/ml oxygen) and the sevoflurane (19 ± 4 ml blood/ml oxygen) groups. With increasing anesthetic depth from 0.5 to 1.0 MAC, the CBF equivalent significantly (P < 0.05) increased in both groups (22 ± 7 and 21 ± 5, respectively). At 1.0 MAC during operation, the CBF equivalent with both anesthetics was maintained with minimal fluctuation for 4 h. There were no significant differences in the average value of the CBF equivalent during a 4-h period at 1.0 MAC between the isoflurane (23 ± 5) and the sevoflurane (20 ± 4) groups. Conclusion. Deepening anesthesia from 0.5 to 1.0 MAC with isoflurane and sevoflurane produced a slight increase in the CBF equivalent. The CBF equivalent at 1.0 MAC was maintained with no difference between the two agents during 4 h of neurosurgery. Received: August 2, 1999 / Accepted: April 3, 2000     

不同剂量异丙酚对家兔肝血流量及肝氧代谢的影响

目的观察输注不同剂量异丙酚对兔肝血流量(BF)和肝氧供需平衡的影响。方法30 只成年雄性健康家兔随机分为高剂量组(n=11,输注异丙酚1.2 mg·kg-1·min-1)、低剂量组(n=10,输注异丙酚0.4mg·kg-1·min-1)和对照组(n=9,输注等容量5%葡萄糖),静脉注射3%戊巴比妥钠麻醉后,气管插管、机械通气,开腹游离门静脉和肝动脉,行颈总动脉、门静脉、肝静脉插管。循环稳定后给药,电磁血流仪连续测定给药后0(给药前即刻)、10、20、30、40、50、60、70、80、90 min的门静脉和肝动脉BF,于给药后0、30、50、70、90 min采颈总动脉、门静脉、肝静脉血各0.5ml作血气分析,计算肝氧供(DO2)、氧耗(VO2)。结果高剂量组在给药后30-90min时肝BF较给药前即刻和对照组增加(P< 0.05或0.01),同期肝DO2、VO2也较对照组增加(P<0.05),肝DO2/VO2组间和组内比较差异无统计学意义。结论高剂量异丙酚可增加肝BF和肝DO2,同时也增加肝VO2,但尚能维持肝DO2/VO2。     

严重烧伤后早期肠道营养加用谷氨酰胺对肠道血流量及氧耗量的影响

采用 TBSA 30%Ⅲ度小型香猪烧伤模型,经肠系膜下静脉门静脉和髂动脉插管,以动态观察早期肠道营养加入谷氨酰胺(0.64g·kg~(-1)·d~(-1))对烧伤后肠道血流量和氧耗量的影响,结果显示谷氨酰胺能明显增加烧伤后肠道的血流量和氧耗量,减轻肠道的再灌注损伤。