Myocardial tissue oxygen during coronary artery constriction and hypotension in dogs

BACKGROUND: Sodium nitroprusside (SNP) may decrease myocardial tissue oxygenation in dogs with normal coronary arteries. We compared SNP- with desflurane-induced hypotension on myocardial tissue oxygen and pH in dogs with left anterior descending artery constriction. METHODS: Twenty-four dogs were anesthetized with 8% desflurane for baseline anesthesia. Catheters were inserted into the femoral artery and vein and the coronary sinus. A flow probe and flow restriction device was placed on the left anterior descending (LAD) artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Baseline measures were made of LAD artery flow, arterial and coronary sinus blood gases, and myocardial tissue gases. A 30% decrease in blood pressure was induced with SNP with unrestricted LAD flow (n=6) or when LAD artery flow was restricted by 30% from baseline (n=6). In separate dogs, a 30% decrease in blood pressure was produced with 14 +/- 1% desflurane with unrestricted LAD flow (n=6) or with baseline LAD artery flow restricted by 30% (n=6). RESULTS: During SNP-induced hypotension with no LAD constriction, LAD artery flow and coronary sinus oxygen tension increased but myocardial tissue oxygen tension (PmO2) decreased by 40%. When baseline artery flow was decreased by 30% by LAD constriction, SNP-induced hypotension decreased tissue oxygen pressure by 80%, and ischemic acidosis was produced. During unrestricted LAD artery flow or with a 30% flow restriction, desflurane-induced hypotension produced no significant change from baseline myocardial tissue oxygen tension or pH. CONCLUSION: During coronary artery constriction, desflurane-induced hypotension maintained myocardial tissue oxygenation and pH better than did SNP-induced hypotension. The divergence between tissue and coronary sinus oxygen tension during SNP suggests that arteriovenous shunting may occur.     

Effects of desflurane and isoflurane on intestinal tissue oxygen pressure during colorectal surgery

Volatile anaesthetics differ in the effects they have on splanchnic haemodynamics and oxygenation. The aim of this study was to evaluate the effects of desflurane and isoflurane as part of a balanced anaesthetic technique on intestinal tissue oxygenation during colorectal surgery. Data were analysed from 44 patients randomly assigned to receive either desflurane (desflurane group, n = 20), or isoflurane (isoflurane group, n = 24) for inhalational anaesthesia. Tissue oxygen pressure (P(tiss)O2) was measured on the serosal side of the large intestine prior to colonic resection (T1) and following the completion of the bowel anastomosis (T2). In addition, haemodynamic and oxygenation parameters were assessed. No difference in mean P(tiss)O2 was observed between the groups at T1 [desflurane group: 8.1 (2.9) kPa vs. isoflurane group: 7.7 (2.7) kPa]. Following completion of the anastomosis (T2) mean P(tiss)O2 was higher in the isoflurane group [9.6 (2.9) kPa] than the desflurane group [7.7 (2.4) kPa, p = 0.025]. During surgery no difference between the groups could be observed with regard to haemodynamics and global oxygenation parameters. The lack of a difference between the groups in P(tiss)O2 before resection of the colon suggests that, under normal conditions, desflurane and isoflurane have comparable effects on intestinal blood flow and oxygenation. However, following local ischaemia, the reactive hyperaemia seems to be better preserved during isoflurane anaesthesia indicated by a local increase in P(tiss)O2blank(p = 0.013) following completion of the bowel anastomosis.     

Influence of desflurane,isoflurane and halothane on regional tissue perfusion in dogs

The actions of desflurane, isoflurane and halothane on regional tissue perfusion were studied using radioactive microspheres in dogs chronically instrumented for measurement of arterial and left ventricular pressure, global (left ventricular dP/dtmax) and regional (percent segment shortening) contractile function, and diastolic coronary blood flow velocity. Systemic and coronary haemodynamics and regional tissue perfusion were measured in the conscious state and during anaesthesia with equihypotensive concentrations of desflurane, isoflurane, and halothane. All three volatile anaesthetics (P < 0.05) increased heart rate and decreased mean arterial pressure, left ventricular systolic pressure, and left ventricular dP/dtmax Myocardial perfusion was unchanged in subendocardial midmyocardial, and subepicardial regions by the administration of either dose of desflurane. No redistribution of intramyocardial blood flow (endo/epi ratio) was observed during desflurane anaesthesia. Although regional myocardial perfusion was reduced (P < 0.05) in a dose-related fashion by halothane and by isoflurane at high concentrations, redistribution of intramyocardial blood flow was not observed during halothane or isoflurane anaesthesia. All three volatile anaesthetics reduced blood flow to the renal cortex, but only desflurane produced a decrease in renal cortical vascular resistance. Hepatic blood flow decreased in response to halothane but not desflurane or isoflurane. Concomitant decreases in hepatic resistance were observed during administration of desflurane and isoflurane. Dose-related decreases in intestinal and skeletal muscle blood flow were observed during halothane and isoflurane but not desflurane anaesthesia. The results suggest that desflurane maintains myocardial, hepatic, intestinal, and skeletal muscle blood flow while halothane and isoflurane decrease regional tissue perfusion in these vascular beds to varying degrees during systemic hypotension in the chronically instrumented dog.     

地氟醚、七氟醚和异氟醚对犬血液动力学和氧供需平衡的影响

目的　采用连续温度稀释法观察不同浓度地氟醚对血液动力学和氧供需平衡的影响 ,并与七氟醚和异氟醚比较。方法　犬 18只 ,1.5 %硫喷妥钠 2 0 mg/ kg、阿曲库胺 0 .8mg/ kg麻醉诱导 ,气管插管后机械通气。左股静脉穿刺置入 7.5 F的六芯肺动脉漂浮导管 ,接 CCO/ SvO2 监测仪 ,连续测定并计算血液动力学及氧供需平衡各项指标。操作完成后平稳 1小时 ,取基础指标。然后随机依次吸入 0 .7、1.2和 1.7MAC的地氟醚、七氟醚或异氟醚 ,呼气末浓度达预定值后稳定 2 0分钟 ,记录各指标 ,再增加吸入浓度达下一个预定浓度。结果　 MAP、SVR和 CO在三组均呈剂量依赖性下降 ,地氟醚和异氟醚组 HR明显增快 ,七氟醚组 HR则明显减慢 ,异氟醚组 1.7MAC时 VO2 增加 ,DO2 和Sv O2 下降。结论　地氟醚对循环功能和氧供需平衡的影响与异氟醚相似 ,与七氟醚则有所不同     

Cardiovascular effects of desflurane and isoflurane in patients with coronary artery disease

Background : Anaesthesia in patients with ischaemic heart disease may cause adverse haemodynamic reactions. This investigation compares the cardiovascular effects of equipotent concentrations of desflurane and isoflurane in 30 patients (ASA III) with coronary artery disease before surgical stimulation. Methods : After standardised induction of anaesthesia with etomidate, fentanyl and pancuronium and tracheal intubation patients randomly received either desflurane (group I, n = 15) or isoflurane (group II, n = 15) in slowly increasing concentrations. ST-segment analysis and haemodynamic measurements were performed at 0.25, 0.5, 0.75 and 1.0 MAC of desflurane or isoflurane. Results : Cardiac index did not change significantly in the two groups during the administration of the inhalational anaesthetics. Desflurane and isoflurane both caused a dose-dependent significant decrease of mean arterial blood pressure (group I: ?16%; group II: ?18%). As with isoflurane, the decrease of mean arterial pressure produced by desflurane primarily resulted from a decrease in systemic vascular resistance (group I: ?26%, group II: ?21%). Central venous pressure was not affected by the two volatile anaesthetics. Pulmonary artery pressure and pulmonary capillary wedge pressure remained unchanged during the administration of isoflurane, but in contrast both parameters significantly increased in patients receiving desflurane (PAP 24%, PCWP 40%). ST-segment analysis provided no signs of myocardial ischaemia. Conclusion : The results of this study demonstrate that in patients with coronary artery disease the haemodynamic effects of equipotent concentrations of desflurane and isoflurane are similar except for a significant increase in PAP and PCWP caused by desflurane. Therefore, desflurane should be administered with great caution if it is used as an alternative anaesthetic in patients with ischaemic heart disease.     

A comparison of desflurane and isoflurane in patients undergoing coronary artery surgery

Animal studies indicate that desflurane and isoflurane have similar hemodynamic effects when administered in equipotent anesthetic concentrations. The authors compared desflurane and isoflurane, used as primary anesthetics for patients undergoing elective coronary artery bypass surgery whose left ventricular ejection fractions were greater than 0.34. After induction of anesthesia with thiopental (dose 180 +/- 45 mg [mean +/- standard deviation]) and fentanyl, 10 micrograms.kg-1, either desflurane or isoflurane was administered to maintain systolic blood pressure within 70-120% of, and heart rates less than 120% of, the patients' average preoperative values. If adjusting the end-tidal anesthetic concentration within the range of 0-2.0 MAC could not maintain these predefined hemodynamic limits, additional fentanyl or vasoactive drugs were used. Induction and maintenance of anesthesia was accompanied by a significant decrease in mean arterial pressure in both groups (desflurane 97 +/- 12 mmHg at control, decreasing to 71 +/- 5 mmHg during skin preparation; isoflurane 95 +/- 9 mmHg at control, 74 +/- 9 mmHg during skin preparation). One minute after sternotomy, mean arterial pressure in the isoflurane group had returned to control, 97 +/- 9 mmHg, which was significantly greater than in the desflurane group, 87 +/- 12 mmHg. Systolic arterial pressure was also significantly greater in the isoflurane group 1 min after intubation, during skin preparation, and 1 min after sternotomy. Otherwise, the hemodynamic effects of these volatile agents were similar. There were no differences between groups in the incidence of ECG changes indicative of myocardial ischemia prior to cardiopulmonary bypass, perioperative myocardial infarction, or perioperative mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Felypressin-induced reduction in coronary blood flow and myocardial tissue oxygen tension during anesthesia in dogs

PURPOSE: To determine whether felypressin reduced myocardial tissue oxygen tension (PmO2). METHODS: Seven open-chest dogs were studied under nitrous oxide and isoflurane anesthesia. Hemodynamic variables including heart rate (HR), blood pressure (BP), mean pulmonary arterial pressure (MPAP), PmO2 and coronary blood flow (CBF) were continuously recorded. After baseline measurements, felypressin was infused at 0.15, 0.3, 0.6 and 1.0 IU x hr(-1) in a successive manner. Hemodynamic variables were evaluated at 3, 6, 9 min after the start of each infusion. RESULTS: Felypressin caused reductions in CBF and inner layer PmO2 (int-PmO2). Decreases in CBF (-23%, P< 0.05) and int-PmO2 (-8%, P<0.05) observed at low dose (0.15 1U x hr(-1)) were not accompanied by changes in BP and HR. Negative correlations between cumulative doses of Felypressin (mIU x kg(-1)) and CBF (% change from base line) (r = -0.69, P<0.05) or int-PmO2 (% change from base line) (r = -0.48, P<0.05) were observed. CONCLUSION: Felypressin reduced PmO2 along with minimal changes in HR and BP.     

Left ventricular oxygen tensions in dogs during coronary vasodilation by enflurane, isoflurane and dipyridamole

The purpose of this study was to investigate the effects of the anesthetics enflurane and isoflurane and of the coronary vasodilator dipyridamole on myocardial oxygen balance and myocardial tissue oxygen tensions. The studies were performed in 24 open-chest dogs during basal anesthesia with a narcotic. Myocardial blood flow (MBF) was measured using radioactive microspheres, myocardial surface tissue PO2 by means of a platinum multiwire surface electrode. One control group and three experimental groups were studied: enflurane (1.1 vol%), isoflurane (0.7 vol%, both end-tidal concentrations), and dipyridamole (0.4 mg/kg). Mean arterial pressure significantly decreased to an average of 70 mm Hg in all three experimental groups. Although MBF was unchanged during enflurane (-18%) and isoflurane (+20%), it increased during dipyridamole (+304% p less than 0.05 vs baseline and control, enflurane, and isoflurane groups). Myocardial oxygen consumption decreased significantly during enflurane and isoflurane but remained unchanged during dipyridamole. Thus, the ratio between myocardial oxygen delivery and consumption increased 6% with enflurane (p less than 0.05 vs baseline), 47% with isoflurane (p less than 0.05 vs baseline and control group) and 280% with dipyridamole (p less than 0.05 vs baseline and control, enflurane, and isoflurane groups). Coronary venous PO2 remained unchanged during enflurane but increased significantly during isoflurane and dipyridamole. Left ventricular surface tissue PO2 was unchanged in enflurane and isoflurane animals and decreased slightly, yet significantly, during dipyridamole. All variables remained unchanged in the control group. Thus, isoflurane and dipyridamole interfered with MBF autoregulation and increased myocardial oxygen delivery out of proportion to myocardial demands.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood pressure response to thermoregulatory vasoconstriction during isoflurane and desflurane anesthesia

BACKGROUND: Mild perioperative hypothermia produces morbid cardiac outcomes that may result from sympathetically induced hypertension. However, volatile anesthetics produce vasodilatation that may reduce the hemodynamic response to hypothermia. We tested the hypothesis that the volatile anesthetics isoflurane and desflurane blunt the normal cold-induced hypertensive response. METHODS: We analyzed prospective data from three analogous studies: 1) 10 volunteers given desflurane (2.6 volume percentage) maintained in left-lateral position; 2) nine volunteers without anesthesia or anesthetized with various doses of desflurane; and 3) eight volunteers given various concentrations of isoflurane. Mean skin temperature was reduced to 31 C, which decreased core body temperature and triggered thermoregulatory vasoconstriction. Mean arterial pressures were determined before and after hypothermia provoked intense thermoregulatory vasoconstriction. RESULTS: The hemodynamic responses to thermoregulatory vasoconstriction were similar without anesthesia and at all concentrations of desflurane and isoflurane. On average, mean arterial pressure increased 14 (SD = 5) mmHg with and without anesthesia. CONCLUSION: We conclude that thermoregulatory vasoconstriction significantly increases arterial pressure with or without isoflurane or desflurane anesthesia.     

Effects of isoflurane on myocardial blood flow, function, and oxygen consumption in the presence of critical coronary stenosis in dogs

Because isoflurane has been reported to produce coronary steal, we studied 12 open chest, anesthetized (pentobarbital) dogs with critical stenosis (CS) of the left circumflex coronary artery (LCA). Sonomicrometers were implanted to measure systolic wall thickening, myocardial blood flow (MBF) was measured with microspheres (15 microns diameter), and regional venous sampling was performed to estimate regional oxygen extraction and myocardial oxygen consumption (MVO2). Anesthetic concentrations of isoflurane reduced arterial blood pressure dramatically, resulting in a maldistribution of MBF distal to the CS consistent with the pattern characterizing a transmural coronary steal effect. Elevation of arterial blood pressure with phenylephrine during high concentration isoflurane (1.7 +/- 0.1%) augmented MBF, but the maldistribution distal to the CS persisted. Despite the maldistribution, however, there was no indication of ischemia in the LCA region because systolic wall thickening, oxygen extraction, and MVO2 were not significantly different between the LCA and left anterior descending coronary artery (LAD) (control) areas. Because wall thickening, oxygen extraction, and MVO2 were markedly reduced by isoflurane in both the LCA and control areas, it was concluded that isoflurane substantially reduced myocardial oxygen requirements by inducing myocardial depression, reducing heart rate, and decreasing afterload. Consequently, the apparent maldistribution of LCA blood flow (coronary steal) was due to the hemodynamic and vasodilatory effects of isoflurane, but did not result in ischemia because the level of blood flow was at or above the requirements of the myocardium.     

Steal-prone coronary circulation in chronically instrumented dogs: isoflurane versus adenosine

The influence of isoflurane and adenosine on left ventricular myocardial blood flow was investigated in dogs chronically instrumented for measurement of systemic and coronary hemodynamics, regional myocardial contractile function (with ultrasonic sonomicrometers), and myocardial perfusion (by the radioactive microsphere method). An Ameroid constrictor was implanted on the left circumflex coronary artery to produce a progressive stenosis that gradually reduced vascular reserve of the distal perfusion territory. The depletion of reserve was evaluated by daily monitoring of the hyperemic response to adenosine. A stenosis of moderate severity was considered present when left circumflex reserve was attenuated by approximately 60-70%. During left circumflex stenosis development, the left anterior descending coronary artery was totally occluded for 2 min each hour eight times daily with a hydraulic occluder to stimulate coronary collateral development over a period of 9-13 days. Contractile dysfunction during and flow debt repayment after each brief occlusion were used to monitor coronary collateral development. After stenosis and collateral development had occurred, the left anterior descending coronary artery was permanently occluded to simulate a condition of multivessel coronary artery disease with enhanced collateral development. In separate groups of experiments, hemodynamics and myocardial perfusion were measured before and after administration of adenosine (0.54 and 1.08 mg/min) or isoflurane (1.1 and 1.9%, end-tidal) and in the presence of either agent during adjustment of diastolic aortic pressure and heart rate to control levels. Total left anterior descending coronary artery occlusion in the presence of a moderate left circumflex stenosis produced an increase in mean arterial and left ventricular end diastolic pressures. Isoflurane decreased arterial pressure, left ventricular systolic pressure, and positive rate of increase of left ventricular pressure (dP/dt50) without altering heart rate. Administration of the high concentration of isoflurane reduced blood flow in normal areas and in regions distal to the partial (from 1.05 +/- 0.10 to 0.76 +/- 0.11 ml.min-1.g-1) or total coronary occlusion (from 0.64 +/- 0.10 to 0.41 +/- 0.11 ml.min-1.g-1). However, when arterial pressure and heart rate were restored to levels present in the conscious state, perfusion in all zones was maintained at control levels (1.06 +/- 0.11 for the stenotic and 0.69 +/- 0.12 ml.min-1.g-1 for the occluded region). Ratios of transmural blood flow between occluded and normal or occluded and stenotic zones were not different from the conscious state during a constant aortic pressure and heart rate.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effect of isoflurane on the extent of myocardial necrosis and on systemic hemodynamics, regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion

Anesthetized dogs were studied in two protocols to determine the effect of isoflurane on the extent of myocardial injury resulting from left anterior descending coronary artery (LAD) occlusion. In 22 dogs (11 treated with isoflurane 1% inspired, beginning 1 hr after LAD occlusion, and 11 control) myocardial infarct size measured postmortem after 6 hr of LAD occlusion was significantly less with isoflurane than without it, 23.4 +/- 3.8% vs 36.2 +/- 2.4% of left ventricle; regional myocardial blood flow (RMBF) did not differ between groups and hemodynamic differences were slight. Fifty-two other dogs underwent two 15-min periods of LAD occlusion separated by 1 hr of reperfusion. Without isoflurane (n = 12), hemodynamic, RMBF, and regional metabolic data did not differ between the two occlusion periods. When isoflurane 1.3% inspired was administered during one of the two occlusion periods by random assignment, coronary perfusion pressure, left ventricular stroke work index, and systolic left ventricular pressure decreased more than when isoflurane was not administered. Both oxygen (O2) consumption and supply in ischemic myocardium decreased proportionately during LAD occlusion, but more so with isoflurane. Neither lactate production, potassium release, glucose extraction, nor coronary venous carbon dioxide (CO2) or O2 content differed between LAD occlusion periods with and without isoflurane. Thus, isoflurane decreased the extent of myocardial necrosis produced by LAD occlusion but neither RMBF nor metabolic indications were improved during transitory ischemia.     

Glyburide decreases myocardial oxygen pressure in dogs

BACKGROUND: Reports show that glyburide, an adenosine triphosphate sensitive potassium (K+ATP) channel blocker, will reverse the myocardial protective effect of inhalational anesthesia. We evaluated the effect of glyburide on myocardial tissue oxygen pressure (PmO2) in dogs anesthetized with desflurane. METHODS: Twelve dogs were anesthetized with 8% end-tidal desflurane for baseline anesthesia. A flow probe was placed on the left anterior descending (LAD) artery. A probe that measured PmO2 was inserted into the middle myocardium in the LAD region. After baseline measures, six dogs received i.v. 1 mg kg(-1) of glyburide and six dogs received sham vehicle treatment. After the glyburide or sham treatment, each dog received an i.v. infusion of adenosine 0.1 microg kg(-1) x min(-1), sodium nitroprusside (SNP) 2-4 microg kg(-1) x min(-1) and 14% end-tidal desflurane in random order. RESULTS: Glyburide decreased LAD artery flow from 59 +/- 9 ml min(-1) to 30 +/- 6 ml min(-1) (P < 0.05) and PmO2 from 44 +/- 16 mmHg to 30 +/- 9 mmHg (P < 0.05). Adenosine infusion increased LAD artery blood flow 180% in the sham-treated dogs but produced no change in the glyburide-treated dogs. Sodium nitroprusside infusion increased LAD artery flow and decreased PmO2 in both the glyburide- and sham-treated dogs. Desflurane (14%) did not reverse the glyburide-induced vasoconstriction but increased PmO2 to 38 +/- 20 mmHg (P < 0.05). CONCLUSION: Glyburide produced myocardial tissue hypoxia, which was not changed by adenosine, worsened by SNP and improved by 14% desflurane. The improvement in PmO2 with desflurane occurred without a change in myocardial blood flow.     

Pulmonary mechanics during isoflurane,sevoflurane and desflurane anaesthesia

This study was designed to investigate the effects of desflurane on bronchial smooth muscle tone, following intubation and to compare these effects with isoflurane and sevoflurane. Patients were randomly divided into three groups to receive, isoflurane (n = 22), sevoflurane (n = 23), or desflurane (n = 22). Peak inspiratory pressure (PIP), respiratory resistance (Rr) and dynamic compliance (Cdyn) measurements were recorded at three time points; After the beginning of ventilation and before inhalation agent was started, following 5 min of ventilation with 1 MAC (minimum alveolar concentration) inhalation agent and following 5 min of 2 MAC inhalation agent. We found that all inhalation agents caused a significant decrease in Peak Inspiratory Pressure (PIP) and respiratory resistance (Rr), and an increase in dynamic compliance (Cdyn) at 1 MAC concentrations. When the agent concentration was increased to 2 MAC, desflurane caused a significant increase in Rr and PIP and a decrease in Cdyn. We concluded that desflurane, like isoflurane and sevoflurane, exhibits a bronchodilator effect at 1 MAC concentration. However, increasing the concentration to 2 MAC caused an increase in airway resistance with desflurane, whilst sevoflurane and isoflurane continued to have a bronchodilator effect.     

Regional blood flow and tissue oxygen pressures of the collateral-dependent myocardium during isoflurane anesthesia in dogs

The authors investigated the effects of isoflurane on blood flow and tissue oxygen pressures of a collateral-dependent myocardium. Seventeen dogs divided into two groups were studied 3-4 weeks after implantation of ameroid coronary artery constrictors to completely occlude the proximal part of the left anterior descending artery. Experiments were performed during anesthesia with an opiate that was infused intravenously throughout the experiments. In Group 1 (n = 9), measurements were obtained during control and during isoflurane- (1.6-2.2 vol%) induced hypotension (mean arterial pressure, 60 mmHg). In Group 2 (n = 8), the identical protocol was applied, but norepinephrine was infused to maintain normotension. Dipyridamole effects were studied in five animals of Group 2 after a second control period at least 1 h after discontinuation of isoflurane. Isoflurane-induced hypotension caused reductions of blood flow and surface tissue oxygen pressures in the collateral flow-dependent area. Vasodilation in the normal left ventricular areas was demonstrated by an unchanged blood flow despite a reduced oxygen consumption and by a significantly increased coronary sinus hemoglobin oxygen saturation. When arterial pressure was maintained at its control level by norepinephrine, tissue oxygen pressures remained constant and collateral as well as normal area flow increased significantly during isoflurane. Coronary vascular resistance was lower during administration of isoflurane and norepinephrine compared with that during isoflurane induced hypotension, suggesting a significant contribution of tissue oxygen demand in regulation of coronary vascular resistance. At comparable levels of arterial pressure and left ventricular oxygen consumption, normal zone blood flow was significantly higher during dipyridamole than during isoflurane and norepinephrine. Thus, isoflurane-induced hypotension decreased blood flow and tissue oxygen pressures of collateral flow-dependent myocardial areas. However, neither isoflurane nor dipyridamole caused such alterations when arterial pressure was normal.     

Vascular responsiveness to brachial artery infusions of phenylephrine during isoflurane and desflurane anesthesia

Compared with equi-minimum alveolar anesthetic concentration (MAC) isoflurane, desflurane is associated with greater levels of sympathetic nerve activity in humans but similar reductions in blood pressure. To explore these divergent effects, we evaluated vascular alpha(1)-adrenoceptor responses in the human forearm during isoflurane and desflurane anesthesia to determine if alpha(1)-adrenoceptor responses were more substantially attenuated during desflurane administration. Bilateral forearm venous occlusion plethysmography was used to examine arterial blood flow and to determine changes in forearm vascular resistance during brachial artery infusions of saline and phenylephrine (0.2, 0.4, 0.8, and 1.6 microg/min) in 22 conscious subjects and during anesthesia with 0.65 and 1.3 MAC isoflurane or desflurane. Infusion of phenylephrine into the brachial artery increased the forearm vascular resistance in a dose-dependent manner. The arterial response to phenylephrine was significantly attenuated by 0.65 and 1.3 MAC desflurane and similarly attenuated during 1.3 MAC isoflurane (P < 0.05). Impaired arterial alpha(1)-adrenoceptor responsiveness occurred during desflurane. However, this effect was statistically similar (P > 0.05) to the impaired responses during isoflurane. Blood pressure decreases during volatile anesthesia may be, in part, caused by decreased alpha(1)-adrenoceptor responsiveness. IMPLICATIONS: alpha-receptors on blood vessels regulate constriction and dilation and therefore modulate blood pressure. This research indicates that vasoconstriction via the alpha(1)-receptor vascular response is impaired during isoflurane and desflurane anesthesia.     

The effects of dopamine and amrinone on myocardial oxygen demand-supply relationship in dogs with coronary artery stenosis

This study examined the effects of dopamine (DA) and amrinone (AM) on myocardial oxygen demand-supply relationship in coronary artery stenotic areas (40-60% reduction of coronary blood flow by a constrictor) by measuring myocardial oxygen tension (PmO2) after administration of either DA or AM in twelve dogs. The results were as follow; 1) PmO2 showed no significant changes with either DA or AM, but it showed a significant inverse correlation with HR with DA or AM. Thus changes in HR affected the myocardial oxygen balance. 2) AM showed strong coronary vasodilating action in non-stenotic areas and possibly led to 'steal'. 3) Looking at indicators of myocardial ischemia, MAP/HR was significantly correlated with PmO2, and it reflected the myocardial oxygen demand-supply relationship better than RPP or DPTI/TTI. When DA or AM is used in patients with coronary artery disease, both drugs seem to maintain myocardial oxygen balance unless they cause tachycardia. Caution is required in the administration of AM because of the possibility of 'steal'.     

地氟醚与异氟醚麻醉对小儿循环功能的影响

目的：比较地氟醚和异氟醚麻醉对小儿血液动力学的影响。方法：28例1－5岁小儿，ASAI－Ⅱ级，快速诱导气管插管后随机分为地氟醚（D）帮异氟醚（I）两组，每组14例。分别测量呼气末麻醉药浓度为0、0．5、1．0和1．5MAC稳定5分钟后的SI、CI、SVR、HR及MAP。结果：与0MAC比较，0．5MAC时两组MAP和SVR均略有降低（P＜0．05），其他指标均无明显变化（P＞0．05）。1．0MAC时，SVR和MAP进一步降低，其幅度两组间无显著差异；HR和SI均略有升高，但无显著差异；CI值D组显著高于I组。达1．5MAC时，D组的HR显著高于I组，而SI下降与0MAC近似；SVR和MAP两组无进一步降低。结论：地氟醚和异氟醚麻醉对小儿心肌收缩功能均有一定抑制作用,但地氟醚使小儿HR增快的作用大于异氟醚。     

Comparison of desflurane and isoflurane in anaesthesia for dental surgery

We studied 50 ASA I-II patients, aged 18-65 yr, undergoing elective orofacial surgery. Anaesthesia was induced with fentanyl and propofol, and maintained with 66% nitrous oxide in oxygen and either desflurane or isoflurane to compare recovery characteristics and cardiovascular stability. Cardiovascular responses to induction, intubation and incision were similar with both agents, although the increase in heart rate in response to intubation was less marked in the desflurane group. Maximum end-tidal concentrations of desflurane required were 4.0-10.6% (mean 6.8%) compared with maximum isoflurane concentrations of 1.1-2.3% (mean 1.6%). Mean duration of anaesthesia was 46 (SD 17.9) min (range 25-89 min) in the desflurane group and 41 (11.5) (23-60) min in the isoflurane group. Times to extubation were 6.7 (2.1) (3-10) min and 11.3 (4.1) (5-23) min, to eye opening 6.8 (2.2) (3-11) min and 12.7 (6.9) (7-37) min, to stating date of birth 9.0 (2.3) (4-12) min and 15.0 (6.9) (8-39) and to discharge from the recovery room 45 (11.6) (22- 80) min and 64 (20.9) (28-134) min, for the desflurane and isoflurane groups, respectively (all P < 0.0001). No serious complications occurred in any patient.