Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation.

This study compared systemic hemodynamic and organ blood flow responses to equipotent concentrations of halothane and sevoflurane during spontaneous ventilation in the rat. The MAC values for halothane and sevoflurane were determined. Cardiac output and organ blood flows were measured using radiolabeled microspheres. Measurements were obtained in awake rats (control values) and at 1.0 MAC halothane or sevoflurane. The MAC values (mean +/- SEM) for halothane and sevoflurane were 1.10% +/- 0.05% and 2.40% +/- 0.05%, respectively. The PaCO2 increased to a similar extent in both groups compared with control values. During halothane anesthesia, heart rate decreased by 12% (P < 0.01), cardiac index by 26% (P < 0.01), and mean arterial blood pressure by 18% (P < 0.01) compared with control values. Stroke volume index and systemic vascular resistance did not change. During sevoflurane anesthesia, hemodynamic variables remained unchanged compared with control values. Coronary blood flow decreased by 21% (P < 0.01) and renal blood flow by 18% (P < 0.01) at 1.0 MAC halothane, whereas both remained unchanged at 1.0 MAC sevoflurane. Cerebral blood flow increased to a greater extent with halothane (63%; P < 0.01) than with sevoflurane (35%; P < 0.05). During halothane anesthesia, hepatic arterial blood flow increased by 48% (P < 0.01), whereas portal tributary blood flow decreased by 28% (P < 0.01). During sevoflurane anesthesia, hepatic arterial blood flow increased by 70% (P < 0.01) without a concomitant reduction in portal tributary blood flow. Total liver blood flow decreased only with halothane (16%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog.

To compare the effects of sevoflurane and isoflurane on hepatic circulation, eighteen dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic and portal blood flows. Each animal was studied while awake and during 1.2 and 2 MAC of either isoflurane or sevoflurane. Both anesthetics induced tachycardia and a dose-dependent decrease in mean aortic blood pressure (isoflurane -27% and -39%; sevoflurane -22% and -37%). Cardiac output decreased only at the highest concentration (isoflurane -10%; sevoflurane -21%). During sevoflurane, portal blood flow decreased at both 1.2 and 2 MAC (-14 and -33%, respectively), whereas an increase in hepatic arterial blood flow was recorded at 2 MAC (+33%). During isoflurane, the only significant change was a decrease in portal blood flow (-16%) at 1.2 MAC. Neither anesthetic significantly changed renal blood flow. Therefore, both anesthetics led to similar systemic and hepatic vasodilation.     

Systemic distribution of blood flow in swine while awake and during 1.0 and 1.5 MAC isoflurane anesthesia with or without 50% nitrous oxide

To examine the effects of isoflurane on systemic distribution of cardiac output, organ/tissue blood flow was measured in 11 isocapnic pigs using 15-micrometer diameter radionuclide-labeled microspheres injected into the left atrium. Measurements were made on each pig during five of the following six conditions; awake (control); 1.0 MAC (1.45% end-tidal)isoflurane anesthesia; 1.5 MAC (2.18% end-tidal) isoflurane anesthesia; 0.95% end-tidal isoflurane and 50% N2O anesthesia equivalent to 1.0 MAC; 1.68% end-tidal isoflurane and 50% N2O anesthesia equivalent to 1.5 MAC; and 50% N2O administration. The order of anesthetized steps was randomized. A period of 60 min was interposed between anesthetized steps to allow pigs to recover towards control values. Mean aortic pressure decreased in a dose-related manner during isoflurane anesthesia, whereas cardiac output decreased only during 1.5 MAC isoflurane anesthesia and heart rate remained unchanged. The addition of N2O attenuated the hypotensive effects of isoflurane and cardiac output was maintained near control values because of increased heart rate. Brain blood flow increased in a dose-dependent manner with isoflurane anesthesia, but myocardial blood flow exhibited a dose-related decrease. The addition of 50% N2O to maintain the same total MAC anesthesia resulted in a larger increase in brain blood flow especially at 1.5 MAC, while myocardial blood flow was maintained near control value. Rate-pressure product and myocardial blood flow at 1.5 MAC anesthesia were higher when N2O was used with isoflurane. While blood flow and fraction of cardiac output going to the adrenal glands were unaltered during isoflurane-N2O anesthesia, blood flow increased at 1.5 MAC isoflurane anesthesia. Splenic blood flow and splenic fraction of cardiac output were increased at both MAC levels of isoflurane as well as isoflurane-N2O anesthesia whereas blood flow to the stomach, small intestine, diaphragm, skeletal muscle, and adipose tissue decreased from control values. Renal, hepatic arterial, and cutaneous blood flow remained unaltered. Fifty percent N2O in the presence of a residual end-tidal isoflurane concentration of 0.20% caused heart rate to increase from control levels, while cardiac output and mean aortic pressure were unaltered. Brain blood flow increased by 27% above control values, but perfusion in the myocardium, adrenal glands, spleen, kidneys, liver, and skin was unchanged. Stomach, small intestine, skeletal muscle, and diaphragm blood flows decreased from control values, whereas perfusion of adipose tissue increased.     

Comparison of the effects of isoflurane and desflurane on cardiovascular dynamics and regional blood flow in the chronically instrumented dog

Seven mongrel dogs were chronically instrumented for the measurement of aortic and left ventricular blood pressures, cardiac output, left ventricular wall thickening, left ventricular dP/dt, and circumflex coronary, renal, hepatic and portal blood flows under the influence of desflurane (D) and isoflurane (I). Administration of the two anesthetics, was randomized, as was the order of the concentrations administered. Each dog was studied awake and at 1.2, 1.4, 1.75, and 2.0 MAC of each anesthetic on different days. Both anesthetics decreased mean arterial pressure, stroke volume, systemic vascular resistance, left ventricular dP/dt, and wall thickness. The decreases were dose-dependent for mean arterial pressure (percent of awake values: D 78, I 85 at 1.2 MAC, and D 67, I 69 at 2.0 MAC); stroke volume (D 66, I 72 at 1.2 MAC, and D 52, I 57 at 2.0 MAC); dP/dt (D 61, I 64 at 1.2 MAC, and D 46, I 49 at 2.0 MAC); and WT (D 68, I 70 at 1.2 MAC, and D 47, I 60 at 2.0 MAC). Systemic vascular resistance decreased approximately the same at 1.2 MAC (D 71, I 87%) as at 2.0 MAC (D 71, I 79%). Heart rate increased but also not in a dose-dependent fashion (percent of awake values: D 177, I 145 at 1.2 MAC, and D 176, I 155 at 2.0 MAC). Coronary blood flow was increased by both anesthetics at all concentrations (percent of awake values: I 136 at 1.2 MAC and 161 at 2.0 MAC of awake, and D 131 at 1.2 MAC and 138 at 2.0 MAC.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Influence of Ventilation Mode (Spontaneous Ventilation,IPPV and PEEP) on Cardiopulmonary Parameters in Sevoflurane Anaesthetized Dogs

The purpose of this study was to investigate the cardiopulmonary influences of sevoflurane in oxygen at two anaesthetic concentrations (1.5 and 2 MAC) during spontaneous and controlled ventilation in dogs. After premedication with fentanyl–droperidol (5 μg/kg and 0.25 mg/kg intramuscularly) and induction with propofol (6 mg/kg intravenously) six dogs were anaesthetized for 3 h. Three types of ventilation were compared: spontaneous ventilation (SpV), intermittent positive pressure ventilation (IPPV), and positive end expiratory pressure ventilation (PEEP, 5 cm H₂O). Heart rate, haemoglobin oxygen saturation, arterial blood pressures, right atrial and pulmonary arterial pressures, pulmonary capillary wedge pressure and cardiac output were measured. End tidal CO₂%, inspiratory oxygen fraction, respiration rate and tidal volume were recorded using a multi‐gas analyser and a respirometer. Acid–base and blood gas analyses were performed. Cardiac index, stroke volume, stroke index, systemic and pulmonary vascular resistance, left and right ventricular stroke work index were calculated. Increasing the MAC value during sevoflurane anaesthesia with spontaneous ventilation induced a marked cardiopulmonary depression; on the other hand, heart rate increased significantly, but the increases were not clinically relevant. The influences of artificial respiration on cardiopulmonary parameters during 1.5 MAC sevoflurane anaesthesia were minimal. In contrast, PEEP ventilation during 2 MAC concentration had more pronounced negative influences, especially on right cardiac parameters. In conclusion, at 1.5 MAC, a surgical anaesthesia level, sevoflurane can be used safely in healthy dogs during spontaneous and controlled ventilation (IPPV and PEEP of 5 cm H₂O).     

Effects of Sevoflurane with and without Nitrous Oxide on Human Cerebral Circulation: Transcranial Doppler Study

Background: This study was designed to evaluate the effects of sevoflurane with and without nitrous oxide on human middle cerebral artery (MCA) flow velocity, cerebrovascular carbon dioxide reactivity, and autoregulation compared with the awake state using transcranial Doppler ultrasonography.

Methods: In 14 patients, the time-mean middle cerebral artery flow velocity (Vmca) was measured when the end-tidal carbon dioxide level was approximately 30, 40, and 50 mmHg under the following conditions: (1) awake; (2) with 2% (1.2 MAC) sevoflurane; and (3) with 1.2 MAC sevoflurane-60% nitrous oxide. In six other patients, the cerebrovascular autoregulation during anesthesia was determined using intravenous phenylephrine to increase blood pressure.

Results: Sevoflurane (1.2 MAC) significantly decreased Vmca compared with the awake value at each level of end-tidal carbon dioxide, whereas 1.2 MAC sevoflurane-60% nitrous oxide did not exert significant influence. The Vmca in normocapnic patients decreased from 69 cm/s to 55 cm/s with 1.2 MAC sevoflurane and then increased to 70 cm/s when nitrous oxide was added. Sevoflurane (1.2 MAC) with and without 60% nitrous oxide had a negligible effect on cerebrovascular carbon dioxide reactivity. A phenylephrine-induced increase of mean arterial pressure did not influence Vmca during anesthesia.     

Haemodynamic and splanchnic organ blood flow responses during sevoflurane-induced hypotension in dogs

BACKGROUND AND OBJECTIVE: The safety of hypotension induced by sevoflurane and splanchnic organ blood flow remains to be clarified. The aim was to investigate the effects of sevoflurane-induced hypotension on systemic haemodynamics and splanchnic organ blood flows in dogs. METHODS: Mean arterial pressure was maintained at 60 mmHg by increasing sevoflurane concentrations. The renal, hepatic and pancreatic blood flows were measured by using the hydrogen clearance method. RESULTS: Hypotension induced by sevoflurane resulted in a 50% decrease of mean arterial pressure due to a 30% reduction in systemic vascular resistance associated with a 30% decrease in cardiac index. The mechanisms causing the lower cardiac index were produced by the decreases in heart rate and left ventricular dP/dt(max). Renal, hepatic and pancreatic blood flow were reduced, but the whole-body oxygen consumption did not change during the hypotensive period. CONCLUSIONS: The haemodynamic changes induced by sevoflurane were caused by the suppression of arterial baroreflexes and myocardial depression, but splanchnic organ blood flows, though reduced, could provide adequate peripheral perfusion to meet the decrease in oxygen supply.     

Direct cerebral vasodilatory effects of sevoflurane and isoflurane.

BACKGROUND: The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. METHODS: Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. RESULTS: Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. CONCLUSIONS: In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.     

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane

Background: The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram.

Methods: Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 [mu]g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels.

Results: Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4 +/- 3 and 17 +/- 3% at 0.5 and 1.5 MAC sevoflurane; 19 +/- 3 and 72 +/- 9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P < 0.05). All patients required phenylephrine (100-300 [mu]g) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia.     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

The minimum alveolar concentration (MAC) and hemodynamic effects of halothane, isoflurane, and sevoflurane in newborn swine

To determine the minimum alveolar concentration (MAC) and hemodynamic responses to halothane, isoflurane, and sevoflurane in newborn swine, 36 fasting swine 4-10 days of age were anesthetized with one of the three volatile anesthetics in 100% oxygen. MAC was determined for each swine. Carotid artery and internal jugular catheters were inserted and each swine was allowed to recover for 48 h. After recovery, heart rate (HR), systemic systolic arterial pressure (SAP), and cardiac index (CI) were measured awake and then at 0.5, 1.0, and 1.5 MAC of the designated anesthetic in random sequence. The (mean +/- SD) MAC for halothane was 0.90 +/- 0.12%; the MAC for isoflurane was 1.48 +/- 0.21%; and the MAC for sevoflurane was 2.12 +/- 0.39%. Awake (mean +/- SD) measurements of HR, SAP, and CI did not differ significantly among the three groups. Compared to the awake HR, the mean HR decreased 35% at 1.5 MAC halothane (P less than 0.001), 19% at 1.5 MAC isoflurane (P less than 0.005), and 31% at 1.5 MAC sevoflurane (P less than 0.005). Compared to awake SAP, mean SAP measurements decreased 46% at 1.5 MAC halothane (P less than 0.001), 43% at 1.5 MAC isoflurane (P less than 0.001), and 36% at 1.5 MAC sevoflurane (P less than 0.005). Mean SAP at 1.0 and 1.5 MAC halothane and isoflurane were significantly less than those measured at equipotent concentrations of sevoflurane (P less than 0.005). Compared to awake CI, mean CI measurements decreased 53% at 1.5 MAC halothane (P less than 0.001) and 43% at 1.5 MAC isoflurane (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral autoregulation in awake versus isoflurane-anesthetized rats

We evaluated regional cerebral and spinal cord blood flow in rats during isoflurane anesthesia. Tissue blood flow was measured in cerebral cortex, subcortex, midbrain, and spinal cord using radioactive microspheres. Blood flow autoregulation was measured within the following arterial blood pressure ranges (mm Hg): 1 = less than 50, 2 = 50-90, 3 = 90-130, 4 = 130-170, 5 = greater than 170. Arterial blood pressure was increased using phenylephrine infusion and decreased with ganglionic blockade and hemorrhage. Three treatment groups were studied: 1 = awake control, 2 = 1.0 minimum alveolar anesthetic concentration (MAC) isoflurane, 3 = 2.0 MAC isoflurane. Autoregulation was seen in awake rats from 50 to 170 mm Hg in all tissues. The autoregulatory coefficient (change in blood flow/change in blood pressure) was increased in midbrain and spinal cord during 1.0 MAC isoflurane and in all tissues during 2.0 MAC isoflurane (P less than 0.05). Within the arterial blood pressure range of 90-130 mm Hg, isoflurane produced the following changes in tissue blood flow (percent of awake control): 1.0 MAC isoflurane: cortex = 87% +/- 8% (P greater than 0.30), subcortex = 124% +/- 11% (P greater than 0.05), midbrain = 263% +/- 20% (P less than 0.001), spinal cord = 278% +/- 19% (P less than 0.001); 2.0 MAC isoflurane: cortex = 137% +/- 13% (P less than 0.05), subcortex = 272% +/- 24% (P less than 0.001), midbrain = 510% +/- 53% (P less than 0.001), spinal cord = 535% +/- 50% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular actions of desflurane with and without nitrous oxide during spontaneous ventilation in humans.

We investigated the cardiovascular actions of desflurane (formerly I-653) during spontaneous ventilation. We gave 0.8-0.9, 1.2-1.3, and 1.6-1.7 MAC desflurane in oxygen (n = 6) and in 60% nitrous oxide, balance oxygen (n = 6) to unmedicated healthy male volunteers. Both anesthetic regimens decreased ventilation, increased partial pressure of arterial carbon dioxide, and produced similar cardiovascular changes. In comparison with values obtained when the volunteers were conscious, desflurane anesthesia with spontaneous ventilation decreased systemic vascular resistance and mean arterial blood pressure. Cardiac index, heart rate, stroke volume index, and central venous blood pressure increased. Left ventricular ejection fraction increased at 0.83 MAC desflurane in oxygen, and otherwise did not differ from the conscious value. The velocity of ventricular circumferential fiber shortening, estimated by echocardiography, increased with desflurane in oxygen but did not change with desflurane in nitrous oxide. Oxygen consumption increased during desflurane and oxygen anesthesia, but not when nitrous oxide plus oxygen was the background gas. Desflurane increased oxygen transport, the ratio of oxygen transport to oxygen consumption, mixed venous partial pressure of oxygen, and oxyhemoglobin saturation. The cardiovascular changes with desflurane during spontaneous ventilation differ from those during controlled ventilation. With both background gases, spontaneous ventilation, in comparison with controlled ventilation, increased cardiac index, stroke volume, central venous pressure, left ventricular ejection fraction, velocity of circumferential fiber shortening, oxygen transport, and the ratio of oxygen transport to oxygen consumption but did not change mean arterial blood pressure except at 1.66 MAC desflurane in oxygen (when it was higher with spontaneous than with controlled ventilation).     

地氟醚、异氟醚和七氟醚对脑血流速率的影响

目的　通过经颅多普勒超声 (TCD)监测大脑中动脉 (MCA)血流速率 ,观察地氟醚、异氟醚和七氟醚三种吸入麻醉药对平均血流速率 (Vm)的影响。方法　 42例 18～ 6 0岁、ASAⅠ～Ⅱ级、择期非颅脑手术病人 ,随机接受地氟醚、异氟醚或七氟醚吸入麻醉。机械通气维持PETCO2 在 40± 1mmHg。当呼气末吸入麻醉药浓度分别为 :1 0MAC平衡 15分钟后 ,快速 (2分钟内 )从 1 0MAC升高至 1 5MAC即时 ,1 5MAC平衡 15分钟后 ,以及稳定于 1 5MAC并且维持和 1 0MAC平衡下相似的MAP时 ,记录Vm、MAP和心率。结果　 (1)吸入浓度从 1 0MAC上升至 1 5MAC ,且MAP维持相同水平的情况下 ,地氟醚和异氟醚使Vm增加非常显著 (分别从 5 6cm/s上升至 6 1cm/s,从47cm/s上升至 5 2cm/s,P <0 0 1) ,而七氟醚无显著变化 (从 6 0cm/s至 6 0cm/s,P >0 0 5 )。 (2 )当吸入浓度快速从 1 0MAC上升至 1 5MAC时 ,地氟醚使血压升高、心率增快 ,同时 ,脑血流速率显著增加 (从 5 6cm/s上升至 6 1cm/s,P <0 0 1)。而异氟醚和七氟醚在MAP显著下降的同时使Vm无显著变化 (从 47cm/s升至 49cm/s,P >0 0 5 ) ,或显著下降 (从 6 0cm/s降至 5 6cm/s,P <0 0 1)。结论　 (1)吸入浓度从 1 0MAC增加到 1 5MCA时 ,地氟醚、异氟醚使脑血流速率显著增加 ,而七氟醚作     

Transfer function analysis of the circulation in patients undergoing sevoflurane anesthesia

PURPOSE: The effects of sevoflurane anesthesia on the interactions between heart rate, blood pressure and respiration were assessed using transfer function analysis. METHODS: Nine ASA 1 or 2 patients undergoing elective surgery were involved. They were paralysed and their lungs were mechanically ventilated during sevoflurane anesthesia. Instantaneous heart rate (IHR) from electrocardiogram, instantaneous lung volume (ILV) by respiratory inductive plethysmography and mean blood pressure (MBP) by arterial tonometry were obtained during conscious state, and 1MAC and 2MAC of sevoflurane anesthesia. Transfer function analysis for the relationships between ILV and IHR, ILV and MBP, MBP and IHR were made for five minute periods during which the respiratory rate was varied in a standardized fashion. RESULTS: In awake patients transfer magnitudes for the relationships between ILV and IHR and between MBP and IHR in the 0.04-0.5Hz frequency band were 8.9 +/- 7.7 bpm x l(-1) and 0.95 +/- 0.44 bpm x mmHg(-1) respectively. Sevoflurane 2MAC decreased these values to 1.2 +/- 0.7 (P = 0.014) and 0.26 +/- 0.14 (P < 0.01) respectively, but phases were not affected. Neither transfer magnitudes nor phases between ILV and MBP were affected during sevoflurane anesthesia. Coherence for the relationships between ILV and IHR and between MBP and IHR were decreased during 1MAC sevoflurane anesthesia but not affected during 2MAC sevoflurane anesthesia. CONCLUSIONS: The interactions between heart rate, blood pressure and respiration were altered by sevoflurane anesthesia. These findings could be explained by the attenuation of autonomic nervous system activity.     

The effect of sevoflurane on cerebral blood flow velocity in children

BACKGROUND: Sevoflurane is a suitable agent for neuroanesthesia in adult patients. In children, cerebrovascular carbon dioxide reactivity is maintained during hypo- and normocapnia under sevoflurane anesthesia. To determine the effects of sevoflurane on middle cerebral artery blood flow velocity (Vmca) in neurologically normal children, Vmca was measured both at different MAC values and at one MAC over a specified time period, using transcranial Doppler sonography. METHODS: Twenty-six healthy children undergoing elective urological surgery were enrolled (16 patients in part I and 10 in part II). In part I of the study anesthesia comprised sevoflurane 0.5, 1.0 and 1.5 MAC in 30% oxygen and a caudal epidural block. Once steady state had been reached at each sevoflurane MAC level, three measurements of Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded. In part II of the study patients received sevoflurane 1.0 MAC over a 90-min period, with the same variables being recorded at 15-min intervals. RESULTS: Vmca did not vary significantly at 0.5, 1.0 and 1.5 MAC sevoflurane. There was a significant decrease in MAP between 0.5 MAC and 1.0 MAC sevoflurane (P < 0.005) and also between 1.0 MAC and 1.5 MAC (P < 0.01). There was no significant change in Vmca over 90 min at 1.0 MAC sevoflurane. CONCLUSION: Sevoflurane does not significantly affect cerebral blood flow velocity in healthy children at working concentrations.     

Decreased respiratory depression during emergence from anesthesia with sevoflurane/N2O than with sevoflurane alone

PURPOSE: To investigate ventilation and gas elimination during the emergence from inhalational anesthesia with controlled normoventilation with either sevoflurane/N2O or sevoflurane alone. METHODS: Twenty-four ASA I-II patients scheduled for abdominal hysterectomy were randomly allocated to receive either 1.3 MAC sevoflurane/N2O (n = 12) or equi-MAC sevoflurane (n = 12) in 30% oxygen (O2). Expired minute ventilation volumes (V(E)), end-tidal (ET) concentrations of O2, carbon dioxide (CO2), sevoflurane and N2O as well as pulse oximetry saturation (SpO2) and CO2 elimination rates (VCO2) were measured. The ET concentrations of sevoflurane and N2O were converted to total MAC values and gas elimination was expressed in terms of MAC reduction. Time to resumption of spontaneous breathing and extubation were recorded and arterial blood gas analysis was performed at the end of controlled normoventilation and at the beginning of spontaneous breathing. RESULTS: Resumption of spontaneous breathing and extubation were 8 and 13 min less, respectively, in the sevoflurane/N2O than in the sevoflurane group. Spontaneous breathing was resumed in both groups when pH had decreased by 0.07-0.08 and PaCO2 increased by 1.3-1.5 kPa. Depression of V(E) and VCO2 were less, and MAC reduction more rapid in the sevoflurane/N2O than in the sevoflurane group. CONCLUSIONS: Respiratory recovery was faster after sevoflurane/N2O than sevoflurane anesthesia. Changes in pH and PaCO2 rather than absolute values were important for resumption of spontaneous breathing after controlled normoventilation. In both groups, the tracheas were extubated at about 0.2 MAC.     

A SHEEP PREPARATION FOR STUDYING INTERACTIONS BETWEEN BLOOD FLOW AND DRUG DISPOSITION: III: EFFECTS OF GENERAL AND SPINAL ANAESTHESIA ON REGIONAL BLOOD FLOW AND OXYGEN TENSIONS

In awake unrestrained sheep the infusions i.v. of five drugs(cefoxitin, pethidine, chlormethiazole, tocainide and lignocaine)with potentially flow-limited clearance were shown to have nosignificant haemodynamic effects of their own, nor to have anyeffects on arterial or venous oxygen tensions. Under generalanaesthesia (1.5% end-tidal halothane), haemodynamic changessimilar to those previously documented in man occurred. Cardiacoutput and hepatic blood flow were decreased to 70%, and renalblood flow to 50% of control vahies; heart rate was unchangedand mean arterial pressure decreased by an average of 10%. Hepaticand renal vein oxygen tensions were decreased significantly.Under spinal anaesthesia, apart from a 10% decrease in hepaticblood flow, there were no significant changes in any haemodynamicvariables or in the arterial or in any of the venous oxygentensions. The i.v. infusion of adequate volumes of saline atthe time of blockade probably contributed to the maintenanceof these indices at their baseline values     

Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans

We have examined cerebral pressure autoregulation while awake, and during 0.5 and 1.5 MAC of sevoflurane anaesthesia in 10 patients undergoing non-intracranial neurosurgical procedures. All patients received a standardized anaesthetic comprising premedication with temazepam 20 mg orally, a sleep dose of propofol, fentanyl 1 microgram kg-1 and vecuronium 0.1 mg kg-1. After tracheal intubation, the lungs were ventilated with a mixture of air and oxygen to mild hypocapnia. Routine monitors included ECG, continuous and intermittent non-invasive arterial pressure, pulse oximetry and end-tidal capnography. In addition, blood flow velocity (vmca) was measured by insonating the middle cerebral artery transtemporally using a 2-MHz transcranial Doppler probe. Cerebral pressure autoregulation was tested by increasing mean arterial pressure (MAP) by approximately 20 mm Hg using an infusion of phenylephrine and simultaneously recording vmca. The index of autoregulation (IOR) during each period of the study, calculated as the ratio of percentage change in estimated cerebral vascular resistance (CVRe = MAP/vmca) to percentage change in MAP, was compared using ANOVA. vmca during 0.5 and 1.5 MAC of sevoflurane anaesthesia was significantly lower than that while awake (mean 79 (SD 24), 54 (15) and 51 (12) cm s-1, respectively; P < 0.05). There was no significant change in vmca with the increase in MAP while awake, or during 0.5 or 1.5 MAC of sevoflurane anaesthesia and IOR was similar under the three conditions (0.82 (0.11), 0.83 (0.04) and 1.0 (0.03), respectively). We conclude that cerebral pressure autoregulation remained intact during sevoflurane anaesthesia in humans.      

Epidural clonidine does not decrease blood pressure or spinal cord blood flow in awake sheep

Preliminary data in animals and humans suggest that epidurally administered clonidine produces antinociception and is not neurotoxic. However, clonidine can produce vasoconstriction, and epidurally administered clonidine decreases spinal cord blood flow in anesthetized pigs. To examine the effect of epidurally administered clonidine on spinal cord blood flow in awake animals, the authors inserted lumbar epidural, femoral arterial and venous, pulmonary arterial, and left ventricular catheters in 13 adult sheep. Following a 24-h recovery, the authors injected saline (N = 6) or clonidine, 750 micrograms (17-25 micrograms/kg; N = 7) epidurally, and measured arterial blood gas tensions; temperature; heart rate; systemic and pulmonary arterial, right atrial, and pulmonary capillary wedge pressures; and spinal cord and renal blood flows (by radioactive microsphere injection) before and at 45 min and 4 h following injection. Epidural saline injection did not affect measured variables. Heart rate decreased from 112 +/- 9 to 86 +/- 4 beats/min (mean +/- SE; P = .003) and arterial PO2 decreased from 99 +/- 3 to 78 +/- 6 mmHg (P = .04) 45 min following clonidine injection. Temperature increased from 39.1 +/- .2 to 40.6 +/- 1 degree C (P = .0001) 4 h following clonidine injection. Epidural clonidine administration did not affect cardiac output, pulmonary and systemic pressures, or renal or spinal cord blood flows, except for an increase in mid-thoracic spinal cord blood flow 45 min following injection. The authors conclude that, in sheep, epidural clonidine does not produce dangerous cardiovascular depression or global spinal cord ischemia.