Peripheral blood flow in the elderly during inhalational anaesthesia

We investigated whether aging altered the peripheral vascular effects of inhaled anaesthetic agents. Forearm blood flow (FBF) was measured in 20 young (18–34 yrs) and 21 healthy elderly (60–79 yrs) patients receiving isoflurane or halothane with 66% nitrous oxide (N₂O) in oxygen (O₂). After etomidate 0.3 mg/kg and vecuronium 0.1 mg/kg, the trachea was intubatcd and controlled ventilation instituted with 66% N₂O in O₂. Halothane or isoflurane were administered to achieve end-tidal concentrations of 0.5% halothane or 0.9% isoflurane after 20 min. FBF was measured by venous occlusion plethysraography during the 20 min study period. Induction of anaesthesia with etomidate decreased FBF below baseline (awake) values in both elderly and young; intubation returned FBF to baseline values in the young but not in the elderly. FBF decreased below baseline values in young and elderly patients receiving halothane and in elderly patients receiving isoflurane but not in young patients receiving isoflurane. FBF was significantly greater in young patients receiving isoflurane than halothane after 20 min administration.
We conclude that perfusion of forearm muscle and skin is maintained in the young but not in the elderly during anaesthesia with isoflurane/N₂O. Perfusion of forearm muscle and skin decreases in both young and elderly patients during anaesthesia with halothane/N₂O. The cardiovascular effects of isoflurane/N₂O and halothane/ N₂O did not differ significantly in healthy elderly patients.     

EFFECT OF HALOTHANE, ENFLURANE AND ISOFLURANE ON BODY TEMPERATURE DURING AND AFTER SURGERY

The superficial and deep body temperatures of 40 healthy femalesundergoing total abdominal hysterectomy were measured duringsurgery and for 4 h afterwards. The patients were allocatedrandomly to one of five groups and anaesthetized to producean end-tidal concentration of 1% halothane, 1% enflurane, 2%enflurane, 1% isoflurane or 2% isoflurane. The patients receivedalso 70% nitrous oxide in oxygen and neuromuscular blockade.The theatre temperature was maintained at 22.0°C. Therewere significant body temperature changes during operation inall groups. The mean (SD) decrease in core temperature over85 min was approximately 1.1 (0.3) °C in the 1% halothane,2% enflurane and 2% isoflurane groups, and 0.6 (0.4) °Cin the 1% enflurane and 1% isoflurane groups (P<0.05). Duringthe recovery period the 1% halothane, 2% enflurane and 2% isofluranegroups took 2 h to rewarm to preoperative temperatures, andthe rate of rewarming during this time was similar for all groups.     

Transkranielle Dopplersonographie Effekte von Sevofluran im Vergleich zu Isofluran

Methods: Using transcranial Doppler sonography (TCD), we studied the effects of sevoflurane compared to equipotent doses of isoflurane on blood-flow velocity in the middle cerebral artery (MCA) before, during, and after general anaesthesia. In random order, 30 patients received sevoflurane (n=15) or isoflurane (n=15) given in stepwise-increasing doses of 0.5, 1.0, and 1.5 MAC in oxygen/air (FiO₂=0.5). Oxygen/air was then replaced by oxygen/nitrous oxide 33%/65% with decreasing doses (1.5, 1.0, 0.5 MAC) of sevoflurane or isoflurane. During each step, ventilation was controlled to provide first normocapnia (end-tidal pCO₂=38 mmHg) and then hypocapnia (end-tidal pCO₂=27 mmHg). MCA blood-flow velocity and pulsatility, arterial blood pressure, heart rate, and body temperature were recorded simultaneously at the end of each period. For statistical analysis, within-group comparison was made by one-way ANOVA. Differences between groups were determined by two-way analysis of variance. Age, weight, and height of the patients were compared using Student’s t-test; P<0.05 was considered significant. Results: Groups were comparable regarding age, weight, and height. TCD parameters were not significantly changed by increasing doses of sevoflurane or isoflurane given in oxygen/air when compared to the awake data. However, increasing MCA blood-flow velocity was found with decreasing doses of sevoflurane or isoflurane given in oxygen/nitrous oxide (P<0.05 for 0.5 MAC, normoventilation) without intergroup differences. In both groups, hyperventilation always decreased MCA blood-flow velocity. Conclusions: We conclude from our TCD data that equipotent doses of sevoflurane and isoflurane comparably affect cerebral perfusion, especially when nitrous oxide is given simultaneously.     

Vomiting, retching, headache and restlessness after halothane-, isoflurane- and enflurane-based anaesthesia: An analysis of pooled data following ear, nose, throat and eye surgery

Background: Isoflurane has exceeded halothane and enflurane in usage. A literature search, however, revealed no data comparing the effects on emesis, headache and restlessness of these three agents.
Methods: With hospital ethics committee approval and patient consent, a prospective, randomised, double-blind study of 556 patients undergoing ENT and eye surgery was undertaken to evaluate the effects of halothane, isoflurane and enflurane on vomiting, retching, headache and restlessness until 24 h after anaesthesia. Balanced general anaesthesia was administered comprising benzodiazepine premedication, induction with thiopentone-atracurium-morphine (ENT patients) or fentanyl (eye patients), controlled ventilation and maintenance with either halothane 0.4–0.6 vol% (n = 186), isoflurane 0.6–0.8 vol% (n = 184) or enflurane 0.8–1 vol% (n=186) in nitrous oxide 67% and oxygen.
Results: The three study groups were comparable, and comprised comparable subgroups having ear, nose, throat, intraocular and non-intraocular surgery. During early recovery from anaesthesia, the respective requirements for halothane, isoflurane and enflurane for analgesia (7%, 9% and 10%), frequency of emesis (6%, 8% and 8%), antiemetic requirements (1%, 1% and 2%), restlessness-pain scores and time spent in the recovery ward (27 SD 10, 31 SD 12 and 26 SD 9 min) were similar. During the ensuing 24-h postoperative period, patients who had isoflurane experienced emesis less often than those who had halothane (36% vs 46%, P <0.025) but did so with similar frequency to those who had enflurane (46% vs 41%). Antiemetic requirements were least in those given isoflurane (isoflurane 12%, halothane and enflurane 23% each, P <0.005), but headache and analgesic requirements were similar.
Conclusion: Isoflurane induces less postoperative emesis than halothane, but headache is similarly frequent after anaesthesia with any of these agents.     

CEREBRAL RESPONSES TO THE ADDITION OF NITROUS OXIDE TO HALOTHANE IN MAN

Cerebral responses to the substitution of 60% nitrous oxidefor nitrogen during halothane anaesthesia (0.84%, end-tidal)were studied in four patients during surgery. The mean (±SEM)cerebral blood flow equivalent and internal jugular venous oxygentension during halothane anaesthesia, 27±3 ml blood/mloxygen and 41±2 mm Hg respectively, increased significantlyto 45±3ml blood/ml oxygen and 54±3 mm Hg followingthe introduction of nitrous oxide. On the withdrawal of nitrousoxide, the mean cerebral blood flow equivalent and internaljugular venous oxygen tension returned gradually to the controlvalues. Cerebral perfusion pressure and blood-gas values, otherthan the internal jugular venous oxygen tension, did not changesignificantly. Marked slowing of the e.e.g. was observed followingthe addition of nitrous oxide to halothane. Upon the withdrawalof nitrous oxide the e.e.g. returned to the control pattern.These results indicate that cerebral blood flow was in excessof oxygen demand during nitrous oxide/halothane anaesthesiain man. This work was performed at the Department of Anaesthesiology,Yamaguchi University Hospital.     

Cardiovascular effects of 50% nitrous oxide in older adult patients anaesthetized with isoflurane or halothane

We have studied the cardiovascular effects of equipotent concentrations of halothane or isoflurane, with or without 50% nitrous oxide in oxygen, in 80 patients, aged 60 yr or more, during 20 min of stable equipotent anaesthesia. Non-invasive measurement techniques were used, with suprasternal Doppler ultrasonography for estimating cardiac output. Both isoflurane and halothane reduced heart rate and systemic arterial pressure. With isoflurane, mean rate decreased from 72 (SD 9.7) to 67 (10.4) beat min-1 and with halothane from 76 (10.1) to 65 (9.1) beat min-1 (P < 0.05). Mean diastolic arterial pressure decreased from 81 (11.3) to 58 (17.0) mm Hg with isoflurane and from 86 (14.7) to 70 (13.3) mm Hg with halothane (P < 0.05). Cardiac index decreased from 3.1 (1.03) to 2.7 (0.71) litre min-1 m-2 with isoflurane and from 3.1 (0.98) to 2.5 (0.57) litre min-1 m-2 with halothane (P < 0.05). Systemic vascular resistance decreased significantly in all groups except those receiving halothane with nitrous oxide. Nitrous oxide resulted in significantly less depression of cardiac index when given with isoflurane than when given with halothane. The mean percentage change in cardiac index during isoflurane anaesthesia without nitrous oxide was 16.7%; with nitrous oxide there was a 0.5% increase. Halothane, in combination with nitrous oxide, resulted in greater depression of cardiac index than isoflurane with nitrous oxide. The mean percentage change with halothane was 20.4% (22.2%); with isoflurane there was a 0.5% (27.1%) increase (P < 0.05). Hypotension was more pronounced in patients anaesthetized with isoflurane (n = 40) than those anaesthetized with halothane (n = 40), irrespective of the presence of nitrous oxide. The mean percentage decrease with isoflurane was 29.7% (21.10%) compared with 16.8% (16.78%) with halothane (P < 0.05).      

Hyperventilation reverses the nitrous oxide-induced increase cerebral blood flow velocity in human volunteers

Because hypocapnia is routine during general anaesthesia forintracranial procedures, we have compared, in 1 3 healthy volunteers,the effect of normocapnia (PE'_CO2 5.3 kPa) and hypocapnia (PE'_CO23.3 kPa) on mean blood flow velocity in the middle cerebralartery (Vmca) during normoventilation and hyperventilation withair and with 50% nitrous oxide in oxygen. After replacementof air with 50% nitrous oxide in oxygen, there was an increasein mean Vmca during normoventilation (air: mean 68.23 (SD 16.98)cm s^–1 vs nitrous oxide in oxygen: 90.69 (20.41) cm s^–1;P < 0.01), whereas during hyperventilation mean Vmca valueswere similar regardless of the inhaled gas mixture (air: 43.46(9.97) cm s^–1 vs nitrous oxide in oxygen: 41.69 (8.08)cm s^–1 Our data suggest that the nitrous oxide-inducedincrease in mean Vmca can be blocked by hyperventilation. (Br.J. Anaesth. 1995; 74: 616–618)     

Halothane-Relaxant Anaesthesia in Elderly Patients

Twenty-three elderly patients, scheduled for elective cholecystectomy, were studied during halothane-relaxant anaesthesia. Anaesthesia was induced with thiopentone and maintained with halothane in 12 patients, six of whom had also received premedication. Eleven patients were anaesthetized with halothane, without thiopentone induction and with no premedication. Measurements of central haemodynamics were performed awake and during anaesthesia at end-tidal halothane concentrations of 0.5 and 1.0%; at the lower concentration, measurements were also made after addition of nitrous oxide. Premedication and thiopentone had no influence on the subsequent halothane anaesthesia. Halothane caused reductions of cardiac index, mean arterial blood pressure and oxygen uptake. However, neither right atrial nor pulmonary capillary venous pressure increased and the arterio-venous oxygen content difference decreased. These findings differ from those made by others in younger subjects and are probably attributable to a dose-dependent reduction in systemic vascular resistance. The addition of nitrous oxide had only minor effects on central circulation. The results suggest that the age of the patients influences their reaction to halothane anaesthesia.     

The divergent actions of volatile anaesthetics on background neuronal activity and reactive capability in the central nervous system in cats

The effects of halothane, isoflurane, and enflurane on background neuronal activity and reactive capability in the central nervous system were studied in cats. The background neuronal activity was assessed by midbrain reticular cell firing, which was measured by the method of multi-unit activity, and the EEG in the cortex, amygdala, and hippocampus. The reactive capability was assessed by evoked responses in the visual neuronal pathway. All anaesthetics studied suppressed reticular cell firing in a dose-dependent manner, and the suppression by halothane (43.8 +/- 10.3% of control, mean +/- SD) was less than isoflurane (66.5 +/- 5.8%, P < 0.01) and enflurane (73.1 +/- 8.8%, P < 0.05) at 1 MAC. Spontaneous EEG spikes developed at 4.8% isoflurane and 3.6% enflurane anaesthesia. Phasic activation of reticular cell firing was associated with EEG spikes during isoflurane and enflurane anaesthesia, and the activation during enflurane anaesthesia was greater than during isoflurane anaesthesia (P < 0.01). Photic stimulation provoked EEG spikes and repetitive stimulation induced seizure activity only at 3.6% enflurane anaesthesia. Halothane and isoflurane suppressed stimulation induced responses in the visual neuronal pathway. The amplitudes of N1 in visual cortical evoked responses induced by photic stimulation were suppressed to 70.1 +/- 24.5% of control at 2.4% halothane and 39.3 +/- 27.3% at 4.8% isoflurane. Enflurane, at 3.6%, augmented the evoked response induced by photic stimulation (398.4 +/- 83.0% of control in the amplitude of N1). These results indicate that all the agents studied had suppressive actions on background neuronal activity in the order halothane < isoflurane = enflurane. The effects on reactive capability were divergent among agents, e.g., enflurane enhanced, halothane suppressed, and the actions of isoflurane were intermediate. We conclude that the anaesthetic effects on background activity and on reactive capability are divergent and that suppression of reactive capability is a factor in determining the ease of clinical application of the anaesthetics.     

ALTERATIONS IN PAIN THRESHOLD AND PSYCHOMOTOR RESPONSE ASSOCIATED WITH SUBANAESTHETIC CONCENTRATIONS OF INHALATION ANAESTHETICS IN HUMANS

We studied the effects of six inhalation anaesthetics at subanaestheticconcentrations of 0.2 MAC on pain threshold and psychomotorfunction in six healthy volunteers. When compared with 100%oxygen inhalation, nitrous oxide and methyoxy-flurane significantlyincreased pain threshold as measured by a radiant heat algometer,and prolonged the response time to auditory stimuli. In contrast,halothane. enflurane, isoflurane and sevo-flourane producedprolongation of the response time to auditory stimuli but didnot influence pain perception. The pain threshold with nitrousoxide remained significantly increased 30 min after its discontinuation,while the response time returned to the preinhalation value.We conclude that nitrous oxide and methoxyflurane possess bothanalgesic and hypnotic actions but halothane, enflurane, isofluraneandsevoflurane do not have an analgesic action at subanaestheticconcentrations, and the analgesic action of nitrous oxide persistsafter its elimination. (Br. J. Anaesth. 1993; 70: 684–686)     

Halothane, but not isoflurane or enflurane, protects against spontaneous and epinephrine-exacerbated acute thrombus formation in stenosed dog coronary arteries

Occlusive platelet thrombi periodically form in mechanically stenosed dog coronary arteries producing cyclical blood flow reductions occurring over 4-7 min. Cyclical coronary flow reductions are exacerbated by IV epinephrine 0.4 microgram.kg-1.min-1 for 15 min. These flow reductions can be abolished by known inhibitors of platelet function. This study assesses the effect of halothane, isoflurane, and enflurane on spontaneous- and epinephrine-exacerbated cyclical coronary flow reductions. Twenty-three open-chest dogs [1% halothane (n = 5), 0.5% halothane (n = 5), 0.25% halothane (n = 3), 1.5% isoflurane (n = 5), and 2.0% enflurane (n = 5)] with a mechanically stenosed coronary artery showed cyclical blood flow reductions. With 1.0% halothane administration, spontaneous cyclical blood flow reductions were abolished (n = 5), whereas during administration of isoflurane 1.5% (n = 5) and enflurane 2.0% (n = 5) cyclical flow reductions and myocardial ischemia continued. Subsequent administration of halothane in the isoflurane and enflurane groups showed abolition of coronary flow reductions in all animals (n = 10). In eight animals a 15-min epinephrine infusion (0.4 microgram.kg-1.min-1) was given following a control period and again following abolition of coronary flow reductions by halothane 0.5% (n = 5) and halothane 0.25% (n = 3). The magnitude of cyclical blood flow reductions (difference between initial and final coronary flow level of each flow reduction) changed from 52 +/- 11 to 61 +/- 12 ml/min (NS), and frequency increased from 0.37 to 0.57/min (P less than 0.05, n = 8) during epinephrine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Nitrous Oxide Augments the Systemic and Coronary Haemodynamic Effects of Isoflurane in Patients with Ischaemic Heart Disease

The effects of 70% nitrous oxide, added to 1% end-tidal isoflurane and administered by intermittent positive pressure ventilation (IPPV), on coronary haemodynamics and myocardial oxygenation were investigated in 10 patients with ischaemic heart disease. Standard methods were used for determination of their central haemodynamic effects. Coronary blood flow was measured by the retrograde thermodilution technique and coronary sinus blood sampled for measurement of myocardial oxygen consumption and lactate extraction. One per cent end-tidal isoflurane decreased systemic blood pressure (-39%) by a combination of systemic vasodilation and reduction in cardiac performance. Coronary blood flow remained unaltered despite the fall in coronary perfusion pressure and myocardial oxygen consumption (-30%) and extraction (-30%) fell significantly. Ischaemic ECG changes parallelled by decreased myocardial lactate extraction or lactate production were recorded in 6 of the 10 patients during steady state isoflurane anaesthesia. When nitrous oxide was added to isoflurane there was a fall in heart rate (-13%), a further reduction in systemic blood pressure (-18%) and myocardial oxygen consumption (-31%) and extraction (-17%) whereas all other variables including coronary blood flow remained unaltered. The myocardial ischaemia was worsened in three of the six patients with ECG and metabolic signs of impaired oxygenation during isoflurane alone. It is concluded that nitrous oxide potentiates the systemic and coronary haemodynamic effects of isoflurane in patients with coronary artery disease. The mechanisms for myocardial ischaemia seem to be decreased coronary perfusion pressure and/or redistribution of coronary blood flow by direct coronary vasodilation.     

The effect of halothane, enflurane and isoflurane on the circulation

This study, in open-chested dogs, sought to explore the relationship between whole-body oxygen delivery and oxygen consumption during anaesthesia, using increasing concentrations of halothane, enflurane and isoflurane. Results indicate that the cardiac index and oxygen delivery became critical at less than 1 MAC (minimal alveolar concentration of anaesthetic) for the three commonly used vapours. Halothane caused the least depression of contractility, but the stroke volume was reduced by the well-maintained afterload at 1 MAC. Enflurane and isoflurane were associated with more depression of contractility, but the cardiac output was maintained by an increase in heart rate in the case of isoflurane and reduced mean arterial pressure during the use of enflurane.     

Antifibrillatory effects of volatile anesthetics in acute occlusion/reperfusion arrhythmias

Halothane, enflurane, and isoflurane were evaluated for antifibrillatory efficacy and compared with lidocaine, propranolol, procainamide, and verapamil in a canine acute left anterior descending (LAD) coronary artery occlusion/reperfusion model with basal pentobarbital anesthesia. Of the antiarrhythmic drugs, only verapamil prevented ventricular fibrillation during occlusion and reperfusion. Halothane 1% inspired after 15 min showed similar protection. Enflurane 2.5% inspired after 15 min resulted in significant protection but caused hypotension after occlusion in 4 of 17 dogs. Isoflurane 1.7% inspired after 15 min showed intermediate results. At inspired concentrations of 0.5% and 1.25%, respectively, halothane and enflurane protected against ventricular fibrillation without hypotension. It is concluded that the volatile anesthetics have antifibrillatory effects in this canine model but differ in their ability to cause hypotension in the presence of proximal LAD coronary artery occlusion.     

CARDIAC RATE AND RHYTHM DURING ANAESTHESIA FOR DENTAL EXTRACTION: A comparison of Halothane, Enflurane and Isoflurane

Cardiac rate and rhythm were compared in 60 patients havingdental extractions under conventional general anaesthesia usinghalothane, enflurane or isoflurane to supplement nitrous oxidein oxygen. The incidence of arrhythmia was higher in the halothanegroup when compared with both the enflurane (P < 0.05) andthe isoflurane (P > 0.05) groups. Heart rates, measured at1-min intervals, tended to be more rapid in the isoflurane groupcompared with the other two groups (P < 0.001 in both instances),and patients anaesthetized with enflurane tended to have morerapid heart rates than those anaesthetized with halothane (P< 0.001).     

Poisoning caused by chronic exposure to volatile anesthetics. Molecular mechanisms and risk anesthetics

The possible molecular mechanisms potentially inducing occupational disease among operating room personnel were examined; and the really dangerous anaesthetic agents were identified. As concerns the molecular mechanisms of parenchymatous injury, we surveyed: those connected with free radicals and biological reactive intermediates produced during halothane and nitrous oxide biotransformation; those coming from inorganic fluoride produced during biotransformation of any halogenated anaesthetic agent, and from inorganic bromide released during halothane metabolism; and, finally, those linked to vitamin B12 inactivation from nitrous oxide. Halothane and nitrous oxide can be considered as really dangerous anaesthetic agents for operating room personnel, and enflurane as an agent with marginal toxic power. On the contrary, isoflurane is a safe, useful compound, totally devoided of viscerotoxic effects. From data examined it is possible to conclude that an isoflurane-oxygen-air anaesthesia is safe for operating room personnel more than a balanced anaesthesia with intravenous drugs and nitrous oxide as maintenance.     

The postoperative effects of halothane versus isoflurane on hepatic artery and portal vein blood flow in humans

Animal studies have shown that halothane decreases total hepatic blood flow (THBF) by reducing both arterial (HABF) and portal (PVBF) inflow, whereas isoflurane appears to preserve them. In this study we assessed the effect of halothane and isoflurane on HABF and PVBF in surgical patients by using the pulsed Doppler technique. A validation study was conducted in six cynomolgus monkeys to compare the values of THBF obtained by the pulsed Doppler and indocyanine green clearance methods. Subsequently, six patients (ASA status I and II) undergoing elective open cholecystectomy were studied after surgery by using implanted pulsed Doppler probes. THBF and liver flow partition were compared during 1% halothane and 1.5% isoflurane (end-tidal concentrations). In the animal study, there was good agreement between the techniques (Bland and Altmann representation). In flunitrazepam-anesthetized patients, THBF was 1120 +/- 284 mL/min. Compared with this baseline and for a similar mean arterial blood pressure decrease (10%), THBF was maintained with isoflurane, whereas it decreased by 36% (P < 0.05) under halothane. With isoflurane, PVBF increased (25%; P = 0.067) with a maintained HABF. With halothane, both PVBF (-44%; P < 0.05) and HABF (-20%; P < 0.05) were reduced. Halothane acted mainly as a vasoconstrictor of the hepatic circulation, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on hepatic oxygen supply. IMPLICATIONS: Volatile anesthetics may alter liver circulation with serious adverse effects. Using implanted pulsed Doppler probes in six anesthetized patients, we showed that halothane acted mainly as a vasoconstrictor of the liver vascular bed, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on liver oxygen supply.     

Role of Adenosine Triphosphate-sensitive Potassium Channels in Coronary Vasodilation by Halothane, Isoflurane, and Enflurane

Background: Halothane, isoflurane, and enflurane cause coronary vasodilation and cardiac depression. This study was performed to assess the role of adenosine triphosphate (ATP)-sensitive potassium channels (K (ATP) channels) in these effects.

Methods: Twenty-five thoracotomized dogs were anesthetized with fentanyl and midazolam. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs. One reservoir was supplied with arterial blood free of a volatile anesthetic, and the second reservoir was supplied with arterial blood equilibrated in an oxygenator with a 1 minimum alveolar concentration of either halothane (0.9%, n = 10), isoflurane (1.4%, n = 28), or enflurane (2.2%, n = 7). Coronary blood flow (CBF) was measured using a Doppler flow transducer, and segmental shortening (SS) was measured with ultrasonic crystals. Responses to the volatile anesthetics were assessed under control conditions, during intracoronary infusion of the KATP channel inhibitor glibenclamide (100 micro gram/min), and after cessation of glibenclamide (recovery). The effectiveness of glibenclamide was verified from inhibition of coronary vasodilator responses to the KATP channel opener cromakalim without effect on those to the KATP channel-independent vasodilators, sodium nitroprusside and acetylcholine.

Results: Under control conditions, the volatile anesthetics caused pronounced increases in CBF (isoflurane > halothane = enflurane), and decreases in SS (enflurane > halothane = isoflurane). Glibenclamide blunted significantly (and reversibly) the increases in CBF, but it had no effect on the decreases in SS.     

Effects of sevoflurane on cerebral blood flow and cerebral metabolic rate of oxygen in human beings: a comparison with isoflurane

BACKGROUND AND OBJECTIVE: Isoflurane is commonly used for neurosurgery but the effects of sevoflurane on human cerebral blood flow and cerebral metabolic rate of oxygen have not been fully evaluated. We therefore assessed the effects of sevoflurane and isoflurane on global cerebral blood flow and cerebral metabolic rate of oxygen in patients without noxious stimuli or neurological disorders. METHODS: General anaesthesia was induced with midazolam (0.2 mg kg(-1)) and fentanyl (5 microg kg(-1)) in 20 ASA I patients undergoing knee joint endoscopic surgery. Epidural anaesthesia was also performed to avoid noxious stimuli during surgery. Cerebral blood flow and cerebral arteriovenous oxygen content difference was measured using the Kety-Schmidt method with 15% nitrous oxide as a tracer before and after administration of either sevoflurane or isoflurane (1.5 minimum alveolar concentration, 60 min) and cerebral metabolic rate of oxygen was then calculated. RESULTS: Sevoflurane and isoflurane both increased cerebral blood flow (17%, P < 0.05; 25%, P < 0.05, respectively) and decreased cerebral metabolic rate of oxygen (26%, P < 0.01; 38%, P < 0.01, respectively). There were no significant differences in cerebral blood flow and cerebral metabolic rate of oxygen between sevoflurane and isoflurane. CONCLUSIONS: Sevoflurane and isoflurane similarly increased cerebral blood flow and decreased cerebral metabolic rate of oxygen in human beings anaesthetized with midazolam and fentanyl.