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The effect of halothane anaesthesia on liver regeneration.

The effects of halothane and diethyl ether on the regenerating liver following 70 per cent hepatectomy were studied in Fisher/344 (F) rats. Our aim was to discover whether halothane administered repeatedly and over prolonged periods could influence the liver regenerative process or hepatocyte function. We also wished to know if the effects of halothane differed from those of diethyl ether. We found: 1. Prolonged halothane or diethyl ether anaesthesia did not inhibit liver mitotic activity, even if administered repeatedly. 2. The effects of halothane and diethyl ether on liver cell division were identical. 3. With reference to liver regeneration, halothane is as safe as diethyl ether when administered during extensive hepatectomy.

Animals↗

The effect of halothane anaesthesia on the asphyxiated foetal lamb in utero.

In a previous study, we examined the effects of halothane on the normal foetal lamb in utero. The most significant finding was a 33 per cent fall in foetal mean arterial blood pressure (MABP). Cardiac output and placental blood flow were not affected. To determine if the asphyxiated foetus would respond similarly, the following study was performed. Seven pregnant ewes were surgically prepared two days prior to study with maternal and foetal indwelling arterial and venous cannulas. An inflatable occlusion loop was secured around the umbilical cord. On the day of study, a tracheostomy was performed on each ewe. Microspheres were injected into the foetal circulation during the control period. The occlusion loop was inflated to produce foetal asphyxia and microspheres were again injected. The ewe was then anesthetized with halothane; and after 15 minutes, microspheres were injected into the asphyxiated foetus and halothane levels were measured. The asphyxiated foetuses showed a significant rise in MABP, fall in heart rate and fall in cardiac output from control. Blood flow to the brain was significantly increased and flow to the placenta and gut decreased. Exposure of the asphyxiated foetus to halothane resulted in a fall of MABP to control but no significant change in cardiac output or brain blood flow. The mean halothane level in the foetus was 46.0 mg X l-1 or 0.32 vol%. Exposure of the asphyxiated foetus to halothane for 15 minutes does not produce significant further deterioration of the foetal lamb in utero.

Acid-Base Equilibrium↗

Reversal by acupuncture of cardiovascular depression induced with morphine during halothane anaesthesia in dogs.

The cardiovascular effects of morphine sulphate and/or acupuncture by means of electrocautery at Jen Chung (Go-26) were studied in 35 dogs. All animals were maintained under anaesthesia with halothane 0.75 per cent supplemented by the intravenous administration of succinylcholine to allow controlled ventilation during a two hour period of monitoring. Cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, [H+] (pH) PaCO2, PaO2 and base deficit were measured in each dog. Morphine 0.5 mg . kg-1, administered alone as a single bolus, significantly (P less than 0.05) decreased cardiac output, heart rate, mean arterial pressure, and significantly increased stroke volume and pulse pressure in dogs under halothane anaesthesia. Acupuncture by electrocautery alone induced a significant increase in cardiac output, stroke volume, heart rate, mean arterial pressure and pulse pressure with a significant decrease in total peripheral resistance following halothane. Acupuncture at Jen Chung (Go-26) for 10 minutes following the intravenous administration of morphine caused a significant increase in cardiac output, heart rate and mean arterial pressure with a significant decrease in central venous pressure and total peripheral resistance during halothane anaesthesia. The depressant effect of morphine on cardiac output, heart rate and mean arterial pressure in dogs under halothane anaesthesia appears to be reversed by acupuncture by electrocautery at Jen Chung (Go-26). Stimulation of this acupuncture locus could be helpful in resuscitating patients whose cardiovascular system is depressed by morphine and/or halothane anaesthesia.

Acupuncture Therapy↗

Subanaesthetic halothane: its effect on regulation of ventilation and relevance to the recovery room.

Ventilation and the ventilatory response to a steady-state of isocapnic hypoxaemia were measured in six healthy volunteers, both awake and while sedated with low doses of halothane (0.05 and 0.1 MAC). Halothane sedation markedly reduced ventilatory responses to sustained hypoxaemia, in a dose-related fashion. We estimated the length of time after anaesthesia that halothane 0.1 MAC would be present in patients in the recovery room. In five healthy patients who had halothane anaesthesia with a mean duration of one hour, halothane 0.1 MAC or more persisted for approximately one hour. We conclude that, during emergence from halothane anaesthesia, patients may have a significant impairment of the ventilatory response to hypoxaemia, which persists for some time even after regaining consciousness.

Adult↗

Safety and efficacy of alfentanil and halothane in paediatric surgical patients.

Alfentanil, a congener of the opioid fentanyl, possesses properties that make it an attractive choice for use during short operative procedures. Since the pharmacodynamic aspects of alfentanil have not been well documented in children, this study was undertaken to evaluate the safety, efficacy, and dose requirements of alfentanil when used with nitrous oxide or halothane in paediatric patients. Eighty unpremedicated patients, ASA physical status I or II and aged 2-12 yr were studied. Patients were randomly assigned to one of four groups. After induction of anaesthesia with nitrous oxide, oxygen, and halothane, the groups were treated as follows. In Group 1 (n = 19), after halothane was discontinued, alfentanil 50 micrograms.kg-1 was infused over 30 sec. In Group 2 (n = 20), the end-tidal halothan was maintained at 0.5% and alfentanil 25 micrograms.kg-1 was infused. In Group 3 (n = 20), the end-tidal halothane concentration was maintained at 1% and alfentanil 12.5 micrograms.kg-1 was infused. In Group 4 (n = 21), the end-tidal halothane concentration was maintained at 1.5% and no alfentanil was administered. Patients in Groups 1, 2, and 3 received bolus doses of alfentanil 12.5 micrograms.kg-1 as needed to maintain haemodynamic stability. After alfentanil administration, there were transient decreases in systolic blood pressure in Groups 1 and 2, and in heart rate in Group 2. With surgical stimulation, haemodynamic stability was well maintained except in patients in Group 1, who had an increase in systolic blood pressure. Children Group 1 were alert sooner and their tracheas were extubated earlier than those in Groups 2, 3, and 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗

Halothane concentrations required to block the cardiovascular responses to incision (MAC CVR) in infants and children.

The purpose of this study was to determine the halothane concentration in N2O required to block the cardiovascular responses to skin incision (MAC CVR) in infants and children. We studied 64 unpremedicated ASA 1 infants and children (one month to seven years). In each infant or child, anaesthesia was induced slowly with halothane and N2O, and an endotracheal tube was placed. The MAC CVR was assessed, after a steady state end-tidal halothane concentration had been established for ten minutes, by the "up and down technique" of Dixon. Positive responses were defined as an increase in MAP or HR > 10%. The MAC CVR50 values of halothane with 60% N2O were 1.16 +/- 0.23% at 1-6 mo, 1.17 +/- 0.18% at 7-12 mo, 0.95 +/- 0.26% at 1-3 yr, and 1.12 +/- 0.16% at 4-7 yr. The value at 1-3 years children was less than those in the other age groups (P < 0.05). The changes of MAP were correlated with changes of both HR and pupillary diameter. These results indicate that the values of MAC CVR50 of halothane in infants and children are higher than those required to block motor responses (MAC). The halothane requirement to block cardiovascular responses is lowest in the children aged one to three years.

Adrenergic Fibers↗

Mechanisms of inhibition of endothelium-dependent relaxation by halothane, isoflurane, and sevoflurane.

Volatile anaesthetics inhibit endothelium-dependent relaxation, but the underlying mechanism(s) have not been clarified. In an attempt to elucidate the mechanism(s), we determined the effects of halothane, isoflurane and sevoflurane on relaxation induced by acetylcholine and sodium nitroprusside (SNP) and the cGMP formation elicited by exogenous nitric oxide (NO) and SNP in rat aortas. Acetylcholine (10(-7)-10(-5) M)-induced relaxation was attenuated by halothane (2%), isoflurane (2%) and sevoflurane (4%). SNP (10(-8) M)-induced relaxation was reduced by halothane (2%), but not by isoflurane (2%) or sevoflurane (4%). The cGMP level of NO-stimulated aorta was reduced by halothane (2%) and sevoflurane (4%), but not by isoflurane (2%). The cGMP level of SNP (10(-7) M)-stimulated aorta was reduced by halothane (2%), but not by isoflurane (2%) and sevoflurane (4%). We conclude that the mechanisms responsible for the inhibition of endothelium-dependent relaxation differ among anaesthetics. Isoflurane inhibits the relaxation mainly by inhibiting the formation of NO in the endothelium. In contrast, the effect of halothane on endothelium-dependent relaxation may be largely due to the inhibition of action of NO in the vascular smooth muscle and the effect of sevoflurane may be to inactivate NO or to inhibit the action of NO.

Anesthetics↗

[Effect of halothane on ventilation and arterial blood gases in rats with and without diaphragmatic paralysis].

Some patients with diaphragmatic paralysis or dysfunction maintain ventilation by use of other muscles. Anaesthesia, in modifying the performance of these muscles, presents a potential risk to such patients. To evaluate this risk, the effects of halothane on ventilation and arterial blood gases were studied on a model of bilateral diaphragmatic paralysis, the phrenectomized rat. The study was performed on 43 rats. Success of phrenectomy was confirmed at laparotomy, which did not result in blood gas changes. Laparotomy was performed in 23 rats and a carotid artery was catheterized. In 11 control rats, phrenic nerves were exposed but not sectioned, and in 12 other rats, the phrenic nerves were sectioned. Ventilation was measured by plethysmography in awake rats before and after surgery and in the same rats anaesthetized with halothane 1.1%. In the 23 rats, a decrease in weight and core temperature was observed after operation and this was more marked in phrenectomized than in control rats. In the 11 control rats, ventilation increased postoperatively without change in blood gases. In these rats, halothane caused a decrease in minute ventilation and PaO2 and an increase in PaCO2. Phrenectomy in awake rats led to an increase in minute ventilation, hypoxaemia and hypercapnia. In these rats, halothane led to death in three and a decrease in minute ventilation, with hypercapnia and hypoxaemia in the nine other rats. Blood gas changes were greater than in anaesthetized controls. In the intact rat, halothane leads to blood gas changes comparable to those observed in other species and humans. The present study confirms the effects of halothane on respiratory muscles other than the diaphragm and demonstrates the severe respiratory risk of anaesthesia in patients whose ventilation is maintained by these muscles.

Anesthesia, Inhalation↗

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children.

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two-dimensional echocardiographic dimensions of the left ventricle and pulmonary artery blood flow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg.kg-1 IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in both groups, but decreases in EF (32 +/- 5 per cent vs 18 +/- 5 per cent) and increases in LVEDV (18 +/- 7 per cent vs 7 +/- 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 +/- 6 per cent), than during isoflurane anaesthesia (18 +/- 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 +/- 4 per cent) following atropine in both groups, and CO returned to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

Pattern of ventilation during halothane anaesthesia in infants less than two months of age.

PURPOSE: To examine the breathing pattern of infants aged less than two months in order to understand better the effect of halothane on ventilation in infants. METHODS: The inspiratory flow waveform, the CO2 waveform and occluded inspiratory pressure waveform were recorded at different inspired concentrations of halothane using a washout of halothane in two groups of infants undergoing elective herniorrhaphy. Data were analyzed for minute ventilation (Vi) and tidal volume (VT), parameters of timing of the breath [Total time (Ttot), Inspiratory time (Ti), and the ratio of the occluded to unoccluded inspiratory time (TiOCC/Ti)], parameters of Amplitude of the neural output [mean inspiratory flow (VT/Ti)] and parameters of the Shape of the inspiratory breath profile [the inspiratory flow centroid (Ci/Ti), the inspiratory duty cycle (Ti/Ttot)]. The airway was occluded at end expiration and the slope of the initial 100 msec of occlusion (dP/dt) together with the maximal negative pressure (PMAX) and occluded inspiratory time (TiOCC) were obtained. We studied ten infants < 48 wk post-conceptional age (PCA) and ten infants > 48 wk. PCA Flow (V), pressure (Pao) and carbon dioxide tension (PCO2) were recorded at three concentrations of inspired halothane (FiH): 0%, 1% and 2% which corresponded to an end-tidal halothane concentration of about 0.2%, 0.8% and 1.2% respectively. RESULTS: In both groups Vi, VT and VT/Ti decreased whereas dP/dt, did not, suggesting that the respiratory pump was impaired. The parameters of breath Shape did not change. Importantly the parameters of Timing showed different tendencies. In infants > 48 wk PCA TiOCC/Ti decreased. In infants < 48 wk PCA, TiOCC/Ti did not change. CONCLUSIONS: The different response in the timing parameter TiOCC/Ti is consistent with a different effect of halothane on parameters of ventilatory timing in infants < 48 wk PCA and this may represent a maturational effect.

Anesthesia, Inhalation↗

Naloxone reverses the hypnotic effect and the depressed baroreceptor reflex of halothane anaesthesia in the dog.

In order to evaluate the effect of an opioid antagonist on depressed intrinsic central vaso-motor drive (carotid sinus reflex) and high voltage slow delta waves in the EEG associated with halothane, naloxone was injected intravenously in a bolus of 100 or 200 micrograms.kg-1 on different days in the anaesthetized dog (0.64 Vol% halothane in oxygen). Only the 200 micrograms.kg-1 dose of naloxone reversed the halothane-induced depression of the blood pressure and heart rate response to clamping of both exteriorized common carotid arteries. The EEG changed from high voltage slow waves to low voltage fast waves, inducing a reduction of power in the delta band in spectral analysis. This effect was most pronounced during the 20th minute post naloxone injection. Naloxone did not reverse the halothane-related hypotension and bradycardia. Because of the late "cortical arousal" reaction during halothane-anaesthesia and the high dose necessary, naloxone appears to exert its action through a generalized increase in CNS excitation. An antagonisation of halothane-induced release of opiate-like peptides therefore is less likely.

Anesthesia, Inhalation↗

Flumazenil improves cognitive and neuromotor emergence and attenuates shivering after halothane-, enflurane- and isoflurane-based anesthesia.

PURPOSE: To conduct a randomized, placebo-controlled, double-blinded, clinical experiment testing the hypothesis that flumazenil, a benzodiazepine antagonist, may affect recovery from halothane-, enflurane- and isoflurane-based anesthesia. METHOD: Patients who underwent surgery under N(2)O/O(2) plus halothane (n=100), enflurane (n=100) or isoflurane (n=70) anesthesia were administered flumazenil 1 mg or placebo upon emergence from anesthesia, and their postanesthesia vital signs, vigilance, neurological recovery, shivering, amnesia reversal, and general subjective feeling were assessed. RESULTS: A ten-point vigilance score showed better recovery of flumazenil-treated patients compared to those who received placebo (60-min after halothane anesthesia: 9.9 +/- 0.1 vs 9.5 +/- 0.2, P <0.01; after enflurane: 10 +/- 0 vs 9.4 +/- 0.2, P <0.01; after isoflurane: 10.0 +/- 0 vs 9.3 +/- 0.1, P <0.01). Halothane- and enflurane-flumazenil-treated patients (but not isoflurane) reached a better neurological score (2.97 +/- 0.05 or 3 +/- 0) compared to placebo (2.8 +/- 0.4 or 2.6 +/- 0.4, P <0.01), respectively. Reversal of amnesia was superior in the flumazenil group at 60 min and at 24 hr postsurgery, and more flumazenil patients rated recovery as "pleasant". Flumazenil patients shivered less than placebo patients despite their lower core temperature (at 30 min: halothane: 11% vs 28%, P <0.05; enflurane: 11% vs 30%, P <0.05; isoflurane: 17% for both groups). CONCLUSION: Flumazenil improves recovery of high cortical and neuromotor functions following halothane, enflurane and isoflurane anesthesia, reduces shivering and improves the overall quality of emergence, including patients' subjective feeling.

Adult↗

Ventilatory parameters in children during propofol anaesthesia: a comparison with halothane.

PURPOSE: The purpose of this study was to compare the effects of propofol on ventilation with those of halothane. METHODS: Respiration was studied in 20 spontaneously breathing children undergoing elective dental restoration randomized to receive either propofol (Group P) or halothane (Group H) anaesthesia. Data were recorded at different inspired concentrations of halothane (F1H) or propofol (RivP) during a washout of the anaesthetic agent. The F1H 2%, 1% and 0% corresponded to an end-tidal halothane concentration of 1.38 +/- 0.06%, 0.857 +/- 0.03% and 0.191 +/- 0.01% respectively. The RivP were 18, 15, 12, 9 and 0 mg.kg-1.hr-1. The inspiratory flow waveform, the CO2 waveform and the occluded inspiratory pressure waveform were recorded. The flow waveform was analyzed for minute ventilation (Vi), and tidal volume (VT), parameters of breath Timing [Total time (Ttot), Inspiratory time (Ti)] and parameters of breath Amplitude [mean inspiratory flow (VT/Ti)]. The slope of the initial 100 msec (dP/dt0.1) of an occluded inspiration, together with the occluded inspiratory time (Tiocc) and the ratio of the occluded to unoccluded inspiratory time (Tiocc/Ti) were obtained. RESULTS: There were intergroup differences in the preemergence values of Ttot, dP/dt0.1 and Tiocc/Ti. In group P the Vi, VT and Ttot increased and PETCO2 decreased during a washout of propofol. The values of dP/dt0.1 in Group P at all RivP were half the values of those in Group H. The ratio Tiocc/Ti did not change in Group P and increased in Group H during a washout of halothane. CONCLUSION: Propofol anaesthesia was associated with a decrease in Vi whereas during halothane anaesthesia, Vi did not change. Ventilation in Group P differed from Group H in parameters of both breath Drive and Timing.

Anesthesia↗

Effect of cocaine on the contracture response to 1% halothane in patients undergoing diagnostic muscle biopsy for malignant hyperthermia.

Two case reports have cited the recreational use of cocaine as possible trigger of a malignant hyperthermia (MH) crisis. We evaluated whether toxic concentrations of cocaine altered the in vitro muscle response to halothane during contracture tests for MH. Twenty-two patients were studied. Muscle biopsies were obtained and first tested for MH susceptibility with 3% halothane and caffeine contracture testing. Ten patients were diagnosed as MH-susceptible and 12 as MH non-susceptible, in accordance with the North American Malignant Hyperthermia Group protocol. Then, muscle strips were exposed to 1% halothane in the presence and absence of 0.1 mmol.L-1 cocaine. Cocaine alone did not affect baseline muscle tension in either group. With 1% halothane, MH non-susceptible muscle showed no contracture with or without cocaine. In contrast, in the presence of 1% halothane, MH-susceptible muscle showed either no change in contracture (six patients), an increase (two patients), or a decrease (two patients) when exposed to cocaine. However, the overall effect of cocaine on muscle contracture in the presence of 1% halothane was insignificant in both groups. We conclude that cocaine, even at toxic levels, does not have a direct effect on skeletal muscle contractility and thus is safe for MH-susceptible patients.

Adult↗

Comparison of the direct effects of sevoflurane, isoflurane and halothane on isolated canine coronary arteries.

We have demonstrated previously, using dog epicardial arteries of different sizes, that isoflurane, like adenosine, is preferentially a small coronary artery dilator, whereas halothane, like nitroglycerin, is a large artery dilator. The present study was designed to compare the direct effects of sevoflurane with those of isoflurane and halothane. Proximal large coronary arteries with an outer diameter (o.d.) of 2.5-3.2 mm and distal small arteries of 0.6-0.9 mm o.d. were isolated from dogs and then cut into vascular rings. They were precontracted with KCl (20 mM), and their relaxant responses to anaesthetics were compared relative to the maximal responses induced by papaverine. Sevoflurane, halothane and isoflurane (1-3 human MAC) induced dose-dependent relaxation of these arteries. The relaxant response to sevoflurane did not differ between large and small arteries. However, the relaxant response of the large arteries to halothane (1.5-2.3%) was greater than that of small arteries (P < 0.01) and the response of small arteries to isoflurane (3.5%) was greater than that of large arteries (P < 0.05). In large arteries, the potency of the relaxant effect at equivalent human MAC could be ranked as halothane > or = sevoflurane > isoflurane, and, in small epicardial arteries as isoflurane > sevoflurane >> halothane. We conclude that, unlike isoflurane, sevoflurane is not a preferential dilator of small coronary arteries.

Anesthetics↗

[No better vigilance after general anesthesia with propofol in colonic surgery. A comparison of three procedures for general anesthesia (propofol, halothane and midazolam/fentanyl) in combination with catheter epidural anesthesia].

Early mental and psychomotor recovery was studied in 67 patients undergoing colorectal surgery under continuous epidural anaesthesia and light general anaesthesia using propofol, halothane, and midazolam/fentanyl. The study was approved by the local ethics committee. All patients received epidural anaesthesia with 0.25% bupivacaine and were then randomly allocated to one of three groups. In group I (halothane), light general anaesthesia was induced with thiopental 3-5 mg/kg and maintained with halothane. The propofol group (II) received 2 mg/kg for induction and a mean continuous infusion of 1.7 mg/kg.h. In group III (Mi/Fe), midazolam and fentanyl were used for induction and maintenance. All patients were intubated, received non-depolarising muscle relaxants, and were manually ventilated with nitrous oxide-oxygen (2:1.2). For postoperative analgesia, 0.05 mg/kg morphine was administrated epidurally 30 min before the end of the operation; 30, 60, 90, and 120 min after arriving in the recovery room, vigilance was assessed using a modified Steward score, the Trieger test, the ability to recall a column of numbers (KAI test), and symbol counting (CI test). Heart rate, blood pressure, arterial oxygen saturation, and blood gases were recorded. RESULTS. The three groups were comparable with regard to age, sex, ASA classification, and duration of anaesthesia and operation (Table 3). There was no difference between the groups in performance of the recovery tests (Figs. 2-5), blood pressure, heart rate, arterial blood gas analysis (Fig. 6), or oxygen saturation. Comparing pre- and postoperative values, we found severe psychomotor and mental impairment in all groups. pCO2 was slightly elevated in all groups, but only 3 patients in the propofol group and 6 in the midazolam/fentanyl group developed hypercapnia above 50 mm Hg. Patients receiving propofol or midazolam/fentanyl had significantly less postoperative nausea and vomiting than those receiving halothane (Table 5). CONCLUSION. It is concluded that propofol offers no advantage over halothane or midazolam/fentanyl where early postoperative recovery is concerned. Intraoperatively, all three techniques provided good anaesthesia. Propofol and midazolam/fentanyl caused less postoperative nausea and vomiting than halothane anaesthesia.

Adult↗

[Orthostasis in halothane anesthesia. A model situation for studying cerebrovascular autoregulation in infants].

Halothane causes impairment of cerebrovascular reactivity and autoregulation. We used transcranial Doppler sonography (TCD) to investigate the reaction patterns of cerebral blood flow velocities (CBFV) during a standardized orthostatic maneuver after premedication and during halothane anesthesia in infants. After premedication orthostasis led to no significant changes in CBFV. During halothane anesthesia CBFV was significantly higher than after premedication, and orthostasis induced a significant decrease in CBFV compared to values obtained in horizontal position. Heart rate and mean blood pressure were significantly lower than before medication during halothane anesthesia. The observed changes in CBFV during halothane anesthesia represent a characteristic pattern of impaired cerebral autoregulation. The changes in CBFV and heart rate demonstrate that neither systemic nor cerebral hemodynamics compensate for hydrostatic inducement during halothane anesthesia. The tilting test is a useful tool for determining cerebral autoregulation capacity in infants.

Anesthesia, Inhalation↗

Comparison of the effects of xenon and halothane on voltage-dependent Ca(2+) fluxes in rabbit T-tubule membranes.

The effects of xenon and halothane on depolarization-induced (45)Ca(2+) fluxes mediated by voltage-dependent Ca(2+) channels were investigated in transverse tubule membrane vesicles from rabbit skeletal muscle. Halothane, in the concentration range of 0.5-2 mM, caused a significant inhibition of (45)Ca(2+) fluxes. Xenon tested in the range of 60%-100% did not affect the (45)Ca(2+) fluxes. Radioligand binding studies indicated that xenon and halothane have different effects on the specific binding of [(3)H]Isradipine to transverse tubule membranes. Halothane caused a significant inhibition on the specific binding of [(3)H]Isradipine. In controls and in presence of 0.5 mM halothane, B(max) values were 26.9 pmole/mg and 15.1 pmole/mg, and K(D) values were 238 pM and 247 pM, respectively. On the other hand, there was no effect of xenon (60%-100%) on the characteristics of [(3)H]Isradipine binding. In conclusion, results indicate that xenon and halothane differ in their effects on the function of voltage-dependent Ca(2+) channels and on the specific binding of [(3)H]Isradipine in skeletal muscle membranes.

Anesthetics, Inhalation↗