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PubMed2003

Effects of halothane on action potential configuration in sub-endocardial and sub-epicardial myocytes from normotensive and hypertensive rat left ventricle.

BACKGROUND: Halothane shortens ventricular action potential duration (APD), as a consequence of its inhibitory effects on a variety of membrane currents, an effect that is greater in sub-endocardial than sub-epicardial myocytes. In hypertrophied ventricle, APD is prolonged as a consequence of electrical remodelling. In this study, we compared the effects of halothane on transmural APD in myocytes from normal and hypertrophied ventricle. METHODS: Myocytes were isolated from the sub-endocardium and sub-epicardium of the left ventricle of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Action potentials were recorded before, during, and after a 1-min exposure to 0.6 mM halothane and APD measured from the peak of the action potential to repolarization at -50 mV (APD(-50 mV)). Data are presented as mean (SEM). RESULTS: In WKY myocytes, halothane reduced APD(-50 mV) from 21 (2) to 18 (2) ms (P<0.001, n=15) in sub-epicardial myocytes but abbreviated APD(-50 mV) to a greater extent in sub-endocardial myocytes (37 (4) to 28 (3) ms; P<0.001, n=14). In SHR myocytes, APD(-50 mV) values were prolonged compared with WKY and APD(-50 mV) was reduced by halothane from 36 (6) to 27 (4) ms (P<0.016) and from 77 (10) to 38 (4) ms (P<0.001) in sub-epicardial and sub-endocardial myocytes, respectively. CONCLUSIONS: In the SHR, hypertrophic remodelling was not homogeneous; APD(-50 mV) was prolonged to a greater extent in sub-endocardial than sub-epicardial cells. Halothane reduced APD to a greater extent in sub-endocardium than sub-epicardium in both WKY and SHR but this effect was larger proportionately in SHR myocytes. The transmural gradient of repolarization was reduced in WKY and effectively abolished in SHR by halothane, which might disturb normal ventricular repolarization.

Action Potentials↗
PubMed2005

Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation.

BACKGROUND: Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. METHODS: Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8x or 1.2x the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED(50)) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). RESULTS: Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from approximately 6 to approximately 8.5 Hz, and the SEF from approximately 25.5 to approximately 27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED(50) propofol, only the tail clamp and 1 Hz stimuli increased MEF ( approximately 8 to approximately 10-10.5 Hz). At the higher propofol infusion rate (1.2 ED(50)) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from approximately 23 to approximately 21.5 Hz). CONCLUSIONS: Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

Anesthetics, Inhalation↗
PubMed2000

The use of halothane gas to identify turkeys prone to developing pale, exudative meat when transported before slaughter.

Halothane screening has been used in the swine industry to identify animals susceptible to stress and prone to developing pale, soft, exudative (PSE) meat. This study evaluated the ability of halothane to identify stress-susceptible turkeys prone to developing PSE meat when reared to market age and transported before slaughter. Male Nicholas turkeys (n = 1,286) were exposed to 3% halothane for 5 min at 4 wk of age in two trials. Birds were classified as halothane sensitive (HAL+) or halothane nonresponder (HAL-), in which HAL+ birds showed signs of muscle rigidity in the legs upon removal from halothane gas, and HAL- birds showed no stiffness response. Approximately 3.5% (45) of the turkeys were HAL+. All HAL+ birds and an equal number of HAL- birds were grown until 20 wk of age. Immediately prior to slaughter, all birds were transported in coops on a flatbed trailer for 2 h and then immediately slaughtered upon arrival at the processing plant. Breast muscle pH (0, 1.5, and 24 h postmortem) and L* value (1.5 h and 24 h postmortem) were measured on the fillets. Drip loss and cook loss were also determined on marinated and nonmarinated breast fillets from each carcass. There were no significant mean differences in any parameter measured between the HAL+ and HAL- turkeys. However, the HAL+ turkeys had a greater percentage of fillets with L* values >51 compared with the HAL- turkeys. These results suggest that either halothane response is only a limited predictor of PSE meat in turkeys or that transportation is not an appropriate stressor to induce the PSE condition.

Anesthetics, Inhalation↗
PubMed1995

Laser-Doppler measurement of the effects of halothane and isoflurane on the cerebrovascular CO2 response in the rat.

We used laser-Doppler flowmetry to compare the effects of the volatile anesthetics, isoflurane and halothane, on the cerebrovascular response to CO2 inhalation in male Sprague-Dawley rats. The effects of 0.5 and 1.5 minimum alveolar anesthetic concentrations (MAC) of halothane and isoflurane on the microcirculatory response to CO2 were compared at 22, 36, and 66 mm Hg end-tidal partial pressure of carbon dioxide (ETCO2). An additional group of animals was anesthetized by continuous barbiturate infusion (10-20 mg.kg-1.h-1). Arterial blood pressure was maintained at control levels throughout the experiment using an infusion of phenylephrine (0.5-5 micrograms.kg-1.min-1). Laser-Doppler flow (LDF) was greater at 1.5 MAC than at 0.5 MAC at each ETCO2 for both anesthetics. The CO2 reactivity (percent LDF change/mm Hg change ETCO2) from hypocapnia to normocapnia was similar to that from normocapnia to hypercapnia. CO2 reactivity with barbiturate infusion and 0.5 MAC isoflurane were 1.78 +/- 0.19 and 2.28 +/- 0.22 (no difference), respectively, both being greater than that with 0.5 MAC halothane at 1.19 +/- 0.14 (P < 0.05). A similar difference was suggested at 1.5 MAC halothane and 1.5 MAC isoflurane (1.99 +/- 0.25 and 2.67 +/- 0.35, respectively). The CO2 reactivity was greater at 1.5 MAC halothane compared to 0.5 MAC halothane. The results of this study suggest that an increase in arterial CO2 may increase cerebrocortical red cell flow more with isoflurane than with halothane, at least at moderate anesthetic concentrations.

Anesthesia↗
PubMed1996

A comparison of the effect of halothane on N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated excitatory synaptic transmission in the hippocampus.

Halothane depresses synaptic transmission in the rat brain. First we determined the concentration of halothane which decreased the amplitude of the population spike recorded in the CA1 region of the hippocampus to 50% of the control value (105 +/- 4.9 micrograms/mL [0.53 mM] halothane). Hippocampal glutamate receptors are divided into N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionate (AMPA) and kainate (non-NMDA) subtypes. The NMDA and non-NMDA receptors were blocked with (+/-)-2-amino-5-phosphonopentanoic acid (AP5) (30 microM), and 6,7-dinitroquinoxaline-2,3-dione (DNQX) (10 microM), respectively, to allow observation of the effects of halothane on the NMDA and non-NMDA receptors, respectively. gamma-Aminobutyric acid type A (GABAA) receptors were blocked in all studies with picrotoxin (PTX) (40 microM). When the non-NMDA receptors were blocked a halothane concentration of 38.1 +/- 5.6 mg/mL was required to produce a further 50% decrease in population spike amplitude. When NMDA receptors were blocked with AP5 or only GABAA receptors were blocked the halothane concentrations needed to produce 50% block were higher than needed for the control (160.8 +/- 17.8 and 190.2 +/- 12.1 microgram/mL, respectively). These studies indicate that the NMDA receptors are more sensitive to the effects of halothane than the non-NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1996

Protein kinase C-induced contraction is inhibited by halothane but enhanced by isoflurane in rat coronary arteries.

Protein kinase C (PKC), important in signal transduction, may help generate and maintain vascular smooth muscle tone. We sought to examine the effect of the volatile anesthetics isoflurane and halothane on PKC agonist-induced vasoconstriction and PKC inhibitor-induced vasorelaxation. Subepicardial resistance arteries were dissected from rat hearts. Changes in vessel diameters were monitored in response to the membrane-bound PKC agonist 12-deoxyphorbol-13-isobutyric-20-acetate (PBE) 10(-8)-10(-7) M or the cytosolic PKC agonist oleic acid 10(-7)-10(-5.5) M either in the presence of isoflurane 1.15%, isoflurane 2.3%, halothane 0.77%, halothane 1.54%, or no volatile anesthetics (control). In addition, after preconstriction with the thromboxane analog U46619 1 microM, relaxation responses to the PKC inhibitor staurosporine 10(-8)-10(-7) M were examined in the presence or absence of the anesthetics as above. PBE-induced constriction was attenuated by either concentration of halothane (P < 0.05) but was unaltered by isoflurane (P > 0.5). Oleic acid-induced constriction was abolished by halothane (P < 0.001) but enhanced by isoflurane (P < 0.01). Staurosporine-induced relaxation of U46619-preconstricted vessels was attenuated by isoflurane (P < 0.05) but unaltered by halothane (P > 0.3). We conclude that isoflurane may enhance cytosolic PKC-mediated vasoconstriction, whereas halothane may attenuate both cytosolic and membrane-bound PKC-mediated vasoconstriction.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

The effect of halothane on phrenic and chemoreceptor responses to hypoxia in anesthetized kittens.

We examined the effect of halothane on phrenic never and carotid sinus discharge during hypoxia in anesthetized kittens. In 12 animals, phrenic amplitude was measured during normoxia, during isocapnic hypoxia, and after a return to normoxia, both with and without halothane. Without halothane, all animals had an increase in phrenic amplitude during hypoxia. With halothane, half the animals showed an increase in phrenic amplitude followed by a decline. In a second group of animals, recordings were obtained from single or a few fiber strands of carotid sinus nerve. Without halothane, an increase in chemoreceptor discharge frequency during hypoxia was seen. With 1.0% halothane, frequency was decreased during normoxia and did not increase during hypoxia. Thus, halothane's effect on the ventilatory response to hypoxia, as measured by phrenic discharge, is at least partially explained by an effect on peripheral chemoreceptors.

Action Potentials↗
PubMed1997

Biotransformation of halothane, enflurane, isoflurane, and desflurane to trifluoroacetylated liver proteins: association between protein acylation and hepatic injury.

In susceptible patients, halothane, enflurane, isoflurane, and desflurane can produce severe hepatic injury by an immune response directed against reactive anesthetic metabolites covalently bound to hepatic proteins. The incidence of hepatotoxicity appears to directly correlate with anesthetic metabolism catalyzed by cytochrome P450 2E1 to trifluoroacetylated hepatic proteins. In the present study, we examined whether the extent of acylation of hepatic proteins in rats by halothane, enflurane, isoflurane, and desflurane correlated with reported relative rates of metabolism. After pretreatment with the P450 2E1 inducer isoniazid, five groups of 10 rats breathed 1.25 minimum alveolar anesthetic concentration (MAC) of halothane, enflurane, isoflurane, or desflurane in oxygen, or oxygen alone, each for 8 h. Immunochemical analysis of livers harvested 18 h after anesthetic exposure showed tissue acylation (greatest to least) after exposure to halothane, enflurane, or isoflurane. Reactivity was not different between isoflurane as compared to desflurane or oxygen alone. An enzyme-linked immunosorbent assay showed halothane reactivity was significantly greater than that of enflurane, isoflurane, desflurane, or oxygen, and that enflurane reactivity was significantly greater than desflurane or oxygen. Sera from patients with a clinical diagnosis of halothane hepatitis showed antibody reactivity against hepatic proteins from rats exposed to halothane or enflurane. No reactivity was detected in rats exposed to isoflurane, desflurane, or oxygen alone. These results indicate that production of acylated proteins may be an important mediator of anesthetic-induced hepatotoxicity.

Acylation↗
PubMed1997

The effects of halothane pretreatment on manganese influx induced by muscarinic stimulation of airway smooth muscle.

We hypothesized that halothane inhibits contraction of canine airway smooth muscle in part by depleting sarcoplasmic reticulum (SR) calcium stores, which affects subsequent force and calcium influx. This hypothesis was tested by using the rate of quenching of fura-2 fluorescence by manganese (Mn2+) as an index of calcium influx. When added 10 min before submaximum muscarinic stimulation (with 0.3 microM acetylcholine [ACh]), halothane (0.60 +/- 0.04 mM [mean +/- SE]) reduced subsequent isometric force and intracellular calcium concentration ([Ca2+]i) measured 10 min after contraction (to 55%) +/- 5% and 69% +/- 4% of control, respectively). The Mn2+ influx measured concurrently was significantly increased by halothane (by 57% +/- 22%). Depletion of SR calcium stores by ACh prior to contraction also increased Mn2+ influx (by 46% +/- 6%) but did not affect developed force or increase [Ca2+]i in response to submaximum muscarinic stimulation. Halothane did not affect [Ca2+]i or Mn2+ influx when added prior to maximum stimulation with 100 microM ACh but significantly reduced developed force. These findings are consistent with the hypothesis that halothane-induced SR depletion prior to contraction stimulates subsequent calcium influx, but they further suggest that halothane-induced SR depletion itself does not contribute significantly to the reduction in contractility produced by halothane in the canine airway smooth muscle.

Acetylcholine↗
PubMed1998

The effect of halothane and sevoflurane on fatigue-induced changes in hamster diaphragmatic contractility.

UNLABELLED: The purpose of this study was to examine the effect of halothane and sevoflurane on fatigue-induced changes in diaphragmatic contractility. Forty-two hamster diaphragm strips were randomly allocated according to anesthetics (no anesthesia control, 1%-3% halothane, 2%-6% sevoflurane) and stimulated directly in an organ bath. Under the influence of the anesthetics, muscle fatigue was induced by repetitive tetanic contraction, and diaphragmatic contractilities (i.e., peak twitch and tetanic tension, twitch contraction time, and half-relaxation time) were measured before and after fatigue. Neither halothane nor sevoflurane changed tension generation before or after fatigue, but each anesthetic significantly enhanced fatigue-induced prolongations of the contraction time and half-relaxation time after fatigue. Specifically, the half-relaxation times after fatigue in the 3% halothane, 4% sevoflurane, and 6% sevoflurane groups (225.6 +/- 37.6, 236.0 +/- 76.5, and 287.3 +/- 55.5 ms, respectively) were more than twice as long as those of the control group (104.7 +/- 19.7 ms, P < 0.05). We conclude that halothane and sevoflurane augment fatigue-induced prolongations of the contraction and relaxation times. Diaphragmatic function may deteriorate when there is a fatiguing task during the clinical administration of halothane or sevoflurane anesthesia. IMPLICATIONS: This study implicates diaphragmatic fatigue during anesthesia. An in vitro hamster diaphragm muscle preparation was used to study the effect of halothane and sevoflurane on fatigue-induced change in contractility. Our findings suggest that increased load on the diaphragm during volatile anesthesia may lead to impaired diaphragmatic contractility.

Anesthetics, Inhalation↗
PubMed1998

Simulation of an epidural test dose with intravenous isoproterenol in sevoflurane- and halothane-anesthetized children.

UNLABELLED: Isoproterenol has been suggested as an alternative marker for epidural test dosing in children receiving halothane anesthesia. The purpose of this prospective, randomized, double-blind study was to determine the chronotropic response to IV isoproterenol in sevoflurane-anesthetized children. Thirty-six ASA physical status I children (0.5-8 yr) were anesthetized with either halothane or sevoflurane at 1 minimum alveolar anesthetic concentration adjusted for age in 70% nitrous oxide. Patients received incremental IV injections of isoproterenol until their heart rate increased > or = 20 bpm above baseline. The minimal effective dose of isoproterenol required to produce an increase of > or = 20 bpm was 55 ng/kg (42-72 ng/kg; 95% confidence interval) in sevoflurane-anesthetized children and 32 ng/kg (26-38 ng/kg; 95% confidence interval) in halothane-anesthetized children (P < 0.05). This dose-response study suggests that sevoflurane antagonizes beta-adrenergic-mediated chronotropic responses to isoproterenol more than halothane. These observations also suggest that larger doses of isoproterenol will be necessary for epidural test dosing in children receiving sevoflurane rather than halothane anesthesia. IMPLICATIONS: Isoproterenol has been suggested as an alternative marker for epidural test dosing in children receiving halothane anesthesia. This isoproterenol dose-response study indicates that larger doses of isoproterenol will be necessary for epidural test dosing in children undergoing sevoflurane rather than halothane anesthesia.

Adrenergic beta-Agonists↗
PubMed1999

Halothane attenuates myogenicity in the rabbit ear artery.

UNLABELLED: The aim of this study was to test the hypothesis that halothane interferes with the myogenic response to an increase in intraluminal pressure. Myogenic responsiveness refers to the intrinsic property of vascular smooth muscle to dilate and then constrict in response to an increase in intraluminal pressure, in an attempt to maintain vessel diameter. Vessel segments taken from the rabbit central ear artery were cannulated, pressurized to 60 mm Hg, and perfused with and suspended in Krebs solution. After exposure to extraluminal l-norepinephrine, vessels contracted to an initial diameter (Di) and were subjected to intraluminal pressure increases to 100 mm Hg. Myogenic reactivity was assessed by measurement of the extent of dilatation after the pressure increase from Di to a maximal diameter (Dm) and then the constriction and recovery (against the pressure increase) to a final (Df) diameter. Myogenicity was further assessed by determining the rate of return of the vessel diameter (angle of recovery) and vessel recovery (defined as Dm - Df/Dm - Di) and expressed as a percentage. Myogenicity was determined before and after exposure to halothane in concentrations of between 1-5%. Halothane significantly attenuated the myogenic response at all concentrations studied. The effect of halothane was maximal at a concentration of 5% where there was virtual abolition of the myogenic response with recovery assessed at 6+/-2.7% (SEM), compared with control (98+/-2.5%, P < 0.05). The angle of recovery was likewise attenuated. These data suggest that halothane, in a dose-dependent manner, attenuates myogenicity in the isolated rabbit ear artery preparation. IMPLICATIONS: Blood pressure is controlled partially by the myogenic response. This refers to the capacity of arteries to dilate and then constrict in response to pressure increase. Using arteries from rabbits, we have shown that administration of halothane reduces or abolishes this response. This observation may be a contributing factor to hypotension caused by halothane.

Anesthetics, Inhalation↗
PubMed2000

Effects of nonimmobilizers and halothane on Caenorhabditis elegans.

We studied the effects of two nonimmobilizers, a transitional compound, and halothane on the nematode, Caenorhabditis elegans, by using reversible immobility as an end point. By themselves, the nonimmobilizers did not immobilize any of the four strains of animals tested. Toluene appears to be a transitional compound for all strains tested. The additive effects of the nonimmobilizers with halothane were also studied. Similar to results seen in studies of mice, the nonimmobilizers were antagonistic to halothane in the wild type nematode. However, the nonimmobilizers did not affect the 50% effective concentrations of halothane for two other mutant strains. For halothane, the slopes of the dose response curves were smaller in more sensitive strains compared with the wild type. As in mammals, nonimmobilizers antagonize the effects of halothane on the nematode, C. elegans. The variation in slopes in the response to halothane in different strains is consistent with multiple sites of action. These results support the use of C. elegans as a model for the study of anesthetics.

Anesthetics↗
PubMed1975

Diphenylhydantoin and lidocaine modification of A-V conduction in halothane-anesthetized dogs.

The effect of halothane on A-V conduction was evaluated in gods during atrial pacing using the technique of His-bundle electrocardiography. In addition, the effects of lidocaine and diphenylkydantoin (DPH) on A-V conuction were examined during halothane anesthesia. Effects of these drugs on three subintervals of A-V conduction were compared. These included the -H (stimulus atifact of His-bundle deflection-atrioventricular conduction), H-Q (His-budnle deflection onset of QRS complex-His-Purkinje conduction), and H-S intervals(His-bundle delfection to end of QRS COmplex-total intraventricular conduction). Linear regression best described the relationship between duration of interval (P-H, H-V,and H-S) and heart rate during incremental increases in the atrial paced rate. Data from these experiments were fitted to a multiple lenear regression model that predicted the effect of increasing concentrations of halothan, lidocaine, and DPH on slope and intercept coefficients. In creasing concentrations of halothan ( 30 and 45 mg/100 ml arterial). Both lidocaine and DPH further depressed conduction at all levels of halothan anesthesia. The P-H interval was particularly sensitive todrug effefts. This may represent potentiation of the normal slowing of conduction through the AVnode in response to incremental increases in heart rate (fatigue response.) We conclude thatboth lidocaine and DPH fail to reverse the depressant effect of halothane on A-V conduction. This may explain their ineffectiveness in treating certain types of arrhythmias during halothane anesthesia.

Anesthesia, Inhalation↗
PubMed1976

Myocardial function and metabolism in the conscious dog and during halothane anesthesia.

Chronically catheterized dogs were studied awake and during anesthesia with high and low concentrations of halothane to assess the relationship between cardiac function and metabolism. Low concentrations of halothane (0.79 per cent endtidal) increased heart rate and decreased left ventricular stroke volume, stroke work, and dP/dt without producing other hemodynamic changes. However, similar heart rate increases produced by atrial pacing in awake animals increased aortic pressure and cardiac output and decreased left atrial pressure. Consequently, the halothane-induced tachycardia partially compensated for the negative inotropic effect of the halothane. High concentrations of halothane (1.74 per cent endtidal) further increased heart rate and elevated left atrial pressures. Cardiac output, stroke volume, stroke work, aortic pressure, LV dP/dt, myocardial blood flow and oxygen consumption were markedly decreased. Myocardial glucose extraction was also decreased. Myocardial oxygen extraction was unchanged, and lactate extraction rose with both concentrations of halothane. Consequently, the dose-dependent negative inotropic effect of halothane resulted in a decrease in cardiac oxygen demand which was equal to or greater than the decrease in oxygen delivery. Whether the same relationship would be seen in the ischemic heart is yet to be demonstrated.

Anesthesia, Inhalation↗
PubMed1978

Microvascular responses to norepinephrine and vasopressin during halothane anesthesia in the rat.

This experiment was designed to determine the microvascular responses to the two known naturally occurring vasoconstrictors, norepinephrine (NE) and vasopressin, at known levels of central vasomotor activity before, during and after halothane anesthesia. The responses to topical application of NE and vasopressin were studied in the microvasculature of the mesentery and cremaster muscle, using microscopic methods. Neural (CNS) stimulation was accomplished through electrodes chronically implanted in vasoactive sites of the forebrain and midbrain. The increase in blood pressure in response to CNS stimulation was decreased during halothane anesthesia (32.4 +/- 5.4 per cent before and 24.7 +/- 6.1 per cent during; P less than 0.001). There was no significant change in the steady-state diameter of the microvasculature under study during or after halothane anesthesia. Marked abatement of arteriolar vasoconstriction in response to CNS stimulation was seen prior to halothane. However, the same target vessel showed increased constriction in response to topically applied NE (from 32.3 +/- 4.7 to 53.2 +/- 7.8 per cent; P less than 0.01) during halothane anesthesia. By contrast, the response to vasopressin decreased (from 42.4 +/- 5.7 to 1.0 +/- 6 per cent; P less than 0.001) with halothane. The precise mechanism(s) underlying the described hypersensitivity to NE and hyposensitivity to vasopressin in the same vascular structure during halothane anesthesia remains undetermined.

Animals↗
PubMed1979

Halothane-induced renal vasodilation.

Halothane-induced changes in renal function have generally been attributed to alterations in systemic hemodynamics, sympathetic tone, and various hormones. Studies were performed to determine whether halothane directly affects the kidney. Twenty-one canine kidneys were perfused in vitro utilizing hemodilution, pulsatile flow, and membrane oxygenation. Temperature and arterial blood-gas variables were controlled and mean and pulse pressures were maintained. Four experimental periods (I-IV)(each consisting of two 10-min sample collection periods) were conducted, with a 20-min "rest" period between succeeding experimental periods (elapsed time = 140 min). Responsiveness was assured by obtaining a normal response to furosemide, acetylcholine, or epinephrine after Period IV. In eight additional kidney preparations halothane was administered to achieve either a "low" (17 +/- 3 mg/100 ml) or "high" (35 +/- 5 mg/100 ml) concentration in Period II, the sequence reversed for Period III, and halothane eliminated by Period IV. Halothane produced marked increases in blood flow (21-26 per cent), total (203-267 per cent) and fractional (173-179 per cent) sodium excretion, osmolal clearance (62-111 per cent) and urinary volume (130-161 per cent). These changes were associated with a shift of microspheres from outer to inner cortex, and were completely reversible by eliminating the halothane. In the absence of external influences, halothane produces renal vasodilation and natriuresis. Direct tubular depression cannot be ruled out.

Acetylcholine↗
PubMed1980

Brain intracellular pH, blood flow, and blood--brain barrier differences with barbiturate and halothane anesthesia in the cat.

The effects of various depths of barbiturate and halothane anesthesia and different arterial blood carbon dioxide tensions (PaCO2) at uniform levels of anesthesia on brain pH, tissue indicator perfusion, and blood flow were studied in 40 cats. Brain pH was measured using a lipid-soluble, pH-sensitive fluorescent indicator (umbelliferone), and its clearance was determined from the slope of its washout curve. Cerebral blood flow (CBF) was determined from the clearance of intra-arterially injected xenon-133. Values for CBF were higher in the halothane-exposed group, and with deep anesthesia they did not decrease as much as did those seen with pentobarbital (47 vs. 27 ml/100 g/min). The barbiturate brain pH-arterial blood PaCO2 regression line had a steeper slope than the corresponding halothane line. The two lines crossed at PaCO2 42 torr and brain pH 7.15. Brain pH was directly related to both PaCO2 and depth of anesthesia in the halothane-exposed group but only to PaCO2 in the barbiturate-exposed group. If light halothane anesthesia (0.1 per cent) can be considered almost equivalent to the waking state, then both anesthetics produce relative brain alkalinity. The clearance of the pH indicator was only modestly sensitive to changes in PaCO2 at anesthetic levels of pentobarbital and halothane. It was not significantly changed by increasing the amount of pentobarbital. However, increasing levels of halothane produced a decrease of more than 50 per cent in its clearance (63 ml/100 g/min at 0.1 per cent vs. 29 ml/100 g/min at 3 per cent). It is concluded that umbelliferone provides a reliable method for the measurement of brain pH and possibly a useful tool for studies of the blood-brain barrier.

Anesthesia, General↗