Influence of halothane, pentobarbital, carbon dioxide and ether anaesthesia on high-energy phosphate levels in mouse and frog skeletal muscle

Three-week-old CD-1 mice infected with the PR-8 (mouse-adapted) strain of influenza virus while exposed to enflurane demonstrated a decrease in virus titers from the lungs of infected animals, less abnormality of lung histology, and an increase in survival in animals as compared with those receiving the other anesthetics tested. Greater than 90% mortality occurred in groups of mice which inhaled aerosolized virus and received no anesthesia, pentobarbital, diethyl ether, or halothane anesthesia 96 h following infection. Infected mice anesthetized with enflurane 96 h post-infection had significantly lower mortality rate (68%) when compared with the other groups. Halothane-anesthetized mice receiving intranasal influenza virus during anesthesia demonstrated increased survival and a delay in the mean day of death when compared with animals receiving either diethyl ether of pentobarbital anesthesia. Animals receiving enflurane during virus inoculation had an even lower mortality rate and a later mean day of death when compared with infected animals receiving day of the other three anesthetics. Examination of lungs from animals infected during anesthesia demonstrated influenza virus titers significantly less in the animals that received enflurane anesthesia when compared with the other groups. Histologic sections of lungs revealed extensive spread of the disease process into the alveoli and interstitium of the lungs of animals infected while receiving pentobarbital or diethyl ether anesthesia. Animals infected during halothane demonstrated pathologic characteristics similar to pentobarbital- and diethyl-ether-treated groups; however, the changes were not as extensive. Mice infected during exposure to enflurane revealed only a mild bronchopneumonia.

The effects of ether and pentobarbital anesthesia on hypothalamic and cerebrospinal fluid (CSF) LH-RH content were studied in male rats. Ether elevated hypothalamic LH-RH 30 min after a 3-min exposure; pentobarbital (30 mg/kgital (30mg/kg) caused no change. The ether-induced increase in LH-RH content was not affected by pretreatment with pentobarbital; however, the increase was abolished in animals subjected to hypothalamic deafferentation. Changes in CSF LH-RH generally paralleled the hypothalamic changes; ether, for example, elicited a significant rise. These results demonstrate the complex hypothalamo-pituitary-CSF interactions which occur in response to general anesthetics.

Changes in the electrocardiogram following bilateral common carotid arteries ligation was observed during the awake state and pentobarbital anesthesia; and the influences of cerebral ischemia, pentobarbital or halothane anesthesia on the cardiotoxicity induced by continuous infusion of ouabain were also studied in Mongolian gerbils. Following ligation, all awake-animals died in about 60 min of ligation, all exhibiting severe neurological symptoms and ventricular arrhythmias. These changes did not appear in the animals under pentobarbital anesthesia. With regards to the amount of ouabain infusion needed to cause cardiotoxicity in pentobarbital-anesthetized animals, there were no significant differences between the vagus-intact group and the vagotomized group. However, the cardiotoxic dose of ouabain in the ligation group during pentobarbital anesthesia was larger than the cardiotoxic dose in the non-ligation group. In halothane anesthesia, the cardiotoxic dose of ouabain decreased more prominently than in pentobarbital anesthesia. The arrhythmias observed with isoproterenol were not enhanced by the halothane anesthesia and vagotomy. Therefore, these findings may indicate that during the cerebral ischemia, there is a heterotopic stimulus formation in the impulse conducting system of the heart; ouabain-induced cardiotoxicity appears to be enhancement via ouabain distribution into the cerebrum; and ventricular fibrillation had no definite effect for lowering sensitization of the myocardium to catecholamine by halothane in Mongolian gerbils.

Laboratories that study Drosophila melanogaster or other insects commonly use carbon dioxide (CO2) anaesthesia for sorting or other work. Unfortunately, the use of CO2 has potential unwanted physiological effects, including altered respiratory and muscle physiology, which impact motor function behaviours. The effects of CO2 at different levels and exposure times were examined on the subsequent recovery of motor function as assessed by climbing and flight assays. With as little as a five minute exposure to 100% CO2, D. melanogaster exhibited climbing deficits up to 24 hours after exposure. Any exposure length over five minutes produced climbing deficits that lasted for days. Flight behaviour was also impaired following CO2 exposure. Overall, there was a positive correlation between CO2 exposure length and recovery time for both behaviours. Furthermore, exposure to as little as 65% CO2 affected the motor capability of D. melanogaster. These negative effects are due to both a CO2-specific mechanism and an anoxic effect. These results indicate a heretofore unconsidered impact of CO2 anaesthesia on subsequent behavioural tests revealing the importance of monitoring and accounting for CO2 exposure when performing physiological or behavioural studies in insects.

The present study determined the effect of halothane on the disposition of morphine by defining the effect of halothane anesthesia on the systemic, renal, and hepatic clearance of the parent compound, morphine, and on the generation of the primary metabolite, morphine-3-glucuronide (M3G) in the dog. Unlabeled morphine, 3H-morphine, and 14C-morphine were simultaneously administered into the portal vein, femoral vein, and renal artery, respectively, first during pentobarbital anesthesia and second during halothane (1.5 MAC) anesthesia; blood samples were taken for estimation of unlabeled plasma morphine and M3G concentrations by high performance liquid chromatography (HPLC). 3H- and 14C-morphine concentrations and corresponding M3G concentrations were determined by dual-channel liquid scintillation counting of the eluant corresponding to the appropriate peak on the HPLC. The portal clearance of morphine was not altered by halothane. However, intravenous (iv) morphine clearance (CLs) decreased (P less than 0.05) by 40% from 963 +/- 131 to 579 +/- 91 ml/min during halothane anesthesia, accompanied by an increase (P less than 0.05) in half-life from 78 +/- 8 to 106 +/- 8 min. The reduction in CLs of morphine occurred putatively on the basis of a halothane-induced decrease in hepatic blood flow, whereas morphine metabolism, reflected by morphine portal (intrinsic) clearance, was not significantly decreased by halothane. There was no significant effect of halothane on the partial metabolic clearance of morphine to M3G, and the ratio of area under the plasma concentration-time curve (AUC)-M3G to AUC unchanged morphine was not significantly altered by halothane, indicating that morphine glucuronidation is unaffected by halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

In rats we assessed the role of the sympathetic nervous system in the increase of plasma renin activity (PRA) following induction of anesthesia by urethane, ether, or pentobarbital and the role of these increased levels of PRA in the maintenance of blood pressure.Urethane and ether induced marked, sustained increases in PRA. Pentobarbital was less effective in this regard. Propranolol inhibited the response of PRA to urethane and ether in a dose-dependent manner but not the renin response to pentobarbital. Similarly, neonatal sympathectomy with 6-hydroxydopamine together with removal of the adrenal medulla prevented the renin response to urethane but not to pentobarbital.Blood pressure changed only slightly during urethane anesthesia, showed a sustained decrease during ether anesthesia, and a gradual return to normal following a marked initial drop during pentobarbital anesthesia. Saralasin pretreatment induced a marked decrease (40–45 mmHg; 1 mmHg = 133.322 Pa) in blood pressure during urethane anesthesia and smaller (10–20 mmHg) additional decreases during ether and pentobarbital anesthesia. In contrast, propranolol pretreatment did not significantly affect blood pressure during ether anesthesia and affected it to a minor degree (by 10–15 mmHg) during urethane and pentobarbital anesthesia.The results indicate that the increases in PRA following induction of anesthesia by urethane or ether, but not by pentobarbital, are mediated through the peripheral sympathetic nervous system via β adrenoceptors. The rennin–angiotensin system appears to be essential for the maintenance of a normal blood pressure during urethane anesthesia but plays a less prominent role in this regard during ether and pentobarbital anesthesia. The propranolol studies suggest that the hypotensive effect of propranolol through blockade of the renin response during urethane- and ether-induced anesthesia is masked by a pressor effect of propranolol.

ArticleBrain CO2 buffering capacity in respiratory acidosis and alkalosis.H Kazemi, D C Shannon, and E Carvallo-GilH Kazemi, D C Shannon, and E Carvallo-GilPublished Online:01 Feb 1967https://doi.org/10.1152/jappl.1967.22.2.241MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByTransport of ions across the choroid plexus epitheliumAcid–base balance and cerebrovascular regulation26 November 2021 | The Journal of Physiology, Vol. 599, No. 24Acid/Base Transporters in CSF Secretion and pH Regulation18 April 2020The choroid plexus sodium-bicarbonate cotransporter NBCe2 regulates mouse cerebrospinal fluid pH12 August 2018 | The Journal of Physiology, Vol. 596, No. 19The murine choroid plexus epithelium expresses the 2Cl−/H+ exchanger ClC-7 and Na+/H+ exchanger NHE6 in the luminal membrane domainHelle H. 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Female hamsters maintained on a 14:10 light-dark schedule with the lights on from 0500 to 1900 were employed to investigate the effects of general anesthetics on the proestrous release of pituitary LH. Ovulation is not blocked in the hamster as in the rat by treatment with pentobarbital (PB) during the critical period. Phenobarbital (Phen) does block ovulation in the hamster if administered at the beginning of the critical period (1300) but fails to block if given two hr later (1500). Neither PB nor ether anesthesia for 2–5 hr blocked ovulation, but did delay the neural stimulus for the ovulatory surge of LH. Ovulation was blocked with Phen administered at 1700 following PB or ether anesthesia from 1300–1700. Deep anesthesia could be maintained for five hr (1300–1800) without blocking ovulation, but six hr under PB or ether prevented ovulation. If the hamsters were allowed to recover for one hr after PB anesthesia from 1300–1500, Phen was ineffective in blocking ovulation. With ether anesthesia from 1300–...

The influence of halothane, pentobarbital, and their interaction on the passage of air across the pulmonary circulation was studied in 12 dogs using transesophageal M-mode echocardiography for air detection in the left atrium and/or aorta. Air was detected in the left atrium and/or aorta after pulmonary artery air injection of 0.04 ml/kg during 1% halothane anesthesia (n = 5). Addition of pentobarbital changed the threshold to 1.0 ml/kg. During pentobarbital anesthesia with and without halothane (n = 7), the thresholds were 1.1 and 1.2 ml/kg, respectively. The authors conclude that the threshold for transpulmonary passage of venous air is higher during anesthesia with pentobarbital with or without halothane than during anesthesia with halothane alone.

Plasma levels of epinephrine which correspond to the arrhythmogenic doses were determined during halothane, enflurane, and pentobarbital anesthesia in the dog. The arrhythmogenic dose was established by a series of 3-min infusion of epinephrine at 10-min intervals. The mean values of the arrhythmogenic doses and the corresponding plasma levels of epinephrine were: 2.18 micrograms X kg-1 X min-1 and 38.7 ng/ml during halothane; 11.43 micrograms X kg-1 X min-1 and 206.3 ng/ml during enflurane; and 15.27 micrograms X kg-1 X min-1 and 296.5 ng/ml during pentobarbital anesthesia. The arrhythmogenic plasma levels of norepinephrine during halothane anesthesia was nearly the same as that of epinephrine.

Hemodynamic alterations and regional myocardial blood flow during supraceliac aortic occlusion in dogs with a critical coronary stenosis

Effects of the use of 5% CO(2) and surface-rewarming or perfusion- rewarming on safe total circulatory occlusion time, blood gases and carbohydrate metabolism were studied in 25 dogs subjected to surface hypothermia (18 C) and 30 minutes of circulatory occlusion under halothane or ether anesthesia. Under halothane anesthesia, all animals with 100% 0(2) developed motor disorders while one of five surface-rewarmed dogs and none of the perfusion-rewarmed dogs developed motor disorders with 5% CO(2). Under ether anesthesia, all were normal with either 100% 0(2) or when 5% CO(2) was added. Ventricular fibrillation occurred in one dog at 21C under halothane anesthesia with 5% CO(2). Blood lactate levels remained low through hypothermic procedures when 5% CO(2) was used. Perfusion rewarming had little effect on lactate levels. The use of 100% 0(2) resulted in slightly higher lactate levels, especially in the ether anesthetized group, but these levels still remained within the upper limit of the normal range. Significant differences in lactate levels between halothane and ether anesthesia suggest different mechanisms of tissue circulation and metabolism during hypothermia. Halothane anesthesia can be useful with the use of CO(2) for surface hypothermia with 30 minutes circulatory occlusion but is still inferior to ether.

The e.c.g., monitored by telemetry, was used to study changes in the heart activity of sheep bled out after electrical stunning or carbon-dioxide anaesthesia. The decrease in ventricular rate which occurs as sheep are bled out after electrical stunning is apparently attributable to increasingly severe anoxia, rather than to changes in blood pressure. The heart rate at sticking is directly related to the heart rate before electrical stunning, but no relationship was found between the wattseconds used and the heart rate at sticking. However, the greater the number of wattseconds applied, the lower the minimum heart rate recorded after sticking. Exposure to carbon dioxide caused an initial tachycardia, followed by a decreased heart rate and then a secondary increase. The rate rose further when the sheep were removed from the gas. As the percentage of carbon dioxide used increased, the duration of heart activity after sticking decreased. Since high stunning currents cause early atrioventricular block, they might adversely affect bleeding out, if this is dependent on heart activity. High concentrations of carbon dioxide results in earlier termination of heart activity and might affect bleeding out similarly. The lower heart rate of sheep before electrical stunning may indicate that it is inherently less stressful than carbon-dioxide anaesthesia and so less likely to affect meat quality.

Electrocardiographic Changes During Surface-Induced Deep Hypothermia: The Influence of Ether, Halothane, Carbon Dioxide, and Perfusion Rewarming

Deformability and Oxidant Stress in Red Blood Cells under the Influence of Halothane and Isoflurane Anesthesia