halothane brands

Molecular formula: C2HBrClF3

Halothane causes general anaethesia due to its actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Its immobilizing effects have been attributed to its binding to potassium channels in cholinergic neurons. Halothane's effect are also likely due to binding to NMDA and calcium channels, causing hyperpolarization. The precise mechanism by which inhalation anesthetics produce loss of perception of sensations and unconsciousness is not known. Inhaled anesthetics act at many areas of the CNS. The Meyer-Overton theory suggests that the site of action of inhaled anesthetics may be the lipid matrix of neuronal membranes or other lipophilic sites. Anesthetics may cause changes in membrane thickness, which in turn effects the gating properties of ion channels in neurons. Interference with the hydrophobic portion of neuronal ion channel membrane proteins may be an important mechanism. In vitro muscle contracture tests for malignant hyperthermia screening are routinely performed using standardized protocols. In the present study online monitoring of halothane concn in the gas phase was demonstrated to be an improved test standard. The kinetics of halothane concn and their effect on in vitro muscle contracture tests were evaluated in two test baths, I and II, which contained 3 and 18 ml Krebs-Ringer solution, respectively. The equilibration kinetics for halothane was significantly faster in bath I (half-life = 8.2 sec) compared with bath II (half-life = 25.6 sec). Twenty one pairs of muscle bundles from 21 potentially malignant hyperthermia susceptible patients were investigated, each test bath receiving one bundle from each pair. The variance of muscle contractures was significantly increased in test bath I compared with test bath II. However, there was no influence on malignant hyperthermia diagnosis, suggesting that, within the ranges of half-life = 8.2 sec-25.6 sec, the test bath volumes need not be standardized. Volatile anesthetics inhibit phagocytic cell function, yet little is known about their effects on target tissues or on the target tissue response to stimulated phagocytes. Experiments were performed to determine how exposure to halothane and isoflurane changes rat pulmonary artery endothelial cell viability in response to the toxic oxygen metabolites produced by stimulated phagocytic cells. Rat pulmonary arterial endothelial cells were grown in monolayer culture. The monolayers were treated with phorbol myristate acetate stimulated human neutrophils at an effector-to-target ratio of 20:1 after equilibration with 0.4% or 1.7% halothane or 0.7% or 2.8% isoflurane. As measured by percent specific release of incorporated (51)Cr label (mean + or - standard error), cytotoxicity in the presence of 1.7% halothane (75.3 + or - 3.4%) was significantly greater (p< 0.02) than cytotoxicity in 5% carbon dioxide in air (44.7 + or - 3.3%) and in 0.4% halothane (57.3 + or - 4.7%). Also, cytotoxicity in 1.7% halothane was significantly greater than in 0.4% halothane (p< 0.02). It was found that rat pulmonary arterial endothelial cells incubated in isoflurane exhibited significantly greater release of (51)Cr than cells incubated in the MAC equivalent concn of halothane: 78.2 + or - 2.6% in 0.7% isoflurane (p= 0.0004) and 83.8 + or - 1% in 2.8% isoflurane (p= 0.005). Because early neutrophil cytotoxicity has been found to be mediated primarily by hydroxyl radical and hydrogen peroxide, hydrogen peroxide production by similar numbers of phorbol myristate acetate stimulated neutrophils under similar exposure conditions was measured. In carrier gas, phorbol myristate acetate stimulated neutrophils produced 20.5 + or - 1.3 nmole hydrogen peroxide/1X10+6 cells/hr. At the higher concn of halothane, hydrogen peroxide production actually was inhibited in comparison with carrier gas (15.4 + or - 1.4 nmole hydrogen peroxide/1X10+6 cells/hr in 1.7% halothane and 16.8 + or - 0.8 in 2.8% halothane),

Source: PubChem (NCBI) · compound 3562