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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is known that narcotics reduce the alveolar concentration of inhalation anesthetics in man and animals. However the magnitude and duration of narcotic effect on inhalation anesthesia is not known. Accordingly, I determined in dogs the temporal effect of various doses of pentazocine, a commonly used anesthetic adjuvant, on the minimum alveolar concentration (MAC) of halothane. In addition, I compared plasma pentazocine concentrations in dogs both awake and during halothane anesthesia using an identical intramuscular dose of pentazocine. Intramuscular injection of pentazocine, group II (2.5 mg/kg), group III (5 mg/kg), group IV (10 mg/kg) reduced MAC of halothane required for anesthesia. The magnitude of MAC depression were 19.3% of control halothane MAC in group II, 36.4% of control in group III and 41.7% of control in group IV. Postinjection plasma concentration was fitted by computer with a 2-compartment open pharmacokinetic model. Plasma pentazocine concentration for awake (group I) and anesthetized (group II) dogs given the same dose (2.5 mg/kg) did not differ significantly on biological half-life, total apparent volume of distribution and body clearance. Halothane minimum alveolar concentration (MAC) was correlated to plasma pentazocine concentration (r= -0.60) and cerebrospinal fluid pentazocine concentration (r= -0.74).
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PMID:[Halothane-pentazocine interaction in dogs (author's transl)]. 46

Halothane (H), kanamycin (KM), streptomycin (SM), and chloramphenicol (CM) had direct negative inotropic effects on isometric contractions of isolated rat-heart muscles. Potassium penicillin-G did not show any significant changes in isometric contractions. The depression produced by these antibiotics was characterized by an abrupt onset, rapid progression, and rapid complete recovery, which suggests direct physicochemical rather than metabolic effects. On the other hand, the depression produced by H progressed slowly. When KM, SM, or CM were combined with H, there was a greater depression in isometric contractions than seen in the absence of H, suggesting that the innate characteristics of the antibiotics are augmented when any of them is administered together with halothane.
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PMID:Interaction of halothane and antibiotics on isometric contractions on rat-heart muscle. 56 Jan 38

Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.
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PMID:Acetate fails to reverse myocardial depression in dogs anesthetized with halothane. 56 99

The influence of halothane, or naloxone, or halothane followed by naloxone was investigated in the in vitro myenteric plexus longitudinal muscle preparation of the guinea pig ileum. Halothane alone in 1.5 to 2.0% (v/v) concentration caused about 50% depression of the twitch and decreased both spontaneous acetylcholine (ACh) release (p less than 0.02) and volley output of ACh (p less than 0.02). Very high concentrations (greater than 1 micron) of naloxone caused a nonspecific, postsynaptic depression of the twitch. Higher than 100 nM concentrations of naloxone increased spontaneous ACh release, but had no effect on the volley output of ACh. Over a wide concentration range, from 15 nM to 3 micron, naloxone did not antagonize in the longitudinal muscle preparation the effects of halothane on any of the parameters investigated. These findings indicate that the sites of action of halothane and naloxone in this preparation are not identical.
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PMID:Naloxone fails to antagonize halothane-induced depression of the longitudinal muscle of the guinea pig ileum. 57 Dec 52

The neutrophil granulocytes of 43 patients undergoing general anesthesia and operation were examined to determine if altered function occurs during these procedures. Neutrophil chemotaxis, random migration, and total and differential leukocyte counts were determined immediately before anesthesia; after 35 to 60 minutes of anesthesia but before operation; 60 minutes after initiation of operation; and 60 minutes after operation. Anesthetic agents included 1 to 3.5% enflurane, 0.5 to 2% halothane, or 0.5 to 1.1 mg/kg of morphine plus N2O-O2 (60:40). Neutrophil and total white blood cell counts were uninfluenced by any of the anesthetics; however, marked rises in both occurred during operation and persisted postoperatively after each of the anesthetic technics. Neutrophil chemotaxis was reduced an average of 36, 32, and 21%, respectively, by halothane, enflurane, and morphine before operation and 20, 10, and 5% intraoperatively. Preoperative reductions in chemotaxis were statistically significant after all anesthetics. However, only halothane produced a significant intraoperative reduction in chemotaxis. Postoperative neutrophil chemotaxis did not differ from control (preanesthesia) values after any of the anesthetics. Halothane and enflurane reduced leukocytic random migration before but not after operation. Morphine had no effect on random migration at any time. These data demonstrate that anesthesia impairs neutrophil function in man but that operation appears to reverse this depression.
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PMID:Neutrophil chemotaxis during and after general anesthesia and operation. 78 49

Halothane depresses myocardial blood flow and metabolism in the dog, but no studies in man have been published. However, the coronary circulation of the pig is remarkably similar to that of man. The authors investigated the effects of halothane-nitrous oxide anesthesia on cardiac function and metabolism in piglets. Thermodilution cardiac output, catheter-tip-manometer measurement of left ventricular function, electro-magnetic flowmeter measurement of coronary blood flow, and blood and tissue measurements of gases and metabolites were made during 0.04 (control), 0.46 (low concentration), and 1.04 (high concentration) per cent halothane vaporized in nitrous oxide, 60 per cent: oxygen, 40 per cent. Compared with control, the low concentration decreased cardiac output (CO) by 10 per cent, left ventricular systolic pressure (LVSP) by 30 per cent, peak contractile element velocity (Vmax by 34 percent, coronary blood flow (CBF) by 36 per cent, and cardiac oxygen uptake (V02) by 55 per cent. Compared with control, the high concentration decreased CO by 32 per cent, LVSP and Vmax by 53 per cent, CBF by 63 per cent and V02 by 62 per cent. This indicates that the dose-related depression in left ventricular function produced by halothane was accompanied by equivalent decreases in coronary blood flow and oxygen comsumption. There was minimal evidence of anaerobic metabolism in these depressed ventricles. Tissue levels of the high-energy phosplates, adenosinetriphosphate and creatine phosphate, and glycogen were unchanged. It is concluded that changes in cardiac oxygenation and metabolism in the pig during halothane anesthesia result from the changes in ventricular function.
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PMID:Dose-dependent depression of cardiac function and metabolism by halothane in swine (Sus scrofa). 86 Aug 43

The effects of halothane on deoxyribonucleic acid (DNA) synthesis and events preceding DNA synthesis have been examined in Chinese hamster fibroblasts in culture.DNA synthesis was studied by the uptake of 3H-thymidine during short periods of incubation that minimized effects on cells in the presynthetic phase (G1). Halothane produced slight but significant dose-related depression of 3H-thymidine uptake (20 per cent depression with 2 per cent halothane). In a separate series of experiments, synchronized cultures were exposed to 1-3 per cent halothane in G 1 phase for three or five hours. Halothane caused a postponement of onset of DNA synthesis (S phase), indicating a delay in G 1. This delay roughly equalled the duration of exposure to 3 per cent halothane but was less with 2 per cent halothane. The delay was only about one hour with 1 per cent halothane.
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PMID:Effects of halothane on DNA synthesis and the presynthetic phase (G 1) in dividing fibroblasts. 97 93

In an experimental study we tried to find out whether halothane, in addition to its effects on vegetative efferents, has also an influence on catecholamine metabolism of the corresponding brain sections. We studied the effects of halothane in the brain stem of rats on dopamine and norepinephrine contents and on the transformation of L-dopa into dopamine and L-norepinephrine. Anaesthesia with 2 vol% halothane reduced dopamine content by 41.4%, norepinephrine content by 17.8%. These findings could be observed even 3 h after narcosis. Electrophysiological studies show that the central nervous sympathetic activity at rest and after central excitation is clearly reduced during anaesthesia with 2 vol% halothane; 70 min after narcosis it returned to normal. Administration of L-dopa led to an increase of dopamine by 43.5% within 45 min. This transformation of L-dopa into dopamine is not affected by concurrent halothane anaesthesia. There is no increase in norepinephrine after administration of L-dopa. Thus, the effect of halothane on catecholamine metabolism in the brain stem affects the precursors of L-dopa. Halothane is said to inhibit transport of the L-dopa precursor L-tyrosine from plasma to brain tissue. Along with such an inhibition goes the depression of the sympathetic activity. In this respect and obviously on the basis of its position within the catecholamine metabolism, dopamine is more important than norepinephrine.
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PMID:[Effect of halothane on catecholamine metabolism in the brain stem of rats]. 98 21

1 The effects of general anaesthetics on the responses of neurones to iontophoretically applied L-glutamate have been examined in slices of the guinea-pig olfactory cortex in vitro. 2 Concentrations of pentobarbitone, ether, methoxyflurance, trichloroethylene and alphaxalone that are known to depress synaptic transmission in the prepiriform cortex also depressed the sensitivity of prepiriform neurones to L-glutamate. 3 Halothane, in concentrations that depress synaptic transmission (less than 1%) did not alter sensitivity of neurones to glutamate. Higher concentrations (greater than 1% produced a dose-related depression of the glutamate sensitivity of neurones. 4 All four volatile anaesthetics tested caused some cells to alter their glutamate-evoked firing pattern to one in which the spike discharges were more closely grouped. Pentobarbitone and alphaxalone had no such effect. 5 If the sensitivity of the neurones to the endogenous excitatory transmitter is affected by anaesthetics in the same way as the glutamate-sensitivity, these results suggest that halothane depresses synaptic transmission by decreasing the amount of transmitter released from the nerve terminals, whereas the other anaesthetics depress the sensitivity of the post-synaptic membrane to the released transmitter.
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PMID:Anaesthetics depress the sensitivity of cortical neurones to L-glutamate. 99 May 90

In an effort to compare the effects of anesthetics on cardiac functions and metabolism, mongrel dogs were anesthetized with morphine (3 mg/kg, N2O 50% in oxygen) or halothane (0.7%, N2O 50% in oxygen). Hb, Ht, pO2, pCO2, pH, O2 content, lactate, and pyruvate in the arterial and coronary sinus blood were measured and ECG, LVP, CVP, AP, and CO were recorded. Aorta was cross-clamped for 30 min under cardiopulmonary bypass (CPB). Hemodynamic and metabolic survey were continued until 120 min of recovery period. Results were as follows: Hemodynamics, such as LVP, AP, and CO, were depressed after CPB, then gradually returned to control level. Subendocardial ischemia observed through ST depression and QRS widening on ECG, as well as DPTI/TTI ratio under 1.0, disappeared in the recovery period. Lactate was produced by the heart after anoxic arrest and was extracted at 120 min after CPB. Halothane and morphine did not show any significant differences of effects on cardiac function and metabolism in this study.
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PMID:Effects of morphine and halothane on canine cardiac function before and after cardiopulmonary bypass. 103 47


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