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

The chronotropic effects of all currently available volatile anesthetics were investigated in isolated rat atrial preparations. Anesthetic ethers, diethyl ether, methoxyflurane, and enflurane elicited a dose-dependent positive chronotropic effect. Fluroxene produced a slight depression at low concentrations. The halogenated hydrocarbon anesthetics, halothane, chloroform, and trichloroethylene, did not show a uniform pattern. Halothane's effect was small and biphasic. Chloroform caused a dose-dependent decrease in heart rate, and trichloroethylene caused a marked positive chronotropic effect. The dose-response curves in all anesthetics remained unaltered in the presence of either 3 x 10(-7) M dl-propranolol or 1 x 10(-6) M atropine. It is concluded that volatile anesthetics elicit significant direct chronotropic actions on rat atrial preparations. The mechanism of their actions does not involve stimulation of beta-adrenergic or cholinergic receptors.
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PMID:Mechanisms of chronotropic effects of volatile inhalation anesthetics. 1 71

Halothane, methoxyflurane, and enflurane produce dose-dependent depression in ventricular function in the dog. Myocardial blood flow and oxygen consumption are decreased accordingly without evidence of myocardial tissue hypoxia. Low-dose fluoxene does not depress the heart, while there is less depression with high-dose fluroxene than with the other anesthetics. In spite of this depression, myocardial blood flow was unchanged, and the decreased oxygen consumption during high-dose fluroxene was a result of decreased oxygen extraction by the heart. Sympathetic nervous system stimulation produced by fluroxene anesthesia is probably responsible for these effects, but further work is necessary for confirmation of this hypothesis.
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PMID:Dose-dependent depression of cardiac function and metabolism by inhalation anesthetics in chronically instrumented dogs. 2 4

Like all inhalation anesthetics, halothane (CF3CHBrCl) has a dose-dependent negative inotropic effect on cardiac muscle. The mechanism of the action has not been determined, although effects on glycolysis, mitochondrial respiration and calcium kinetics, and sarcoplasmic reticulum ATPase activity have been suggested. Previous studies of the effect of halothane on the ATPase of contractile protein suffered from design and dosing defects. We have measured ATP splitting by canine cardiac natural actomyosin using extraction and equilibration procedures described previously (Honig, C. R. and Reddy, Y. C. 1973, J. Pharmacol. 184: 330-338). Drug dosing calculations were facilitated by measurement of the partition coefficient of halothane in protein. Halothane shifted the Ca++ concentration effect curve for actomyosin ATPase activity to the right. The maximum depression occurred at pCa 7.0 or 6.5. The effect was dose dependent with less than 10 percent depression at threshold and 50-60 percent depression at peak. Enzyme inhibition was antagonized by high Ca++ concentration, and was reversed by removing halothane from the reaction mixture. We suggest that inhibition of ATP utilization by the contractile system may be a mechanism of the in vivo myocardial depression produced by halothane.
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PMID:Halothane decreases actomyosin ATPase activity: a possible mechanism of the negative inotropic effect. 12 60

The effects of ether, chloroform, and halothane on calcium accumulation and ATPase activity of rat heart microsomes and mitochondria as well as on myofibrillar ATPase activity were investigated. Chloroform and halothane depressed microsomal and mitochondrial calcium uptake and binding in a parallel fashion. Ether decreased microsomal calcium binding and mitochondrial calcium uptake to varying degrees, while mitochondrial calcium binding was slightly enhanced. Whereas ether had no effect, chloroform depressed microsomal and mitochondrial total APTase activities and halothane decreased microsomsl ATPase and slightly stimulated mitochondrial total ATPase activities. Halothane was found to depress myofibrillar Mg2+-ATPase and ether was capable of decreasing myofibrillar Ca2+-ATPase. Chloroform was seen to inhibit both myofibrillar enzymes. These results suggest that the cardiodepressant actions of volatile anesthetic agents may be due to alterations in the calcium accumulating abilities of microsomal and mitochondrial membranes while direct myofibrillar effects may contribute to the depression seen with relatively higher concentrations of anesthetics.
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PMID:Subcellular effects of some anesthetic agents on rat myocardium. 15 65

Experiments were performed to determine whether depression of venomotor responses with halothane results from interference with sympathetic activation or from an effect on venous smooth muscle cells. Changes in isometric tension of isolated canine saphenous-vein strips were recorded. Adrenergic activation was achieved by transmural electrical stimulation, by addition of tyramine, and by addition of morepinephrine. Halothane (0.5 to 3 per cent) did not significantly alter basal tension. It lessened the reaction of the veins to electrical stimulation but not their response to norepinephrine; it increased the response to tyramine. Since the responses to norepinephrine and tyramine were not decreased, halothane appears to act on the nerve terminal to prevent release of neurotransmitter associated with nerve-terminal depolarization. Thus, halothane causes inhibition of electrically induced venoconstriction in cutaneous veins, probably by interfering with the release of norepinephrine from nerve terminals rather than by an inhibitory effect on the smooth muscle cells.
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PMID:Venomotor changes caused by halothane acting on the sympathetic nerves. 23 34

Changes in heart rate and arterial pressure caused by enflurane and halothane anaesthesia were investigated in patients premedicated with diazepam and scopolamine. Enflurane caused a significant (12%) increase in heart rate and depression of arterial pressure (23%). Halothane depressed heart rate significantly (14%), whereas arterial pressure was unaffected. The authors conclude that enflurane possesses a positive chronotropic effect.
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PMID:Heart rate changes caused by enflurane and halothane anaesthesia in man. 27 56

In order to study the influence of two inhalational anaesthetics on metabolic activity of macrophages, we exposed alveolar macrophages (AM) from guinea pigs to both nitrous oxide (N2O) and halothane-N2O in vitro. We examined the enzymatic activity, which is bound to an intact metabolic phase, by application of the triphenyltetrazolium-chloride test (TTC-test). The content of the enzymatically to formazan reduced TTC was measured spectro-photometrically. Incubation of AM for 60 min in 1 to 4 percent halothane vaporized in air produced only a minimal, statistically insignificant depression of TTC reduction activity (TTC-RA). Halothane plus N2O-O2 (80:20) caused a statistically significant depression of TTC-RA. The reponse is graded in relation to the halothane dose. Exposure to monoanaesthesia with N2O also resulted in reduction of metabolic activity. These data demonstrate that inhalational anaesthetics inhibit the capability of AM to reduce TTC.
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PMID:[TTC-reducing activity of alveolar macrophages under the influence of halothane and nitrous oxide (author's transl)]. 43 25

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.
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PMID:Halothane-induced renal vasodilation. 43 86

A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P less than .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V5 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.
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PMID:Indices of myocardial oxygenation during coronary-artery revascularization in man with morphine versus halothane anesthesia. 43 35

Halothane (0.05--1.7 vol per cent end-tidal) in nitrous oxide (N2O), 60 per cent: oxygen (O2), 40 per cent was administered to nonmedicated, closed-chest pigs. Ventricular function was analyzed from cardiac output (thermodilution) and left ventricular (LV) pressure indices. Ventricular volumes and compliance were estimated from single and biplane LV angiography. In separate experiments, the effects of N2O, time, and the angiographic dye injections were shown to be minimal. Halothane caused dose-dependent decreases in aortic blood pressure, cardiac output, peak first derivative of left ventricular pressure (LV dP/dt), the in-vivo maximum velocity of fiber shortening (Vmax), and ejection fraction; non-dose-dependent decreases in heart rate and circumferential fiber shortening rate. Although a pronounced dose-related negative inotropic effect of halothane in the pig heart was demonstrated, there was no definite effect on ventricular pressure-volume relationships (compliance). If there was any such effect of halothane, it was obscured by the cardiac depression produced.
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PMID:Left ventricular function and compliance in swine during halothane anesthesia. 45 58


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