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

Sensory evoked field potentials were recorded from the mesencephalic reticular formation (MRF), central gray (CG) and somatosensory cortex (SCX), following incremental doses of halothane in freely-moving rats. Halothane concentrations of 0.25%, 0.5% 1.0% and 2.0% were used. In general, the responses from each structure were affected in dose response manner. The averaged acoustic evoked responses (AAER) exhibit more sensitivity to halothane than the averaged visual evoked responses (AVER). The evoked response and its components obtained from each structure were affected differently by halothane mainly following the initial two halothane doses, (0.25% and 0.5%); mainly increase in amplitude was observed in the recording obtained from the MRF, decrease in the CG, and mixed (increase and/or decrease) in SCX. The degree of the depression of the sensory evoked responses was directly correlated to the level of anesthesia as assessed by sural nerve stimulation.
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PMID:Dose effects of halothane on sensory evoked responses obtained from the cortex, reticular formation and central gray. 401 66

The effects of intravenous (iv) nifedipine (7.5 micrograms/kg over 10 min) on systemic hemodynamics and myocardial contractility were investigated under steady state conditions of halothane anesthesia (0.5 MAC) in 8 patients scheduled for elective coronary artery bypass surgery. All patients received long-term medication in the form of beta adrenergic receptor blockers and had a normal global left ventricular function at rest. Halothane produced a marked reduction in left ventricular contractility as documented by a considerable fall in LV max dP/dt. Nifedipine caused a small additional depression of LV max dP/dt without affecting LVEDP significantly. The slight myocardial depressant effect of nifedipine was counterbalanced by a concomitant reduction in left ventricular afterload due to a decrease in the systemic vascular resistance resulting in unchanged or even improved cardiac output. The results indicate that iv nifedipine in the doses used here is safe for patients with ischemic heart disease, even in the presence of already compromised myocardial contractility due to halothane anesthesia and chronic low-dose beta blocker therapy.
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PMID:Cardiovascular interactions of halothane anesthesia and nifedipine in patients subjected to elective coronary artery bypass surgery. 619 57

The effect of halothane on cardiac sarcoplasmic reticulum Ca2+-ATPase activity was studied at low calcium concentrations (0.4-20 microM). Clinical concentrations of halothane (1%-3%, v/v) were found to depress Ca2+-ATPase activity more severely at lower calcium levels than at the higher calcium levels previously reported (greater than 0.1 mM). An increase in calcium concentration in the external medium of a preparation of isolated cardiac sarcoplasmic reticulum vesicles antagonized the halothane-induced depression of the Ca2+-ATPase activity. The depression of calcium-activated ATPase activity by halothane appears to take place by a competitive-type inhibition. The Ca2+-ATPase Vmax remained constant at 0.175 mumole/min/mg of protein with an increasing Km (0.47 microM-4.09 microM). Halothane depression of sarcoplasmic reticulum function may in part explain the ability of halothane to depress myocardial function.
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PMID:Effect of halothane on cardiac sarcoplasmic reticulum Ca2+-ATPase at low calcium concentrations. 621 5

Halothane depresses the inotropic state of the heart, possibly by decreasing the rate of formation of cyclic 3',5'-adenosine monophosphate (cAMP) through depression of the activity of adenylate cyclase, the cAMP-generating enzyme. As catecholamines regulate the inotropic state and adenylate cyclase activity by binding to myocardial beta-adrenergic receptors, the effect of halothane on binding to these receptors was studied to determine whether this was a site of halothane effect. Beta-adrenergic binding was measured at binding equilibrium in vitro in a canine myocardial membrane preparation in the absence and presence of halothane, 3 to 5 vol%, using as the radioligand 3H-dihydroalprenolol (3H-DHA), a beta-adrenergic antagonist with high affinity and radioactivity. In addition, the effect of halothane on the binding of l-isoproterenol, a beta-adrenergic agonist, was measured by displacement of 3H-DHA. The results indicate that halothane has no effect on either the affinity of canine myocardial beta-adrenergic receptors for 3H-DHA or l-isoproterenol, nor does it alter the number of available receptors at binding equilibrium.
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PMID:Halothane effect on beta-adrenergic receptors in canine myocardium. 626 32

The effects of halothane on ganglionic transmission were studied in the stellate ganglion of the guinea pig using intracellular recordings in vitro. Depression of synaptic transmission is one of the actions common to many general anesthetics. The aim of this study was to investigate which of the processes involved in synaptic transmission are affected by halothane in concentrations comparable to those used during surgical anesthesia. The neurons of the stellate ganglion were depolarized using preganglionic nerve stimulation, postganglionic nerve stimulation, and intracellular stimulation before ad after introduction of halothane (vaporizer settings of 0.75% and 1.5% produced bath concentrations of 8 and 18 mg/dl, respectively). Halothane at both concentrations depressed sympathetic ganglionic transmission which was induced by stimulation of preganglionic nerves. Axonal transmission and the excitability of the postganglionic neurons to direct intracellular stimulation was far less sensitive to halothane than synaptic transmission. The depression of ganglionic transmission seen in the present study was most likely due to a decrease in transmitter release although alterations in postsynaptic receptor properties could have been involved as well. The decrease in sympathetic activity resulting from depression of ganglionic transmission probably contributes to the arterial hypotension seen during halothane anesthesia, along with direct myocardial depression, inhibition of catecholamine release from the adrenal medulla, direct action on vascular smooth muscle, and central sympathetic depression.
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PMID:The effects of halothane on sympathetic ganglionic transmission. 629 45

The interaction of halothane anesthesia and intravenous verapamil (0.15 mg/kg over 10 min) was investigated in eight patients scheduled for coronary artery bypass surgery. All patients had a normal left ventricular (LV) function at rest and were on chronic beta-blocker therapy. Halothane produced a marked reduction in mean arterial pressure (MAP), cardiac index, and in LV contractility as documented by a decrease in LV peak positive dP/dt. Verapamil caused an additional depression (16%) of LV peak positive dP/dt accompanied by a small increase (3 mm Hg) in LV end-diastolic pressure. The combined negative inotropic propensities of halothane and verapamil did not produce any overt untoward effects even in the presence of chronic low dose beta-blocker therapy. The predominant hemodynamic effect of verapamil was a systemic vasodilation resulting in a further reduction in MAP (12%) while heart rate remained unaffected. Despite reducing myocardial oxygen demand, caution must be exercised in dose selection in each drug to avoid regional myocardial ischemia due to the combined hypotensive effects of halothane and verapamil.
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PMID:Combined effects of halothane anesthesia and verapamil on systemic hemodynamics and left ventricular myocardial contractility in patients with ischemic heart disease. 633 75

End-tidal Pco2 (petco2) and ventilation of the rat anesthetized with halothane were measured. The Petco2 measured by an infrared analyzer agreed well with the simultaneously measured Paco2 in the range from 20-60mm Hg (2.7-8.0 kPa). When the level of anesthesia was deepened by increasing the halothane concentration from 0.9-3.0%, minute ventilation was decreased progressively accompanied by a rise in Petco2 and the CO2 output was reduced. Halothane induced a progressive decrease in frequency of respiration (f) with almost constant or even slight increase in tidal volume (VT)). Decrease in f was caused largely by the prolongation of expiratory duration (TE). Changes in inspiratory duration (T1) were small and the mean VT/T1 ratio remained unaltered at different levels of anesthesia. These changes in respiratory pattern induced by halothane anesthesia contrasted with the simultaneous decrease in VT, f and VT/T1 ratio and apparent changes of both T1 an TE reported in other species. Species differences in effects of anesthesia on ventilation were discussed. Restraining the rat on a stereotaxic apparatus with head holders, especially with ear bars, elicited an initial transient stimulation of ventilation which was followed by a strong depression.
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PMID:Effect of halothane anesthesia on end-tidal PCO and pattern of respiration in the rat. 646 40

Depressive effect of halothane on carotid sinus baroreceptor function may be due to direct local action, in the CNS, or both. Paris of dogs were anesthetized with pentobarbital and ventilated with oxygen. The carotid sinus of the recipient dog was isolated and perfused with blood from the common carotid artery of the donor dog. Blood from the recipient sinus was returned through its external carotid to the donor common carotid. Thus, both carotid sinuses of the donor and the contralateral carotid sinus of the recipient dog received uninterrupted circulation. Carotid sinus nerve action potentials and lingual artery pressure of the isolated recipient sinus were recorded before and during steady state end-tidal halothane concentrations of 0, 0.5, 1.0, 1.5, 2.0, and 2.5% in oxygen, given randomly first to the donor dog (to evaluate direct local effect) and then to the recipient dog (to determine central effect). The dog not given halothane received pentobarbital. Plots of normalized nerve activity versus halothane concentrations showed approximately zero slope when the donor was given halothane but showed significant decrease in nerve activity when the recipient was given halothane. Halothane appears to have no direct local effect but causes depression of baroreceptor nerve activity, possibly via CNS inhibition of sympathetic efferents to the carotid sinus.
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PMID:Local versus central effect of halothane on carotid sinus baroreceptor function. 646

Alcohol as well as anesthetic and sedative agents depress the respiratory activity of the hypoglossal-genioglossal system more than that of the phrenic-diaphragmatic system. The mechanisms for this selective depression remain unclear. To evaluate the contribution of pathways traversing the spinal cord, the response of phrenic and hypoglossal nerve activities to 0.5% halothane was obtained in decerebrate cats before and after transection of the spinal cord at T1 and again following transection at C1. Halothane produced a much greater decrease in hypoglossal than phrenic activity before and after spinal cord section at T1. Following cord section at C1, which eliminates phrenic activity, 0.5% halothane still produced a marked depression of hypoglossal activity. Therefore, the selective depression of the hypoglossal-genioglossal system does not depend on spinal mechanisms and appears to be mediated in the brain stem.
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PMID:Anesthesia selectively reduces hypoglossal nerve activity by actions upon the brain stem. 648 84

Responses to ligation of the left anterior descending coronary artery (blood pressure, heart rate, ECG, arrhythmias, myocardial tissue loss, and mortality) were investigated in chronically prepared rats anesthetized with one of various halogenated hydrocarbon anesthetics. Halothane (inhaled concentrations of 0, 0.25, 0.5, 1.0, and 2.0%) reduced arrhythmias, mortality, and "S-T" segment changes in the ECG in a dose-related manner. The most effective antiarrhythmic concentrations were 0.5 and 1.0%. Other halogenated hydrocarbon anesthetics (chloroform, enflurane, isoflurane, methoxyflurane, and trichlorethylene) were investigated at minimal anesthetic concentrations. Of these, only chloroform and enflurane reduced arrhythmias. However, both increased mortality as a result of nonarrhythmic causes. At one-half anesthetic concentrations, chloroform (0.25%) and enflurane (0.75%) were not antiarrhythmic and mortality resulting from nonarrhythmic causes was not increased. In the chronically prepared rat, halothane at anesthetic and subanesthetic concentrations has antiarrhythmic actions against ligation-induced arrhythmias, reducing mortality. Of the other halogenated hydrocarbons tested, only enflurane and chloroform had antiarrhythmic actions, however, mortality was high with both agents because of accompanying cardiovascular depression.
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PMID:Effects of halogenated hydrocarbon anesthetics on responses to ligation of a coronary artery in chronically prepared rats. 661 41


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