Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Raman spectroscopy has been used to monitor the concentration of halothane (1-bromo-1-chloro-2,2,2-trifluoroethane) in 20% aqueous dispersions of dipalmitoylphosphatidylcholine (DPPC) as well as to follow changes in the acyl chain order within the hydrocarbon interior of the liposomes. Temperature profiles for the gel to liquid-crystalline phase transitions for the liposomes were constructed from changes in peak height intensity ratios in the C-H stretching mode and C-C stretching mode regions. Halothane present at the clinical level produces a change of -0.5 degrees C in the phase transition temperature. A limiting transition temperature of about 21 degrees C and saturation of the gel phase occur when the molar ratio of halothane to DPPC reaches about 1.25. At molar ratios above 2.1, the liquid-crystalline phase is also saturated with halothane. Calculations of the distribution of halothane between the various phases in the system are presented and used to interpret literature data as well as the present experiments. Ideal solution theory accounts rather well for the depression in the transition temperature over most of the mole ratio range, an outcome which implies that halothane is excluded from the hydrocarbon interior but not the head-group region in the gel phase. The role of halothane in the head-group region is discussed.
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PMID:Effects of halothane on dipalmitoylphosphatidylcholine liposomes: a Raman spectroscopic study. 360 27

The effect of halothane on myocardial contractility was studied in isolated right ventricular muscle preparations from newborn and adult rabbits. Right ventricular strips were mounted in oxygenated Krebs' solution and stimulated with supramaximal voltages at 1.0 Hz, while isometric force of contraction was continuously recorded. Halothane (0.4, 0.7, and 1.1%) caused a significant dose-dependent depression of both peak developed tension (42, 61, and 70%, respectively) and maximum rate of rise of isometric tension (40, 56, and 64%, respectively) of newborn myocardium. Newborn myocardial preparations exhibited approximately 20% greater depression of contractility than adult myocardium at each concentration studied (P less than 0.05), thus a parallel shift of the dose-response curves was observed. It was concluded that halothane exerts a potent depressant effect on newborn myocardium that is greater than that on adult myocardium. The depression effect of halothane on the newborn myocardium may contribute to its hypotensive effect in newborn infants.
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PMID:Comparison of the effects of halothane on newborn and adult rabbit myocardium. 368 96

Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent-induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMRO2 of 3.21 +/- 0.17 (SEM) ml X 100 g-1 X min-1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMRO2 of 1.76 +/- 0.16 ml X 100 g-1 X min-1. In rabbits receiving a background of morphine sulfate/N2O, halothane resulted in a significantly greater CBF (65 +/- 10 ml X 100 g-1 X min-1) than did isoflurane (40 +/- 5 ml X 100 g-1 X min-1). Both agents caused a reduction in CMRO2, but CMRO2 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the direct cerebral vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit. 377 75

Nine patients with unilateral ponto-cerebellar tumour, one with epidermoid, eight with acoustic neuroma had intraoperative monitoring of the brainstem auditory evoked potentials (BAEP) using bilateral scalp recording (Cz-A1 and Cz-A2) and binaural stimulation in order to monitor brainstem function during the surgery. Results were correlated with preoperative and postoperative BAEP findings. There was some intraoperative BAEP change in all the patients. Halothane anaesthesia caused bilateral wave V. prolongation in six patients. Lumbar drainage produced ipsilateral or bilateral wave V. prolongation in three of four patients in whom lumbar drainage was established. Opening the dura produced ipsilateral or bilateral wave V. depression or bilateral prolongation in four patients. Tumour dissection caused BAEP changes in all the patients: bilateral prolongation or depression in five patients, and ipsilateral prolongation and/or depression in six patients, three of them together with bilateral changes. The only patient who had no changes in wave I-IV. but in whom a big wave VI. appeared at the tumour side during removal, had epidermoid tumour. At the end of surgery there was some improvement in all patients, but in two the improvement was not striking: in one BAEP remained flat ipsilaterally, and in other, latency did not improve. All the patients had a good clinical recovery a few days later, but the control BAEP performed from the 3rd-7th postoperative day was not yet completely recovered in four patients. Intraoperative BAEP monitoring can be a useful technique to monitor brainstem function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of brainstem auditory evoked potentials during posterior fossa surgery as a monitor of brainstem function. 378 75

During normovolemia, nitrous oxide causes mild sympathetic stimulation and direct myocardial depression; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during hypovolemia this balance would change and depression predominate, 10 swine were made hypovolemic (30% blood loss) and then were given 70% N2O (0.25 MAC in swine) or an equipotent concentration of halothane, an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same hypovolemic swine on another day. Five minutes after induction of anesthesia during hypovolemia, both N2O and halothane caused significant, physiologically important deterioration of compensation for hemorrhage. Halothane decreased systemic vascular resistance (SVR); N2O was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, stroke volume, oxygen consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma renin activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma norepinephrine concentration increased only in the N2O group and was greater in that group than in the halothane group. The deterioration of cardiovascular compensation for hemorrhage was expressed metabolically by similar decreases in the two groups in partial pressure of oxygen of mixed venous blood and by increases in blood lactate concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular actions of nitrous oxide or halothane in hypovolemic swine. 390 22

Synaptosomes isolated from rat cerebra were used to study the effects of the inhalational anesthetic, halothane, on cholinergic processes. To identify possible mechanisms responsible for the depression of acetylcholine synthesis, we examined the effects of halothane on precursor metabolite metabolism involved with supplying the cytosol with acetyl-CoA for acetylcholine synthesis. Three percent halothane/air (vol/vol) depressed 14CO2 evolution from labeled pyruvate and glucose. Steady-state 14CO2 evolution from [1-14C]glucose was depressed 84% by halothane, while 14CO2 evolution from [6-14C]glucose and [3,4-14C]glucose was decreased 67 and 52%, respectively, when compared with control conditions. Halothane inhibited the activities of both pyruvate dehydrogenase (14% depression) and ATP-citrate lyase (32% depression). Total synaptosomal acetyl-CoA concentrations were unaffected by halothane. Three percent halothane/air (vol/vol) caused a 77% increase in medium glucose depletion rate from 1.38 nmol (mg protein)-1 min-1 to 2.44 nmol (mg protein)-1 min-1. Production of lactate by the synaptosomes in the presence of halothane increased by 231% from a control rate of 1.44 nmol (mg protein)-1 min-1 to 4.77 nmol (mg protein)-1 min-1. Lactate production rate from pyruvate was also enhanced by 56% in the presence of halothane. These data lend support to the concept that the NAD+/NADH potential may be involved in the halothane-induced depression of acetylcholine synthesis.
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PMID:Halothane-induced alterations of glucose and pyruvate metabolism in rat cerebra synaptosomes. 392 66

The hemodynamic and cardiovascular effects of isoflurane and halothane anesthesia were studied in 15 unpremedicated ASA I children using measurements of heart rate, blood pressure and M-mode echocardiography (echo). The children (ages 2 to 7.3 yr) were randomly assigned to receive either isoflurane (N = 8) or halothane (N = 7) with oxygen. End-tidal carbon dioxide concentrations (range 30-44 mmHg) were monitored throughout the study in each child. The experimental protocol was completed prior to intubation and the initiation of surgery. Within each anesthetic group, preinduction (control) hemodynamic and echo measurements were compared with measurements obtained at two sequential equipotent end-tidal anesthetic concentrations (0.74% and 2.22% isoflurane; or 0.5% and 1.5% halothane). We also compared the data of the isoflurane group with that of the halothane group at each equipotent end-tidal anesthetic concentration. Preinduction hemodynamic (heart rate, blood pressure) and echo measurements (left ventricular dimensions and function) were similar between the two anesthetic groups. With isoflurane or halothane administration, blood pressure decreased significantly, while heart rate remained essentially unchanged. The observed alterations in heart rate and blood pressure were similar in both study groups at each equipotent end-tidal anesthetic concentration. In contrast, there were marked differences in the echo measurements of the two anesthetic groups. Halothane was associated with a significant dose-dependent decrease in echo-measured left-ventricular shortening fraction and mean velocity of circumferential fiber shortening. These echo measurements were not significantly altered by isoflurane at either end-tidal anesthetic concentration. These alterations suggest halothane is associated with significant myocardial depression in normal children, while myocardial function is well preserved during isoflurane anesthesia.
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PMID:The hemodynamic and cardiovascular effects of isoflurane and halothane anesthesia in children. 395 27

The effects on baroreflex control of heart rate of halothane or methohexitone used to supplement 67% nitrous oxide in oxygen have been studied in 21 patients. Stable anaesthesia with either agent caused depression of baroreflex sensitivity by more than 50%. The set point of the reflex was also changed by both agents, but in opposite directions. Halothane administration resulted in slower heart rates at lower arterial pressures, whereas the infusion of methohexitone caused faster heart rates at lower arterial pressure. During recovery from anaesthesia, there was a rapid return of baroreflex sensitivity to normal and this was achieved before the patients regained consciousness, with no difference between the two groups. The reflex was reset rapidly and repeatedly during the recovery phase.
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PMID:Restoration of baroreflex control of heart rate during recovery from anaesthesia. 395 22

The combined depressant effects of verapamil and halothane on myocardial contractility were studied using isolated papillary muscle from the rabbit. Verapamil alone (0.5 microM) significantly decreased peak developed tension (PDT) by 15 +/- 2%, time to peak tension (TPT) by 10 +/- 1%, and maximum rate of increase of tension (+dT/dt) by 5 +/- 1%, but not maximum rate of decrease of tension (-dT/dt). Halothane alone (0.8%) significantly decreased PDT by 56 +/- 2%, TPT by 11 +/- 2%, +dT/dt by 53 +/- 2%, and -dT/dt by 56 +/- 2%. During the exposure period, the combination of verapamil and halothane together produced a simple additive effect (no significant interaction effect by two-way analysis of variance), with PDT decreased by 68 +/- 2%, TPT by 20 +/- 3%, +dT/dt by 62 +/- 2%, and -dT/dt by 65 +/- 2%. The reversibility of halothane-induced depression was also studied. Peak developed tension showed complete reversibility 30 min after discontinuing halothane. In the presence of verapamil, however, the reversibility of halothane-induced depression was not complete, and significant residual depression of PDT (19 +/- 3%) was observed. We conclude that the acute depressant effect of verapamil plus halothane in isolated papillary muscle is additive, but reversibility of halothane-induced depression may be impaired or prolonged in the presence of verapamil.
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PMID:Interaction of halothane and verapamil in isolated papillary muscle. 396 31

It is reported that benzodiazepines such as diazepam will stimulate the opiate receptor system and that B-carboline drugs, which are benzodiazepine antagonists, may interact with opiate receptors directly. The ability of 3-hydroxymethyl-B-carboline (3-HMC) to antagonize several parameters of fentanyl anesthesia was tested here in rats. Fentanyl (25 and 100 micrograms/kg iv) produced dose dependent depression of cerebral blood flow (CBF), measured by radioactive microspheres, and cerebral oxygen consumption (CMRO2). These effects were significantly inhibited by 10 mg/kg 3-HMC iv. To test for the specificity of this effect, 3-HMC was also given to rats ventilated with inspire concentrations of 2% halothane. Halothane depressed CMRO2 equally in 3-HMC and vehicle treated rats, indicating no significant effect of the benzodiazepine antagonist. Blood pressure was increased in 3-HMC compared to vehicle treated animals during both fentanyl and halothane anesthesia. CBF was increased in 3-HMC vs vehicle treated rats during halothane anesthesia but this could be accounted for by the elevated blood pressure and lack of cerebral autoregulation rather than a direct cerebrovascular effect. 3-HMC decreased the sleep time and respiratory depressant effects of fentanyl but enhanced the analgesic effects of the opiate, as measured by time to respond to a hot plate stimulus. These results indicate that 3-HMC has the ability to specifically antagonize fentanyl anesthesia. These effects may be produced by an action of 3-HMC at the benzodiazepine receptor and/or by an action of the B-carboline at opioid receptors.
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PMID:A benzodiazepine antagonist inhibits the cerebral metabolic and respiratory depressant effects of fentanyl. 399 26


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