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

The effects of 1.2, 1.7, and 2.3 MAC enflurane (ENF), halothane (HAL), and isoflurane (ISO) on specialized atrioventricular (AV) conduction times were compared with awake (control) in 23 dogs that were chronically instrumented for His bundle studies. Compared with awake, 1.2 MAC ENF and HAL produced 17% and 18% increases in AV nodal conduction time, respectively. There was little added prolongation related to depth of ENF or HAL. ISO did not prolong AV nodal conduction compared with awake at 1.7 (9%) and 2.3 MAC (12%). All agents produced an approximate 5% increase in His-Purkinje and ventricular conduction times compared with awake, with little additional effect related to depth of anesthesia. In separate experiments in ten of these dogs, anesthetic effects on conduction were determined following combined autonomic blockade with atropine and propranolol. During autonomic blockade, there was no effect of any anesthetic compared with awake, or to increased level of anesthesia, on specialized AV conduction times. The authors conclude that of the major inhalation anesthetics in current clinical use, ISO is least depressant of and ENF and HAL about equally depressant of AV nodal and His-Purkinje conduction times. Furthermore, depression of AV nodal conduction appears to be an indirect rather than direct effect of anesthesia. Finally, most depression of conduction occurs with light anesthesia, with little added depression related to depth of anesthesia over levels likely to be encountered clinically.
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PMID:Conscious-state comparisons of the effects of inhalation anesthetics on specialized atrioventricular conduction times in dogs. 371 34

Haemodynamic effects of 1 MAC halothane, enflurane and isoflurane were studied in 15 healthy children using pulsed Doppler echo cardiography. Heart rate was significantly increased with isoflurane, but not with the other two agents. All three caused comparable decreases in arterial pressure. Cardiac output was increased with isoflurane, but remained unchanged with halothane and enflurane. Aortic peak flow velocity, a sensitive index of myocardial contractility, was decreased with halothane and enflurane, but not with isoflurane. These findings indicate that isoflurane causes less myocardial depression than halothane or enflurane in children.
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PMID:Isoflurane does not reduce aortic peak flow velocity in children. 376 23

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

Changes in haemodynamics and blood gases were investigated before and after administration of 0.5, 1 and 1.5 MAC of halothane, enflurane and isoflurane in respectively 7, 7 and 9 dogs ventilated alternatively with a fraction of inspired O2 in N2 (FiO2) of 0.4 and with brief periods (10 min) of FiO2 of 0.1. Anaesthesia was induced with pentobarbital and the animals were paralysed with pancuronium. Acute hypoxic challenges with FiO2 of 0.1 consistently decreased arterial PO2 to 3.5-4.5 kPa and increased pulmonary vascular resistances by 60-100%. At identical inspired concentrations, as expressed in MAC units, all three inhaled anaesthetics induced a broadly comparable dose-related decrease in systemic blood pressures, due to a depression in cardiac performance as well as a reduction in systemic vascular resistances. Enflurane was the most potent myocardial depressor and isoflurane the most potent vasodilator, halothane being intermediate. Oxygen deprivation was associated with some enhancement of the cardiovascular depressant effects of the inhaled anaesthetics but, in spite of this, matching of O2 transport to tissue O2 demand appeared to be improved, probably in relation to a concomitant reduction in metabolic rate. Only isoflurane inhibited the hypoxic pulmonary pressor response, and this was associated with a slight deterioration in arterial oxygenation in both normoxic and hypoxic conditions.
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PMID:Cardiovascular and blood gas responses to inhaled anaesthetics in normoxic and hypoxic dogs. 381 97

The respiratory effects of sevoflurane were studied in seven patients and compared with values obtained in another seven patients anesthetized with halothane. Resting ventilation, resting PaCO2, and ventilatory response to CO2 were measured awake and at 1.1 and 1.4 MAC levels of both anesthetic agents. We found that with sevoflurane, tidal volume and the slopes of the CO2 response curves decreased and PaCO2 increased with increasing depth of anesthesia, as with other inhaled anesthetics. A compensatory increase in respiratory frequency was not enough to prevent a decrease in minute volume with increasing depth of anesthesia. At 1.1 MAC, sevoflurane produced almost the same degree of respiratory depression as halothane. At 1.4 MAC, sevoflurane produced more profound respiratory depression than halothane.
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PMID:Respiratory effects of sevoflurane. 382 66

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

The authors determined the neuromuscular effects of vecuronium (ORG NC45, Norcuron) during anesthesia with nitrous oxide and 0.9 MAC halothane. To determine potency, they administered vecuronium (15, 20, or 25 micrograms/kg) to 18 infants (less than 1 year old) and 18 children (1-8 years old). They then compared these dose-response relationships with values obtained for adults (greater than 18 years old) under comparable anesthetic conditions. The ED50S (dose producing 50% depression of adductor pollicis twitch tension) of 16.5, 19.0, and 15.0 micrograms/kg for infants, children, and adults, respectively, did not differ significantly. To determine the time course of neuromuscular blockade, the authors administered vecuronium, 70 micrograms/kg, to six infants, six children, and six adults. Onset time (time to maximal effect) was shortest for infants (1.5 +/- 0.6 min, mean +/- SD) compared with that for children (2.4 +/- 1.4 min) and adults (2.9 +/- 0.2 min). Duration (time from injection to 90% recovery) was longest for infants (73 +/- 27 min) compared with that for children (35 +/- 6 min) and adults (53 +/- 21 min). The authors conclude that vecuronium can be used in infants and children in doses similar to those recommended for adults. The time interval for supplemental doses will be longest in infants and shortest in children.
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PMID:Neuromuscular effects of vecuronium (ORG NC45) in infants and children during N2O, halothane anesthesia. 613 83

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

Of all the available halogenated anaesthetic agents, isoflurane appears to be the most advantageous for the neurosurgical patient. Concentrations which produce satisfactory anaesthesia for neurosurgical procedures cause little or no depression of myocardial function, and no increase in intracranial pressure. Cerebral perfusion pressure is maintained. Autoregulation remains effective at concentrations of up to 1.5 MAC. Vascular reactivity to carbon dioxide is also maintained. Cerebral metabolic rate is decreased in a dose-related fashion and a cerebral protective effect, maximal at clinical concentrations, has been demonstrated. Isoflurane produces predictable electroencephalographic changes as anaesthesia deepens. Because the metabolism of isoflurane in vivo is so low, the risk of interference with organ function after surgery or adverse drug interactions is reduced. The potency is such that adequate anaesthetic and surgical conditions for most intracranial procedures may be achieved with 0.5-1% isoflurane combined with hyperventilation with or without nitrous oxide. The rapid, precise adjustment of depth of anaesthesia made possible by the low blood/gas solubility of isoflurane is especially beneficial in neurosurgical procedures because of the great variability of surgical stimulation. Prompt elimination of isoflurane allows fast return to consciousness and permits early neurological examination after surgery.
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PMID:Inhalation anaesthetic agents in neurosurgery. 639 28

In rats pretreated with phenobarbital breathing 10% oxygen, subanesthetic doses of halothane, isoflurane, enflurane, thiopental, and fentanyl caused hepatic injury. Because hypoxia per se can produce such injury, we hypothesized that the anesthetic-induced injury resulted from increased hypoxemia secondary to respiratory depression. Male Sprague-Dawley rats were pretreated with phenobarbital; half of the rats were fed and the other half were deprived of food for the 24 h before study. Isoflurane anesthesia was given for the placement of a catheter into the femoral artery. After 1 h of recovery, the rats were exposed to 10% oxygen. Control samples were obtained and halothane, isoflurane, enflurane, thiopental, or fentanyl was administered. Rats given food had higher PaCO2 and lower pH values than starved rats. Also, arterial oxygen saturation (SaO2) tended to be lower in rats given food. At concentrations of 0.15-0.2 MAC or higher, halothane, isoflurane, and enflurane slightly increased PaCO2 values relative to values for a control group exposed only to hypoxia. However, SaO2 and PaO2 did not show significant drug-induced changes. Fentanyl transiently decreased PaO2 and SaO2. Thiopental caused no changes. Thus, we conclude that subanesthetic doses of anesthetics may depress the ventilatory response to hypoxia but that this depression is inconsistent and appears to be too small to cause hepatic damage.
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PMID:Effects of halothane, isoflurane, enflurane, thiopental, and fentanyl on blood gas values in rats exposed to hypoxia. 640 54


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