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

The respiratory and haemodynamic changes produced by three inspired concentrations of isoflurane (1, 1.5, and 2%) were evaluated in a healthy children (mean age 4 yrs) breathing spontaneously during anaesthesia. Isoflurane produced respiratory depression; end tidal carbon dioxide tension increased from 38.8 +/- 3.6 mmHg at 1%, to 42.6 +/- 4.3 mmHg and 48.8 +/- 4.9 mmHg at 1.5 and 2% respectively. Respiratory frequency was not modified at the different inspired concentrations of isoflurane. Heart rate and arterial pressure decreased after induction of anaesthesia with isoflurane and remained at the same level throughout the study.
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PMID:[Effects of isoflurane administered during spontaneous ventilation in the child]. 374 91

Isoflurane-oxygen was given for induction and maintenance of anesthesia to ten patients having coronary artery bypass grafts. All had preserved ventricular function without hypertension or other cardiac lesions; treatment with beta-blocking drugs was maintained until the operation in all patients. Cardiac output, arterial and central pressures, coronary sinus (CS) blood flow, arterial and CS oxygen, Hb, and lactate contents were measured before, six times during, and twice after anesthesia. On induction, systolic arterial pressure was purposely reduced 33% along with systemic resistance by increasing the concentration of isoflurane; cardiac index, heart rate, and coronary flow did not change. Coronary resistance decreased 23% and CS oxygen content increased 56%; but in three of ten patients myocardial lactate production took place, evidence of global ischemia. Induction of anesthesia was not smooth in three patients. Controlled hemodynamic depression could be maintained with isoflurane-oxygen, but the frequency of myocardial lactate production before and after perfusion was greater than with other general anesthetics. Isoflurane dilated portions of the coronary bed but, because anaerobic metabolism occurred concomitantly, the theory that redistribution of flow can take place resulting in ischemic areas of ventricle is supported.
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PMID:Myocardial metabolism and hemodynamic responses with isoflurane anesthesia for coronary arterial surgery. 394 Apr 70

The cardiovascular actions of isoflurane-nitrous oxide anesthesia were studied in 20 patients (age rage 46-76 yr) undergoing laparatomy (group A = 13 patients) or peripheral vascular surgery (group B = 7 patients). Measurements were performed in the awake state, 20 min after induction of anesthesia and during surgical stimulation. Isoflurane produced small changes in heart rate but a significant reduction in mean arterial pressure which was due to a reduction in peripheral vascular resistance and myocardial contractility. During surgical stimulation arterial pressure rose above control values in group A but remained below control in group B. Cardiac index and stroke volume index both decreased after induction of anesthesia in group A and B. During surgical stimulation cardiac index increased in group A due to an increase in heart rate but remained below control in group B, while stroke volume index was reduced in both groups throughout the whole procedure. These results suggest, that contrary to the findings in human volunteers, isoflurane produces a significant cardiovascular depression in aged surgical patient.
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PMID:[Cardiovascular effects of isoflurane-nitrous oxide anesthesia in peripheral and abdominal surgical interventions]. 399 96

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

The physical and pharmacological properties of the structural isomers isoflurane and enflurane differ from each other and from those of other potent inhaled anaesthetics. The minimum alveolar concentration (MAC) for isoflurane (1.15%) is one-and-one-half times that for halothane (0.75%) and two-thirds that for enflurane (1.7%). The blood/gas partition coefficient (1.4) for isoflurane is lower than the coefficients for all other potent inhaled agents. Despite this lower blood solubility, induction of anaesthesia is slightly faster with halothane because of isoflurane's mild pungency. Enflurane depresses ventilation more than isoflurane, which in turn is slightly more depressant than halothane. All these agents dilate constricted bronchi, and thus are useful in the anaesthetic management of patients who have asthma or chronic obstructive pulmonary disease. Isoflurane has the largest circulatory margin of safety of all potent halogenated agents; it produces the least myocardial depression at a given multiple of MAC. Isoflurane may increase heart rate, particularly in younger patients, and occasionally is associated with tachycardia. It decreases total peripheral resistance, thereby decreasing systemic arterial pressure. Although results from one study suggest that isoflurane may produce a "steal" or coronary blood flow in patients with coronary artery disease, results from other studies suggest that, even in the presence of coronary artery disease, coronary blood flow to all parts of the heart remains as adequate with isoflurane as with other anaesthetics. Greater concentrations of isoflurane (1.6 MAC) increase cerebral blood flow less than does halothane. Isoflurane does not produce convulsive activity, but can produce profound muscle relaxation. It enhances the action of tubocurarine or pancuronium, and (to a lesser extent) vecuronium or atracurium. The enhancement is comparable to that produced by enflurane. Less enhancement is produced by halothane or nitrous oxide-narcotic. Only 0.17% of isoflurane taken up in man appears as urinary metabolites. This resistance to biodegradation may explain the minimal or absent hepatotoxicity and nephrotoxicity of isoflurane.
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PMID:The pharmacology of isoflurane. 639 30

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

The hypotension accompanying isoflurane suggests that the anesthetic produces an attenuation of sympathetic tone. Previous studies examining the effects of isoflurane on sympathetic efferent nerve activity have required concomitant use of a basal anesthetic or decerebration, both of which independently alter sympathetic activity. This study was performed to examine the effects of isoflurane on sympathetic efferent nerve activity in the absence of basal anesthetic or decerebration. Five mongrel dogs were anesthetized with 4% isoflurane by mask. Platinum electrodes chronically were implanted around a renal nerve adjacent to the renal artery in order to measure renal sympathetic efferent nerve activity in the conscious and anesthetized animal. After 5-24 h for recovery, renal nerve activity and arterial pressure (via an implanted femoral artery cannula) were measured in the conscious, resting animal (control); during induction (4% isoflurane) and intubation; in the anesthetized animal (1.5% and 2.5% isoflurane); and during recovery and extubation. Isoflurane produced a significant dose-dependent depression of arterial blood pressure but did not significantly change heart rate from control. Renal sympathetic efferent nerve activity at 1.5% isoflurane was not significantly different from that in conscious animals, but nerve activity at 2.5% isoflurane was depressed significantly from both control and 1.5% isoflurane. Both intubation and extubation were accompanied by an increase in sympathetic nerve activity. Isoflurane appeared to directly depress sympathetic activity at both levels of anesthesia, but the direct depression of activity at 1.5% isoflurane seemed to be countered by reflex increases in sympathetic tone due to the hypotension accompanying the anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic efferent nerve activity in conscious and isoflurane-anesthetized dogs. 647 34

The hemodynamic interactions of verapamil and isoflurane were studied in eight dogs. Left ventricular function was analyzed using a right heart bypass preparation to permit rigid hemodynamic control. Hemodynamic studies were performed at 0.7, 1.05, and 1.40% isoflurane before and during the maintenance of two stable levels of verapamil, administered intravenously by combining a bolus dose (0.2 mg X kg-1) with an infusion (3.0 and 6.0 micrograms X kg-1 X min-1). Isoflurane produced a concentration-dependent depression of left ventricular function as indicated by dP/dt max, per cent systolic shortening, and left ventricular function curves. This depression was enhanced in a dose-plasma concentration-dependent manner by verapamil and was reversed by calcium chloride. Isoflurane alone and the combination of verapamil and isoflurane decreased systemic vascular resistance in a dose-dependent fashion that was antagonized partially by calcium chloride. Therefore, verapamil can enhance the hemodynamic effects of isoflurane in a dose-related manner that needs to be considered when both drugs are administered together.
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PMID:Hemodynamic interactions of verapamil and isoflurane. 686 70

Circulatory and respiratory effects of alveolar concentrations of 1.31, 1.97, and 2.62 vol% of isoflurane in oxygen were studied in eight young, healthy horses during spontaneous and controlled ventilation. These isoflurane concentrations were equivalent, respectively, to 1.0, 1.5, and 2.0 times the minimal alveolar concentration of isoflurane, which prevents movement in horses in response to a standard pain stimulus. Results of the isoflurane studies were compared with similarly derived findings in these same horses during equipotent halothane in oxygen anesthesia. Isoflurane, similar to halothane, produced a dose-related depression of cardiovascular function which was less severe during spontaneous ventilation and associated hypercapnia. The two anesthetic agents produced similar circulatory effects during controlled ventilation and constant arterial carbon dioxide tension except for a significantly (P less than 0.05) less depressed cardiac output/kg of body weight and stroke volume that occurred with minimal alveolar concentration 1.5 and 2.0 isoflurane. Total peripheral resistance was greatest when these horses were anesthetized with halothane regardless of the alveolar dose. In horses, isoflurane was, in general, no more depressing than was halothane to circulatory and respiratory function.
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PMID:Comparison of circulatory and respiratory effects of isoflurane and halothane anesthesia in horses. 740 5

Heart muscle is dependent on the entry of calcium from the extracellular fluid to support contraction, and neonatal hearts are particularly sensitive to reductions in transsarcolemmal entry of calcium. Accordingly, this study evaluated the ability of the calcium channel agonist BAY K8644 to prevent or reverse the myocardial depressant effects of halothane or isoflurane in right ventricular papillary muscles from neonatal rabbits. The ability of BAY K8644 to reverse reductions in force (F) and dF/dt (halothane and isoflurane) or prevent reduction (halothane) was studied. Halothane decreased F to 24 +/- 2% of baseline values (p = 0.001). The addition of BAY K8644 reversed F to only 54 +/- 3% of baseline (p = 0.001 vs. baseline and p = 0.002 vs. halothane alone). Isoflurane decreased F to 20 +/- 2% of baseline (p = 0.001) with a return to 45 +/- 4% of baseline with the addition of BAY K8644 (p = 0.0001 vs. baseline and p = 0.0025 vs. isoflurane alone). With BAY K8644 in the bath prior to the addition of halothane, halothane decreased F to 38 +/- 4% of baseline (p = 0.001). dF/dt mirrored changes in F in all studies. These data show that a calcium channel agonist is only partially effective in modulating volatile anesthetic-induced depression in neonatal rabbit ventricular papillary muscle.
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PMID:Effect of calcium channel agonist (BAY K8644) on volatile anesthetic-mediated depression in neonatal rabbit papillary muscle. 752 47


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