Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Information on species differences in responses to inhalation anesthetics has been established in a variety of mammalian and non-mammalian species, but comparable studies have not been reported in birds. The purpose of this study was to determine minimal anesthetic concentration and cardiopulmonary concentration-response effects of isoflurane in Sandhill cranes. Six cranes were anesthetized with isoflurane in oxygen. Gases sampled through a polyethylene tube inserted to the distal end of an endotracheal tube were used for measurements of isoflurane concentrations using an infrared gas analyzer. Body temperature was maintained at 40 +/- 0.5 degrees C. The minimal anesthetic concentration for isoflurane was determined during spontaneous ventilation, and concentration-response data were collected at 1, 1.5, and 2.0 times the minimal anesthetic concentration. Concentration-response data were repeated during mechanically controlled breathing with PaCO2 maintained between 27 and 35 mm Hg. The minimal anesthetic concentration for isoflurane was 1.34 +/- 0.14 vol% (mean +/- SD). Concentration-dependent respiratory depression during spontaneous breathing was evidenced in all cranes by an increase in PaCO2. Isoflurane induced apnea in two of the cranes during spontaneous ventilation at 2 times the minimal anesthetic concentration. As the concentration of isoflurane was increased, mean arterial blood pressure decreased during both spontaneous and controlled ventilation. Mean arterial blood pressure was higher during controlled ventilation than during spontaneous ventilation. The minimal anesthetic concentration for isoflurane in Sandhill cranes is similar to values for isoflurane minimal anesthetic concentration in mammals. Isoflurane has dose-dependent effects on cardiopulmonary function qualitatively similar to those observed in mammals.
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PMID:Isoflurane anesthesia in sandhill cranes (Grus canadensis): minimal anesthetic concentration and cardiopulmonary dose-response during spontaneous and controlled breathing. 292 84

The cardiovascular and respiratory effects of the new inhalational anaesthetic agent isoflurane were investigated in dogs. Anaesthesia was induced with thiopentone after premedication with acepromazine. Isoflurane was administered with nitrous oxide and oxygen by spontaneous ventilation after base line values had been determined. Arterial blood pressure decreased as the concentration of administered isoflurane increased. Isoflurane produced a profound and dose related respiratory depression as measured by the increase in end tidal carbon dioxide levels. Isoflurane administration did not produce any visible muscle twitching.
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PMID:Experimental investigation of the cardiovascular and respiratory effects of increasing concentrations of isoflurane in the dog. 308 81

This study compares halothane with isoflurane for short ENT procedures performed under spontaneous breathing in 80 children. Monitoring included ECG, arterial pressure, PECO2 and respiratory rate. Induction, maintenance and recovery durations were recorded. Induction time was further subdivided into an initial phase followed by a plateau according to delivered halogen concentrations. Inhalation induction was possible with isoflurane without major side effects as long as the drug concentration was increased slowly. This precaution was not needed with halothane. No respiratory depression could be attributed to either of the tested drugs. Isoflurane elicited a significant drop in arterial pressure with a concomitant increase in heart rate. Recovery times were shorter in the isoflurane group.
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PMID:Halothane versus isoflurane for short ENT procedures with spontaneous respiration in children. 311 17

Isoflurane and fentanyl have been compared as anaesthetic agents for outpatient laparoscopy. In 50 female patients anaesthesia was induced with thiopentone and maintained with nitrous oxide 66% in oxygen combined with either isoflurane 1-2% or fentanyl 0.3 mg according to a randomized list. Suxamethonium was used to facilitate intubation and for further muscle relaxation. Immediate recovery from anaesthesia was assessed by eye opening and time before giving the date of birth. Additional observations made hourly for 4 h were: nausea or vomiting; clinical assessment of wakefulness; psychic or motor agitation; antiemetic or analgesic drugs given; reaction time; respiratory depression. Immediate recovery was more rapid in the fentanyl group (P less than 0.05). Reaction times in the isoflurane patients returned to control by 3 h, whereas the fentanyl patients were 10% slower than control at 4 h (P less than 0.05 at 2 h, 3 h, 4 h). Nausea and vomiting were more frequent in the fentanyl group, and four of the fentanyl patients required naloxone. Both anaesthetic techniques provided satisfactory operating conditions, but isoflurane appeared to provide a better recovery with less side effects than fentanyl.
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PMID:Isoflurane v fentanyl for outpatient laparoscopy. 315 46

The myocardial depressant effects of isoflurane and halothane were compared using feline right ventricular papillary muscles bathed in Krebs-bicarbonate solution. In experiment 1 muscles were stimulated by field electrodes (0.2 Hz) to obtain control measurements of developed tension (dt) and maximal rate of tension development (dF/dt) prior to exposing the papillary muscles to four concentrations of either isoflurane (4.0%, 2.0%, 1.0%, 0.5%) or halothane (2.0%, 1.0%, 0.5%, 0.25%). Repeat measurements of dt and dF/dt were recorded after 20 min at each concentration. Isoflurane and halothane both caused dose-dependent depression of dt and dF/dt, but at 0.5%, 1.0%, and 2.0%, halothane was significantly more depressant than isoflurane (P less than 0.01 for dt and dF/dt). Quadratic equations were fitted to the dose-response data by least squares analysis (R2 greater than .985 for both anesthetics), and the isoflurane and halothane concentrations that decreased dt to 90%, 70%, 50%, and 30% of control were determined to compare the relative myocardial depressant potency of isoflurane and halothane by linear regression analysis. This potency relationship is described by the equation: isoflurane concentration = -0.005 + 1.445 (halothane concentration). In experiment 2 papillary muscle responses at two similar cardiodepressant concentrations of isoflurane (1.25% and 2.0%) or halothane (0.80% and 1.35%) were compared at stimulus frequencies of 0.05, 0.1, 0.2, 0.4, 0.8, 1.0, and 2.0 Hz. The concentrations of isoflurane and halothane were selected from the data obtained in experiment 1 and represent the anesthetic concentrations that diminish muscle function to approximately 70% and 50% of control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the in vitro myocardial depressant effects of isoflurane and halothane anesthesia. 318 13

The influence of isoflurane on membrane currents, action potentials, and contraction was investigated in single cells isolated from guinea-pig ventricle. Isoflurane (1.65-4.45%) reduced the action potential duration at 20% and 90% repolarization times. When step depolarizations were applied under voltage-clamp conditions, there was a depression by isoflurane both of the second inward (calcium) current and of the contraction (measured by an optical method). Isoflurane also depressed "tail" currents, which were recorded on repolarization following a voltage-clamp step to 0 mV and which are thought to be activated by cytosolic calcium. Additional actions of isoflurane were investigated using a paired-pulse protocol. The observations were consistent with a reduction by isoflurane of calcium release. This action together with the reduction of calcium influx during the second inward current would contribute to the negative inotropic effect of isoflurane.
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PMID:Isoflurane depresses membrane currents associated with contraction in myocytes isolated from guinea-pig ventricle. 318 20

In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (PaCO2 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n = 7). CBF was measured after intravenous administration of 133xenon and CMRO2 was calculated from the arterial venous differences of oxygen content (AVDO2) determined in arterial and jugular venous bulb blood. CBF and CMRO2 (means +/- s.e. mean) determined prior to administration of volatile agents were 28 +/- 5 ml x 100(-1) x min-1 and 2.0 +/- 0.3 ml x 100 g-1 x min-1, respectively, in the isoflurane group. In the halothane group, CBF was 25 +/- 0.4 ml x 100 g-1 x min-1 and CMRO2 was 2.0 +/- 0.4 ml x 100 g-1 x ml-1. There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P less than 0.05) compared to values obtained during fentanyl/N2O anesthesia. In addition, isoflurane caused a further decrease in CMRO2 of 12% (P less than 0.01) as compared to a 20% increase (P less than 0.05) with halothane. The cerebral metabolic depression caused by the short-acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMRO2 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.
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PMID:Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man. 327 96

Segments of viable human left ventricular trabeculae were obtained at the time of endocardial resection for intractable ventricular ectopy. Muscle segments which showed suitable and reproducible contractions in 26 mM K Tyrode solution with 1 microM isoproterenol were electrically stimulated after rest, and at frequencies of 0.1, 0.25, 0.5, and 1 Hz. Effects of 0.75% halothane and 1.3% isoflurane on peak tension, maximum rate of tension development (dT/dt-max), and on slow (calcium dependent) action potential (AP) characteristics were studied. Halothane depressed peak tension, dT/dt-max, and slow AP maximum rate of depolarization (Vmax) at all frequencies, and caused a significantly greater depression of peak tension and dT/dt-max at 0.5-1 Hz than after rest and at 0.1-0.25 Hz. Isoflurane did not significantly depress slow AP Vmax, showed no frequency dependent contractile depression, and depressed dT/dt-max less than halothane at 0.5 and 1 Hz. Halothane and isoflurane caused differing depression in the pattern of developed tension. The differential depression by halothane and isoflurane of human ventricular myocardium was similar to that previously observed in isolated animal ventricular tissue.
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PMID:Effects of halothane and isoflurane on isolated human ventricular myocardium. 334 98

The effects of enflurane, halothane, and isoflurane on myocardial potentiated-state contractions were examined in a study in which each of the anesthetics was presented, in random order, to each of eight isolated rabbit papillary muscles. Post-rest potentiated-state contractions were elicited by imposing a stimulus at precisely timed intervals following a 2-Hz steady-state stimulus train. The strength of these contractions is known to be highly dependent on sarcoplasmic reticulum (SR) Ca2+ release. The increment in tension developed in potentiated state, as compared to the steady state, is directly attributed to the potentiation process, and is defined here as potentiated-state strength (PSS). Effects of enflurane, halothane, and isoflurane on the time course of development of the potentiated state were characterized, as were the effects of incremental doses of these anesthetics on PSS. Anesthetic gas phase concentrations that produced 50% depression of contractile tension at 0.05 Hz steady-state stimulation were 0.6% halothane, 1.4% isoflurane, and 1.6% enflurane. Muscles exhibited maximal PSS of 0.91 +/- 0.01 g/mm2 in the absence of anesthetics. Halothane (0.6%) and enflurane (1.6%) caused significant depression of PSS to 0.45 +/- 0.06 and 0.61 +/- 0.06 g/mm2, respectively, while isoflurane (1.4%) preserved PSS at 0.95 +/- 0.09 g/mm2. Concentration profiles showed that the depression of PSS by halothane and enflurane was dose dependent. Isoflurane, up to 2.3%, failed to depress PSS. The time interval for development of optimum PSS, 1.5 to 2.0 s, was unaffected by any of the anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of inhalation anesthetics on myocardial potentiated-state contractions in vitro. 335 90

At present, the most widely used inhalational anaesthetics are the halogenated, inflammable vapours halothane, enflurane, isoflurane and the gas nitrous oxide. The anaesthetic effect of these agents is related to their tension or partial pressure in the brain, represented at equilibrium by the alveolar concentration. The minimum alveolar concentration for a specific agent is remarkably constant between individuals. The uptake and distribution of inhalational anaesthetics depends on inhaled concentration, pulmonary ventilation, solubility in blood, cardiac output and tissue uptake. Inhalational anaesthetics are mainly eliminated by pulmonary exhalation, but significant amounts of halothane are removed by hepatic metabolism. Inhalational agents currently in use have acceptable pharmacokinetic characteristics, and clinical acceptance depends on their potential for adverse effects. Induction of anaesthesia with halothane is rapid and relatively pleasant and it is the agent of choice for paediatric anaesthesia. Between 20 and 50% is metabolised, and the parent drug is a potent inhibitor of drug metabolism. Post-operatively enzyme induction may follow. The major disadvantages of halothane are myocardial depression, propensity to evoke cardiac arrhythmias and the rare but serious halothane hepatitis. Induction and recovery from enflurane anaesthesia is rapid. Metabolism accounts for 5 to 9% of the elimination. The metabolic product inorganic fluoride may in rare cases cause renal toxicity. Enflurane is a weak inhibitor of drug metabolism at anaesthetic concentrations. Enflurane depresses circulation more than halothane by reducing both myocardial contractility and systemic vascular resistance, but cardiac rhythm is stable. Enflurane anaesthesia may, unlike the other agents, induce epileptic activity. Enflurane is widely used as replacement for halothane in adults. Despite its low blood-gas solubility, the airway irritability of isoflurane precludes a faster induction of anaesthesia than with halothane. Isoflurane is almost resistant to biodegradation. Myocardial contractility is maintained during isoflurane anaesthesia and cardiac rhythm is stable except for the occurrence of tachycardia in some patients. Isoflurane is the inhalational agent of choice for neurosurgical operations. Sevoflurane is an experimental ether vapour: induction and recovery is fast and pleasant. It is metabolised to the same extent as enflurane and subnephrotoxic concentrations of inorganic fluoride may result. Sevoflurane has fewer respiratory and cardiovascular depressant effects than halothane and may be a future alternative for paediatric anaesthesia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of the inhalational anaesthetics. 355 39


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