Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated perfused rat livers exposed to 1.5% halothane (equivalent to 1.35 MAC) in O2/CO2 or to O2/CO2 alone produced urea, as well as albumin and transferrin (both measured by immunodiffusion), at constant rates during a 4.25-h perfusion. Urea production did not differ in the two treatment groups, but halothane depressed albumin and transferrin synthesis 43% and 45%, respectively. Intact rats were also exposed to halothane, after which albumin synthesis was measured by the (14C)carbonate technique. The minimum halothane concentration required to insure sufficient relaxation for ventilation was selected and ranged from 1.0 to 1.5%. Measurements were made in control rats not exposed to halothane (group I) and in halothane exposed rats immediately after 1 h of anesthesia (group II), 24 h after the start of 1 h of anesthesia (group III), and immediately after 1/2 h of anesthesia preceded by a 1-h exposure 24 h earlier (group IV). Single exposures to halothane (groups II and III) resulted in a decrease in albumin synthesis immediately or 24 h later that did not differ significantly from controls (group I). However, halothane given twice to rats at 24-h intervals (group IV) reduced their mean albumin synthesis rate to half that of controls. The early onset and constancy of halothane depression of export protein synthesis by isolated, perfused livers may reflect a response to halothane itself, rather than an effect resulting from the accumulation of halothane metabolites. Similarly, reduction of albumin synthesis in intact rats immediately after a second halothane exposure may indicate a response to halothane, rather than to halothane metabolites.
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PMID:Halothane decreases albumin and transferrin synthesis: studies in the isolated, perfused rat liver and in the intact rat. 335 89

The effects of similar anaesthetic levels of halothane (1.3 MAC), enflurane (1.2 MAC) and isoflurane (1.1 MAC) on pulmonary ventilation and gas exchange were investigated in 24 children subjected to minor and intermediate paediatric surgical procedures. Eight children were anaesthetized with each agent, pneumotachography and capnography were used, and airway as well as oesophageal pressures were measured. Minute ventilation (VE) was lower with enflurane than with halothane (P less than 0.001) and isoflurane (ns). Tidal volumes were, however, similar and variations in VE were thus caused by lower respiratory rates with enflurane than with the two other agents. Alveolar ventilation (VABohr) and carbon dioxide elimination (VCO2) were smaller and end-tidal CO2 tension higher with enflurane. Ventilatory efficiency was, however, somewhat better with enflurane as indicated by lower VDBohr/VT (ns) and VE/VCO2 (P less than 0.05) ratios compared with the two other agents. The effects of all three agents on dynamic compliance were similar, while total pulmonary resistance was less with isoflurane than with halothane and enflurane. It is concluded that although minute ventilation was smaller with enflurane than with halothane and isoflurane, ventilatory efficiency was similar due to a smaller dead space ventilation as a result of the lower respiratory rates in children anaesthetized with enflurane.
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PMID:Pulmonary ventilation and gas exchange in children anaesthetized with halothane, enflurane and isoflurane. 363 May 81

Respiratory effects of nitrous oxide and isoflurane were studied in 13 children (mean age 45.6 +/- 19.3 months, mean weight 14.9 +/- 4.8 kg) during surgery under continuous extradural anaesthesia. Three different anaesthetic states were studied: isoflurane 0.5 MAC in oxygen (27 study periods), isoflurane 0.5 MAC with 50% nitrous oxide (32), isoflurane 1 MAC in oxygen (25). End-tidal carbon dioxide (PE' CO2) and isoflurane, respiratory indices (tidal volume, VT; minute ventilation, VE; mean inspiratory flow, VI; respiratory frequency f, effective inspiratory timing TI/Ttot were measured. The addition of nitrous oxide (comparison of respiratory variables obtained in 25 successive periods at (1) and (2)) produced a significant increase in PE' CO2' significant decreases in VT, VE and VI, a significant increase in f. The increase in alveolar concentration of isoflurane ((1) compared with (3) in 25 successive periods) was associated with a significant increase in PE' CO2' significant decreases in VT, VE, VI and a significant increase in f. The equipotent anaesthetic states (2) and (3) were compared in 21 successive periods. In children, the net result of substituting nitrous oxide for an equal MAC fraction of isoflurane was to produce a smaller decrease in VT responsible for a smaller decrease in VE without significant change in respiratory rate.
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PMID:Respiratory effects of nitrous oxide during isoflurane anaesthesia in children. 376 24

The MAC 16 is a transplantable murine carcinoma of the colon producing extensive weight loss in tumour-bearing animals. The weight loss is proportional to the size of the tumour and occurs without a reduction in food intake when compared with non tumour-bearing control mice. Weight loss produced by the MAC 16 tumour is accompanied by hypoglycaemia which becomes more extensive as the tumour mass increases. In order to understand the mechanism of the cachexia produced by the MAC 16 tumour the rate of substrate utilization and CO2 formation from both glucose and palmitate has been compared in vitro, with other colon carcinoma cell lines known not to produce cachexia as well as a range of murine and human tumour cell lines. The rate of glucose consumption, lactate production and CO2 formation from both glucose and palmitate is much higher for the MAC 16 than for the other tumour cells. For all cell lines in vitro the consumption of glucose exceeds that of palmitate by a factor of 10(3). Excessive consumption of glucose by the MAC 16 tumour may account for the hypoglycaemic effect on the host. The level of 3 oxo acid CoA transferase, an initiator of ketone body utilization, was found to be much lower in the MAC 16 tumour than non-involved colon. This suggests that the tumour may not be able to metabolize ketone bodies effectively.
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PMID:Metabolic substrate utilization by a tumour cell line which induces cachexia in vivo. 377 4

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

The effects of halothane and isoflurane on hypocapnic increases in pulmonary collateral resistance were studied in dogs. A bronchoscope with a double lumen catheter in the suction port obstructed a peripheral airway and allowed gas to flow out of the isolated segment of lung only via collateral channels. The collateral gas flow (Vcoll) was measured with a flowmeter and delivered through one lumen of the catheter, while the other lumen measured distal pressure (Pb). At FRC, the resistance to collateral ventilation (Rcoll) was calculated as Rcoll = Pb/Vcoll. The rest of the lung was ventilated with air, while air (hypocapnia), 10% CO2 in air, or air and halothane or isoflurane were delivered to the isolated segment. A measurement of resistance was made after 4 min of test gas flow. For each segment, when air replaced 10% CO2, the average increase in Rcoll was calculated and called Rmax. When 10% CO2 in air was infused into segments the mean Rcoll (n = 50) was 0.0196 +/- 0.0022 cmH2O X ml-1 X min. This increased to 0.0285 +/- 0.0031 cmH2O X ml-1 X min (mean +/- E) when air was infused, a mean increase in resistance of 52 +/- 3%. When halothane or isoflurane was added to air the hypocapnic increase in Rcoll was attenuated with a 50% decrease at 1.3% (1.4 MAC and 0.8 MAC, respectively). These two inhalational anesthetics reduce active changes in the flow resistance to collateral ventilation. When collateral resistance acts to adjust ventilation perfusion deviations, this action of halothane and isoflurane may make this regulation less effective.
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PMID:The influence of halothane and isoflurane on pulmonary collateral ventilation. 391 81

The reduction in cerebral blood flow (CBF) caused by hypocapnia is an important element of neuroanesthetic techniques. While it has been demonstrated previously that the CO2 response of the cerebral circulation (CO2 X R) is enhanced (i.e., greater delta CBF/delta PaCO2) during halothane administration, the effect of isoflurane on CO2 X R has not been evaluated completely. Accordingly, the authors examined CO2 X R in cats during anesthesia with 1.0 MAC isoflurane (with 75% N2O) and compared it with CO2 X R during anesthesia with 1.0 MAC halothane (with 75% N2O) and with CO2 X R during the administration of 75% N2O alone. CO2 X R during anesthesia with isoflurane-N2O was enhanced relative to that observed during administration of both halothane-N2O (P less than 0.025) and N2O alone (P less than .001). CO2 X R during anesthesia with halothane-N2O was, in turn, greater than that observed during the administration of N2O alone (P less than 0.025). Furthermore, at similar levels of hypocapnia (PaCO2 18-20 mmHg), CBF was significantly lower (P less than 0.01) during administration of isoflurane-N2O (29.0 +/- 4.5 ml X 100 g-1 X min-1) than during administration of either N2O (40.6 +/- 5.5 ml X 100 g-1 X min-1) or halothane-N2O (39.6 +/- 7.8 ml X 100 g-1 X min-1). CBF values during administration of the N2O alone and halothane-N2O were not different during hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of the feline cerebral circulation to PaCO2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide. 391 14

The authors studied the influence of locally administered isoflurane anesthesia on the pulmonary vascular response to regional alveolar hypoxia (hypoxic pulmonary vasoconstriction [HPV]) over a range of cardiac outputs (COs) in seven mechanically ventilated, closed-chest dogs. The right lung was ventilated with 100% O2 throughout the study. The left lung was ventilated with either 100% O2 (normoxia) or an hypoxic gas mixture (hypoxia). Different alveolar concentrations of isoflurane (0, 1, and 2.5 MAC) were administered to the left lung in a randomized sequence. The CO was altered by opening and closing surgically produced arteriovenous fistulae, at all isoflurane concentrations, and by hemorrhage at 0 MAC isoflurane. The magnitude of the HPV response was measured by differential CO2 elimination in the absence of isoflurane and by venous admixtures in all phases. During normoxia, the left lung effective flow (QL%) measured from differential CO2 excretion was 39.9 +/- 1.2% of the total blood flow and decreased to 18.8 +/- 2.6% when ventilated with the hypoxic gas mixture. Venous admixture (QVA/QT%) was significantly correlated with QL% during hypoxic ventilation in the absence of isoflurane. QVA/QT% was 22.3 +/- 2.7% during hypoxia with normal CO, and it increased significantly to 27.7 +/- 1.1% when the CO was increased 43%. It was not significantly altered (23.6 +/- 3.6%) when the CO was decreased by 54%. Isoflurane 2.5 MAC significantly increased QVA/QT% during hypoxic ventilation of the left lung to 33.9 +/- 2.6% with low CO and 35.4 +/- 1.7% with normal CO. Isoflurane 1 MAC increased QVA/QT% to 27.2 +/- 2.7% with normal CO and 28.1 +/- 2.6% with high CO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of isoflurane on hypoxic pulmonary vasoconstriction in dogs. 396 50

Halothane, enflurane, isoflurane, and fentanyl were examined for their potential to exacerbate liver dysfunction in rats with preexisting cirrhosis. Male Wistar rats given sodium phenobarbital for 2 weeks are assigned randomly to two groups. One group (cirrhotic) was exposed by inhalation to carbon tetrachloride (CCl4) in air at weekly intervals for 12 weeks to induce cirrhosis. The other group (noncirrhotic) was handled similarly but received air only. Five weeks after the last exposure to CCl4, cirrhotic and noncirrhotic rats were given three hours of 1 MAC halothane, enflurane, or isoflurane in 50% oxygen, or 350 micrograms fentanyl per kg of body weight and 50% oxygen, or 50% oxygen only. Blood gas tensions and blood glucose levels were measured before, during, and at the end of exposure. Forty-eight hours after exposure, serum chemistries were measured in each rat for comparison with preexposure values. Rats were then killed by CO2 overdose, and liver, kidney, and testis were prepared for microscopic examination. Enflurane, isoflurane, and halothane, but not fentanyl, produced mild respiratory acidosis and no change in serum glucose levels. All anesthetics resulted in a mild but similar degree of acute liver dysfunction as indicated by small increases in SGOT or SGPT in both cirrhotic and noncirrhotic rats. Liver histology revealed mild to moderate portal cirrhosis with fibrosis and well-developed micronodules in rats exposed to CCl4, but no superimposed acute hepatocellular damage was noted. It is concluded that all the anesthetics used in this study were associated with the same minimal degree of postanesthetic hepatic dysfunction and that the dysfunction was similar in both cirrhotic and noncirrhotic rats.
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PMID:Effects of volatile anesthetics or fentanyl on hepatic function in cirrhotic rats. 406

To assess the effects of isoflurane on chemical regulation of ventilation, we studied the ventilatory responses to (1) hyperoxic hypercarbia, (2) isocapnic hypoxaemia, and (3) a single half vital capacity breath of carbon dioxide 20 per cent in oxygen in 12 human subjects, awake and sedated or anaesthetized with isoflurane, 0.1 or 1.1 MAC. Sedation did not alter ventilation nor the ventilatory response to hypercarbia but reduced the responses to hypoxaemia and to the half vital capacity breath of CO2. Anaesthesia reduced ventilation and the response to hypercarbia and nearly abolished the responses to hypoxaemia and to the breath of CO2. The results indicate that isoflurane reduces ventilatory responses to several chemical drives and that it selectively impairs those responses mediated by peripheral chemoreceptors. In these respects, isoflurane is similar to halothane and enflurane.
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PMID:Chemical regulation of ventilation during isoflurane sedation and anaesthesia in humans. 641 54


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