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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inspiratory mechanical loads were applied to the airway continuously for 5 min in healthy young adult volunteers maintained in a near steady-state of halothane anesthesia 1.1 MAC. The loads, both flow resistive and elastic in nature, had been selected to reduce the first loaded tidal volume approximately 10, 30 or 50%--these being designated "small," "medium," and "large" loads, respectively. The actual magnitudes of resistive load were 8 +/- 1, 21 +/- 3, and 48 +/- 6 cmH2O X l-1 X s, and of elastic load 6 +/- 1, 18 +/- 1, and 41 +/- 5 cmH2O X l-1 (mean +/- SEM). All loads caused an immediate reduction of ventilation proportional to the size of the load. This was followed by a gradual recovery of ventilation toward control values over approximately 2 min and then nearly stable ventilation for the rest of the loading period. Respiratory frequency was unchanged throughout. At 5 min of loading, ventilation and PaCO2 had been nearly steady for 3 min and O2 uptake and CO2 output at the airway were unchanged from control, suggesting the establishment of a near steady respiratory state. With the small and medium loads of both types, ventilation and PaCO2 in this near steady-state were not detectably different from control. With the large loads, however, ventilation was significantly reduced and PaCO2 slightly increased. The end-expiratory position of the chest wall and the relative contributions of the rib cage and abdomen-diaphragm to ventilation, as estimated by anteroposterior chest wall magnetometers, were not consistently altered by any load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory compensation for continuous inspiratory resistive and elastic loads during halothane anesthesia in humans. 293 23

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.
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PMID:Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits. 308 28

A number of clinically important features of isoflurane anaesthesia were studied in comparison to those of halothane. Two groups of dogs were used. After light premedication, anaesthesia was induced by mask, and both groups of dogs were maintained for 30 minutes at 1.5 X MAC value of either halothane or isoflurane in a combination of oxygen and nitrous oxide (50:50). All animals were ventilating spontaneously. There was no difference in the speed of induction of the halothane and isoflurane groups. Blood pressure in both groups dropped to approximately 7.5 kPa (56 mm Hg) during maintenance anesthesia (1.5 MAC), while the heart rate was significantly higher in the isoflurane group. Individual respiratory variables were not significantly different between the two groups, however the differences between the trends of the mean values were significant (Sign-test). In general, with isoflurane, respiration rates were lower, with the tidal volume and end tidal CO2 being greater. The trends in pH and arterial pCO2 showed a slightly more severe respiratory acidosis in the isoflurane group. However, neither group showed values corresponding to any expected clinical problems. Speed of recovery (determined by times to head-lift and righting-reflex) was greater in the isoflurane group. Previously known important features of isoflurane are low biodegradability, low blood: gas partition coefficient, and decreased myocardial sensitivity to catecholamines. It is concluded from this study that isoflurane deserves a place in canine anesthesia whenever these specific pharmacologic properties are desired.
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PMID:Comparison of isoflurane and halothane as inhalation anaesthetics in the dog. 309 32

Pulmonary ventilation, CO2 response and inspiratory drive were studied during halothane anaesthesia prior to surgery in 13 spontaneously breathing infants less than 6 months of age. Pneumotachography and capnography were used. Airway and oesophageal pressures were measured and occlusion tests were performed at functional residual capacity. Measurements were made before and during 8 min of 4% CO2 stimulation. Inspiratory drive increased significantly (P less than 0.001) at CO2 stimulation. This resulted in increased minute ventilation (P less than 0.001) and tidal volume (P less than 0.001) while respiratory rate was unchanged. As VBohrD/VT ratios were the same, the net effect was increased alveolar ventilation (P less than 0.001). CO2 elimination was unpredictable in these young infants and decreased during CO2 stimulation (P less than 0.05), while mean end-tidal CO2 concentration only increased from 5.2 to 6.3% (P less than 0.001). The ventilatory response to 4% CO2 could therefore be deemed to be adequate during the short period (8 min) of CO2 breathing. However, this was achieved at the cost of increased work as witnessed by the increased ratio between minute ventilation and CO2 elimination (P less than 0.01). Stabilisation of end-tidal CO2 concentrations during CO2 inhalation took only 10 s while the maximal increase in ventilation volumes was not achieved until after 150 s. It is concluded that young spontaneously breathing infants anaesthetized with halothane (MAC 1.3) have an increased respiratory drive with greater tidal volumes during CO2 stimulations. Respiratory timing, dynamic compliance and total pulmonary resistance were, however, uninfluenced by 4% CO2 stimulation. Increased monitoring of CO2 output in anaesthetized infants is suggested.
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PMID:Pulmonary ventilation, CO2 response and inspiratory drive in spontaneously breathing young infants during halothane anaesthesia. 309 64

The effect of halothane on the pressor responses to hypoxia (3% O2, 5% CO2, balance N2) and to Angiotensin II (Ang II) (0.2 microgram) has been compared in an in vitro perfused and ventilated rat lung preparation in the presence and absence of agents known to block the lipoxygenase (BW755C) and/or the cyclooxygenase (ibuprofen) pathways for arachidonic acid metabolism. Preliminary studies established the stability of the preparation (experiment 1) during two hours of observation and allowed estimation of (experiment 2) the concentration of BW755C that inhibited the HPV response by 50% (ED50 = 125 microM). In experiment 3, the rat lungs were subdivided into four groups: A, B, C, and D. Group A received the drug solvent, and B received 17 microM ibuprofen. Groups C and D received ibuprofen and, in addition, an ED50 dose of BW755C. The lungs were then tested for their response to hypoxia. In addition, groups C and D were tested for their response to 0.2 microgram Ang II. 0.5 MAC halothane was introduced into the ventilatory circuit of A, B, and D. Group C received no halothane. Responses to hypoxia and Ang II (groups C and D) were measured. Halothane was terminated and a further hypoxic response was tested in groups A and B. The results show, in group A, that the addition of halothane reduced the response to hypoxia from (mean +/- SE cm H2O) 13.4 +/- 1.56 to 6.5 +/- 1.28, a 50% reduction. The addition of ibuprofen in group B caused a 33% increase in the response, and the addition of halothane now caused only a 30% decrease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The actions of halothane, ibuprofen and BW755C on hypoxic pulmonary vasoconstriction. 310 60

The intracranial pressure (ICP) responses to administration of either halothane or isoflurane were compared in New Zealand white rabbits following a standardized cryogenic brain injury. Animals were tracheally intubated and paralyzed, and background anesthesia was maintained with morphine sulfate and nitrous oxide. Following injury and attainment of an elevated and stable ICP, animals were divided into four groups. Animals in groups I and III were maintained normocapnic throughout the experiment and administered 1 MAC halothane or isoflurane, respectively. Group II and IV animals were made hypocapnic (PaCO2 = 20 mmHg) prior to the administration of either 1 MAC halothane or isoflurane, respectively. Monitored variables were mean arterial blood pressure, ICP (ventriculostomy), end-tidal (ET) CO2, ET volatile anesthetic, the electroencephalogram, temperature, and arterial blood gases. Prior to producing the lesion, ICP was approximately 5 mmHg in all animals with no differences among groups. Sixty to ninety minutes after injury, ICP increased significantly to approximately 20 mmHg in all animals. Introduction of either halothane or isoflurane was associated with significant increases in ICP in all groups to approximately 30 mmHg. These data suggest that further significant increases in ICP may occur following introduction of either halothane or isoflurane in the presence of acute brain injury and elevated ICP. Furthermore, these ICP increases may not be altered by the prior establishment of hypocapnia.
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PMID:The intracranial pressure effects of isoflurane and halothane administered following cryogenic brain injury in rabbits. 311 88

Ventilatory CO2 response, respiratory drive and timing were investigated during anaesthesia prior to surgery in 24 spontaneously breathing cardiopulmonary healthy children. Anaesthesia was maintained with halothane, enflurane or isoflurane combined with oxygen-nitrous oxide (FIO2 0.5). The MAC values were 0.97 for halothane, 0.92 for enflurane and 0.92 for isoflurane. Pneumotachography and capnography were used and airway pressures were measured before and during breathing of 4% CO2 as well as during airway occlusion. Changes in minute ventilation were less with enflurane than with halothane and isoflurane in response to 4% CO2; however, tidal volumes were equally increased with all three agents. End-tidal CO2 tensions were significantly higher during enflurane than during both halothane and isoflurane anaesthesia, before as well as during CO2 stimulation. Respiratory rates were lower in children anaesthetized with enflurane and were unresponsive to CO2 when all three volatile agents were used. During CO2 challenge, mean inspiratory flow and maximal occlusion pressure were similarly increased in all groups.
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PMID:Ventilatory CO2 response, respiratory drive and timing in children anaesthetized with halothane, enflurane or isoflurane. 312 22

Regional (frontal, parietal, occipital, cortical, and basal ganglia) cerebral blood flow (rCBF) was examined at 1.5 and 3.5 MAC inspired isoflurane/O2 anesthesia in the rat using the radioactive microsphere technique to determine the effects of controlled hypotension with deep isoflurane anesthesia on rCBF and the response of rCBF to changes in PaCO2 when mean blood pressure (BP) was decreased to levels below the lower limit of the autoregulatory threshold. Four groups of six rats were studied with rCBF 1 determined at 1.5 MAC (mean BP 80-90 mm Hg) followed by two rCBF determinations at 3.5 MAC (mean BP 46-48 mm Hg). For CBF 1 the regional CO2 response was a 3.1-3.9% increase in rCBF/mm Hg increase in CO2. Regional cerebral blood flow (ml/g/min) ranged from 0.64 +/- 0.05-0.83 +/- 0.15 at PaCO2 of 19 mm Hg to 1.34 +/- 0.11-1.80 +/- 0.33 at PaCO2 of 41 mm Hg to 2.61 +/- 0.26-3.72 +/- 0.37 at PaCO2 of 59 mm Hg (mean +/- SEM). With controlled hypotension (CBF 2) rCBF was unchanged during normocarbia, increased 100% during hypocarbia, P less than 0.01 vs CBF 1 and decreased 30% during hypercarbia, P less than 0.01 vs CBF 1. For rCBF 3 measurements, the BP and inspired concentration of isoflurane were kept constant, while PaCO2 was increased in two and decreased in two of the four groups. Within-group comparisons between rCBF 2 and rCBF 3 results demonstrated loss of CO2 responsiveness of the rat cerebrovasculature in every region during controlled hypotension to below the autoregulatory threshold at 3.5 MAC isoflurane/O2 anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow and response to carbon dioxide during controlled hypotension with isoflurane anesthesia in the rat. 312 43

The effects of isoflurane (1 MAC) and enflurane (1 MAC) on cerebral blood flow and cerebral oxygen consumption were studied in 20 male patients without intracranial disease undergoing coronary artery bypass surgery (mean age 57 and 59 years respectively). The aim of the study was to investigate whether both agents diminish autoregulation of cerebral blood flow and CO2 reactivity of cerebral blood vessels. Patients were randomly assigned to one of two groups (10 patients each) receiving either isoflurane 1.15 vol.% or enflurane 1.68 vol.% endexpiratory. Measurements were performed and blood samples were taken in the awake state (I); 15 min after achievement of steady-state conditions with 1.68 vol.% enflurane or 1.5 vol.% isoflurane without blood pressure support (II); during norepinephrine-induced hypertension at a cerebral perfusion pressure of 110 mmHg (III); and during controlled hyperventilation at a PaCO2 of 27 mmHg and normotension (IV). Cerebral blood flow was measured by the argon wash-in technique. Isoflurane and enflurane produced a significant drop in cardiac index and cerebral perfusion pressure and reduced cerebral blood flow significantly by 35% and 39% respectively. Cerebral oxygen consumption was also significantly decreased by 49% (isoflurane) and 50% (enflurane). Induced hypertension with norepinephrine increased cerebral blood flow significantly by 32% (isoflurane) and 26% (enflurane), while hypocapnia reduced cerebral blood flow significantly by 26% (isoflurane) and 29% (enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of isoflurane and enflurane on cerebral hemodynamics and cerebral oxygen consumption in humans]. 326 82

The respiratory effects of nitrous oxide (N2O) were studied during halothane and enflurane anaesthesia in 12 children (mean age 46.4 +/- 29.3 months, mean weight 15.3 +/- 4.2 kg) during surgery under continuous extradural anaesthesia. Four equipotent anaesthetic states were studied in random order: 1) halothane 1 MAC in oxygen, 2) halothane 0.5 MAC + 50% N2O, 3) enflurane 1 MAC in oxygen, 4) enflurane 0.5 MAC +50% N2O. End-tidal fractions of CO2 (PetCO2) and halothane and enflurane were measured using infrared analysers. The respiratory variables (tidal volume VT, minute ventilation VE, respiratory frequency F, inspiratory time Ti, mean inspiratory flow VI, effective inspiratory time Ti/Ttot) were measured using a pneumotachograph. Significant changes were observed between the four states for VE, VI, F and PetCO2, whereas the values of VT, Ti and Ti/Tot did not differ significantly. The respiratory depressant effect of 1 MAC of either halothane alone or of the mixture of halothane and N2O was very similar. During enflurane anaesthesia, PetCO2 was less increased when N2O was substituted for enflurane, owing to a significant increase in respiratory frequency. A marked decrease in VE together with an increase in PetCO2 was observed during enflurane anaesthesia (states 3 and 4) when compared to the corresponding states during halothane anaesthesia (states 1 and 2). The respiratory depressant effect of enflurane is greater than that of halothane in unpremedicated children, even when substituting N2O for an equal MAC fraction of enflurane.2+ The effect of N2O on respiratory patterns seems to depend on the inhalational agent used and/or on the vesting respiratory frequency.
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PMID:Respiratory effects of nitrous oxide during halothane or enflurane anaesthesia in children. 328 67


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