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)

The authors measured resting ventilation, the ventilatory response to added CO2, the VD/VT ratio, the rate of carbon dioxide output, and arterial PCO2 in four healthy volunteers, awake and anesthetized with, in order (I) enflurane 0.4 MAC with nitrous oxide 70 per cent, (II) enflurane 1.1 MAC with nitrous oxide 70 per cent, and (III) enflurane 1.1 MAC alone. Enflurane 1.1 MAC reduced ventilation and the response to added CO2 markedly, increased the VD/VT radio, reduced rate of CO2 output, and elevated values of PaCO2 from 41 +/- 1 to 65 +/- 3 mmHg (mean +/- SEM). Enflurane 1.1 MAC with nitrous oxide 70 per cent had similar effects. Enflurane 1.1 MAC with nitrous oxide 70 per cent had similar effects. Enflurane 0.4 MAC with nitrous oxide 70 per cent caused much smaller changes in each measured respiratory variable, increasing PaCO2 values to only 49 +/- 1 mmHg. The results indicate that enflurane 1.1 MAC alone is too potent a depressant of alveolar ventilation to permit spontaneous breathing, but that the "equi-anesthetic" enflurane 0.4 MAC with nitrous oxide 70 per cent may not be. The magnitude of the beneficial respiratory effects of substituting nitrous oxide for an equivalent amount of vapor is substantially greater with enflurane than with either halothane or isoflurane.
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PMID:Respiratory effects of nitrous during enflurane anesthesia in humans. 680 35

Nalbuphin is a new agonist-antagonist opioid, with a noteworthy ceiling-effect in terms of analgesia and respiratory depression, a proper cardiocirculatory innocuousness, so that it seems to be a safe analgesic in children. Our study reports 40 thoracic or abdominal surgical procedures, with nalbuphine 0.22 +/- 0.04 mg.kg-1 as sole analgesic. To ensure maintenance of anaesthesia, a volatile anaesthetic agent is inhaled at 1.1 +/- 0.4 MAC concentration, and vecuronium 0.08 +/- 0.05 mg.kg-1 is administered at induction. There was no evidence of haemodynamic changes, and no change in CO2 production. There was no analgesia related adverse effect, and awakening occurred promptly. This report suggests that nalbuphin is a suitable analgesic for paediatric surgery.
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PMID:[Peroperative evaluation of nalbuphine in pediatric thoracic and abdominal surgery]. 767 Oct 57

In order to evaluate the difference between poikilo-capnic (no CO2 added to inspired gas) and iso-capnic (CO2 added to keep end-tidal CO2 constant) hypoxic ventilatory responses (HVR) awake and during 0.6 MAC isoflurane anaesthesia, seven cardio-pulmonary healthy patients were investigated. Pneumotachography and capnography were used before and during hypoxia (end-tidal O2 tension approx. 7 kPa). In the awake state, poikilo-capnic hypoxic challenges resulted in an increased HVR as indicated by a VE that on average increased by 1.4 +/- 1.0 (mean +/- s.d.) l.min-1, whereas the iso-capnic hypoxic challenges resulted in a VE increase that was 4.7 +/- 2.3 l.min-1 on average. In the anaesthetized state, the corresponding value during poikilocapnia was 1.3 +/- 0.8 l.min-1 (88% of the awake responses, n.s.) and during iso-capnia 2.3 +/- 1.4 l.min-1 (49% of the awake, P < 0.02). Awake HVR was achieved by greater tidal volumes during poikilocapnia as well as during isocapnic challenges, while respiratory rates were unchanged. In the anaesthetized state, during poikilocapnia, however, HVR was mediated by an increased respiratory rate, (from 17.5 +/- 1.7 breath.min-1 to 20.2 +/- 2.2) and during isocapnia by a combination of increased rate (from 17.1 +/- 1.9 breath.min-1 to 19.1 +/- 1.8) and tidal volume (from 496 +/- 80 to 560 +/- 83 ml). It is concluded that poikilocapnic HVR is maintained at 0.6 MAC isoflurane whereas iso-capnic HVR is depressed by 50%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans. 772 78

Inhalation anesthetics diminish cerebrovascular resistance, augmenting cerebral blood flow (CBF) and hematic volume. This may lead to a dangerous increase in intracranial pressure (ICP). It has been observed that isoflurane used in hypocapnia does not appear to cause an increase in ICP equal to that caused by other inhalation anesthetics. The authors aimed to evaluate the effects of isoflurane on ICP and on intracranial vessel reactivity to changes in CO2 using a pulsed intracranial Doppler technique which measures cerebral flow velocity (CFV). A prospective study was performed at the Neurosurgery Clinic of the University of Milan in 10 in-patients due to undergo surgical removal of supratentorial intracranial expansion. Patients were anesthetised with isoflurane 1 MAC in air and O2. The following parameters were monitored: ICP at a spinal subarachnoid level; mean arterial pressure (MAP); cerebral perfusion pressure (CPP); ECG; CFV; EtCO2. The study was subdivided into 5 stages: basal (before induction); hypocapnia lasting 30 min; registration of data for 10 min; stabilisation phase in normocapnia; registration in normocapnia. The results show that during hypocapnia isoflurane causes significant reductions in MAP and CCP whereas ICP and CFV tend to diminish but not significantly. On the contrary, isoflurane in normocapnia causes an increase in ICP and a further and more marked reduction in CPP with a corresponding but not significant increase in CFV. In conclusion, in the light of these results the increase in ICP and the contemporary reduction of MAP would appear to restrict the use of isoflurane in normocapnia in patients with intracranial pathologies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of inhalation anesthetics on intracranial pressure and cerebral blood flow velocity]. 776 Oct 12

Mechanical hyperventilation may produce hypocapnic apnoea below the carbon dioxide off-switch threshold whereas an increase in arterial PCO2 after post-hyperventilation apnoea causes reappearance of respiratory effort above the carbon dioxide on-switch threshold. To study the effects of surgical stimulation on these two thresholds, we have measured end-tidal PCO2 (PE'CO2) at the two thresholds, before and during surgical stimulation, in 14 patients undergoing mastectomy, anaesthetized with sevoflurane (1.2 MAC). Based on the reproducibility of the results, data from 11 patients were analysed and data from the three other patients were discarded. Before surgical stimulation, mean resting PE'CO2' off-switch threshold and on-switch threshold were 5.7 (SEM 0.2), 5.2 (0.2) and 6.1 (0.2) kPa, respectively. The off-switch threshold was significantly less than resting PE'CO2 (P < 0.01) but the on-switch threshold was significantly greater than resting PE'CO2 (P < 0.01). During surgical stimulation, resting PE'CO2' off-switch threshold and on-switch threshold were 4.8 (0.2), 4.1 (0.2) and 4.7 (0.2) kPa, respectively. Although the off-switch threshold was significantly less than resting PE'CO2 (P < 0.01), there were no significant differences between resting PE'CO2 and on-switch threshold. These results indicate that surgical stimulation does not affect equally the carbon dioxide on- and off-switch thresholds.
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PMID:Effects of surgical stimulation on the apnoeic thresholds for carbon dioxide during anaesthesia with sevoflurane. 782 82

The relationship between intracranial pressure and arterial blood pressure during sevoflurane or halothane anesthesia was evaluated in New Zealand white rabbits after cryogenic brain injury. Fourteen rabbits were randomized to be anesthetized with 1.5 MAC of sevoflurane or halothane in oxygen. All animals were paralyzed with pancuronium, and mechanically ventilated. A cryogenic lesion was created over the left hemisphere. Thirty minutes later, the intracranial pressure had risen to a mean value of 15 mm Hg. The inhaled concentration of anesthetic drugs was then increased to achieve a blood pressure of 35 mm Hg. Baseline measurements were made of monitored variables including mean arterial pressure, intracranial pressure, esophageal temperature, end-tidal CO2, and arterial blood gases. Neosynephrine was then infused to raise the blood pressure from 35 to 100 mm Hg during 20 min. The PaCO2 was maintained between 38 and 42 mm Hg. At baseline, there were no significant differences in mean arterial pressure, intracranial pressure, and blood gas values between the two groups. The intracranial pressure in the sevoflurane anesthesia group increased from 11 +/- 1 to 44 +/- 4 mm Hg as mean arterial pressure increased from 35 to 100 mm Hg. Intracranial pressure in the halothane anesthesia group increased from 9 +/- 1 to 32 +/- 3 mm Hg during the same range of blood pressure. Linear regressions of intracranial pressure on mean arterial pressure were performed for each of the two anesthetic groups. The slope of the regression line for the sevoflurane animals (0.491) was significantly greater than that for the halothane animals (0.323, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sevoflurane versus halothane anesthesia after acute cryogenic brain injury in rabbits: relationship between arterial and intracranial pressure. 800 Jan 96

Although volatile anesthetic is known as a cerebral vasodilator, its mechanism is not clear. The purpose of this study was to investigate effects of sevoflurane or halothane on contractions induced by high K+ and serotonin in the isolated canine basilar artery. Cylindrical segments of canine basilar artery were placed in Krebs solution oxygenated with 95% O2 and 5% CO2 at 37 degrees C. They were then constricted with cumulative administration of 10 to 60 mM KCl, or with 10(-9) to 10(-6) M serotonin and exposed to either sevoflurane or halothane at concentration of 1.0 and 2.0 MAC. Halothane and sevoflurane at concentration of 1.0 and 2.0 MAC decreased contractile responses evoked by KCl to a similar degree. The attenuation by either of the two anesthetics at concentration of 2.0 MAC were equivalent to the inhibitions by diltiazem 2 x 10(-7) M. Contractile responses to serotonin above 3 x 10(-7) M were depressed by halothane 1.0 MAC, but not by sevoflurane 1.0 MAC. Sevoflurane and halothane at concentration of 2.0 MAC decreased contractile responses evoked by serotonin at concentrations above 3 x 10(-8) M and 10(-8) M. Removal of the endothelium did not alter the response of the basilar artery contracted by serotonin to either anesthetic. These findings suggest that sevoflurane and halothane depress the voltage-dependent Ca2+ channels due to decreases of contractile responses to high K+. Our results also demonstrate that sevoflurane is a less potent vasodilator of the basilar artery contracted by serotonin than halothane.
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PMID:[Effects of sevoflurane or halothane on contractile responses of isolated canine basilar artery]. 801 53

We have studied the effects of hypocapnia on cerebrovascular changes in two MAC-equivalent anaesthetic regimens, using the transcranial Doppler technique as an index of cerebral blood flow (CBF) in 24 healthy ASA I patients undergoing spinal surgery. Eight of the patients were subjected to carbon dioxide reactivity challenges in the awake state. Before surgery, the other 16 patients received, in random order, either 1.15% isoflurane in oxygen or 0.5% isoflurane with 70% nitrous oxide. Carbon dioxide reactivity was calculated for each group as the increase in flow velocity per kPa change in PE'CO2 (cm s-1 kPa-1). It was significantly greater for the isoflurane group (14.09 (SD 2.44) cm s-1 kPa-1) and significantly less for the isoflurane-nitrous oxide group (7.95 (1.32) cm s-1 kPa-1) compared with the awake group (11.24 (0.95) cm s-1 kPa-1). We conclude that cerebrovascular responsiveness to changes in arterial carbon dioxide concentration is influenced markedly by the anaesthetic procedure. Hyperventilation is more likely to affect CBF during isoflurane anaesthesia than during an MAC-equivalent isoflurane-nitrous oxide anaesthesia.
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PMID:Cerebrovascular carbon dioxide reactivity during exposure to equipotent isoflurane and isoflurane in nitrous oxide anaesthesia. 812 6

Ventilatory responses to hypoxia (HVR) were investigated using poikilocapnic conditions (i.e. end-tidal CO2's allowed to seek it's own level) in 15 cardio-pulmonary healthy patients who were first studied awake and then at 0.85 MAC isoflurane. The influence of hypercapnia (HyperCapnic Ventilatory Response, HCVR) was also elucidated. Pneumotachography, capnography and airway occlusion pressures at 0.1 s (P degree 0.1) were used before and during both mild hypoxia (end-tidal O2 tension 8.7 kPa) and hypercapnia achieved by an inspired CO2 concentration of 5%. HCVR was attenuated by 60% during anesthesia (P < 0.01). In the awake state, five of the 15 patients decreased HVR during hypoxia as compared with during normoxia. This resulted in a VE that on average increased by 0.6 l.min-1 (P < 0.05) whereas P degree 0.1 was unchanged. In the anesthetized state, no case of decreased HVR was seen and hypoxia induced a mean VE increase (+/- s.d.) by 1.0 +/- 0.2 l.min-1 (P < 0.001) and a P degree 0.1 that on average was improved by 0.63 +/- 0.27 cm H2O (P < 0.01). It is suggested that when the aim is to evaluate the influence of volatile anesthetic agents on HVR and to quantitate its clinical relevance during and immediately after anesthesia, a poikilocapnic technique should be used. It is concluded that the poikilocapnic HVR to PEO2's of 8.7 kPa was maintained during 0.85 MAC isoflurane.
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PMID:Poikilocapnic hypoxic ventilatory response in humans during 0.85 MAC isoflurane anesthesia. 817 50

Twenty-two methionine-containing di- to octapeptides were evaluated for their ability to be a source of methionine to support protein accretion in C2C12 myogenic and MAC-T bovine mammary epithelial cells. The cell cultures were incubated for 72 h at 37 degrees C in a humidified environment of 90% air: 10% CO2 for C2C12 cells or 95% air: 5% CO2 for MAC-T cells. The basal medium contained methionine-free Dulbecco's modified Eagle's medium and 6% desalted fetal bovine serum. Treatments included basal medium, the basal medium supplemented with one of the 22 methionine-containing peptides, or the basal medium supplemented with free L-methionine. Methionine-containing peptides with the exception of glycylmethionine and prolylmethionine in C2C12 cells were able to support protein accretion with responses ranging from 29.1 to 123.3% of the response of L-methionine. Dipeptides with methionine at the N-terminus promoted greater (P < 0.0001) protein accretion than dipeptides with methionine at the C-terminus. Stimulation of protein accretion by seven pairs of dipeptides with methionine at either the C- or the N-terminus was linearly (P < 0.0001) related to the hydrophobicity of the dipeptides. These results indicate that C2C12 myogenic and MAC-T mammary epithelial cells have the ability to utilize methionine-containing peptides as sources of methionine to support protein accretion.
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PMID:Methionine-containing peptides can be used as methionine sources for protein accretion in cultured C2C12 and MAC-T cells. 855 6


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