Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although changes in cerebral blood flow (CBF) and the electroencephalogram (EEG) have been reported with nitrous oxide (N2O) administration, the interaction of these parameters is unclear. The purpose of this study was to measure CBF and EEG during N2O administration in eight patients. A craniotomy was performed and CBF was measured in major brain arteries using a transit time Doppler flowmeter. EEG was recorded bilaterally from frontooccipital leads. Power spectrum analysis was performed on the EEG and power for delta, theta, alpha, and beta frequency bands analyzed over time. Arterial blood pressure was recorded continuously. N2O (66%) was added to the inspired gases during isoflurane anesthesia (0.8% end tidal) under hypocapnic (Paco2 = 29 mm Hg) and normocapnic conditions (Paco2 = 39 mm Hg). During hypocapnia, N2O administration decreased alpha EEG activity and increased delta activity but did not change CBF. During normacapnia, N2O produced similar but greater changes in EEG and increased CBF 39%. In three patients, the isoflurane concentration was increased to 1.6% end tidal during normocapnia. N2O administration in these patients also enhanced delta EEG activity and increased CBF. The slowing of EEG activity with N2O is temporally related to increases in CBF during normocapnia. Hypocapnia abolished the increase in CBF during N2O and attenuated the shift of EEG to delta activity.
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PMID:Nitrous oxide added to isoflurane increases brain artery blood flow and low frequency brain electrical activity. 777 71

To study the pathophysiology of idiopathic postoperative brain swelling or hemorrhage after arteriovenous malformation resection, termed normal perfusion pressure breakthrough (NPPB), we performed cerebral blood flow (CBF) studies during 152 operations in 143 patients, using the xenon-133 intravenous injection method. In the first part of the study, CBF was intraoperatively measured (isoflurane/N2O anesthesia) during relative hypocapnia in 95 patients before and after resection. The NPPB group had a greater increase (P < 0.0001) in mean +/- standard deviation global CBF (28 +/- 6 to 47 +/- 16 ml/100 g/min, n = 5) than did the non-NPPB group (25 +/- 7 to 29 +/- 10 ml/100 g/min, n = 90); both arteriovenous malformation groups showed greater increase (P < 0.05) than did controls undergoing craniotomy for tumor (23 +/- 6 to 23 +/- 6 ml/100 g/min, n = 22). Ipsilateral and contralateral CBF changes were similar. In a second cohort of patients with arteriovenous malformations, CBF was measured at relative normocapnia and it increased (P < 0.002) from pre- to postresection (40 +/- 13 to 49 +/- 15 ml/100 g/min, n = 57). There were no NPPB patients in this latter cohort. The feeding mean arterial pressure was measured intraoperatively before resection or at the last embolization before surgery (n = 64). The feeding mean arterial pressure (44 +/- 16 mm Hg) was 56% of the systemic arterial pressure (78 +/- 12 mm Hg, P < 0.0001) and was not related to changes in CBF from pre- to postresection. There was an association between increases in global CBF from pre- to postresection and NPPB-type complications, but there was no relationship of these CBF changes to preoperative regional arterial hypotension. These data do not support a uniquely hemodynamic mechanism that explains cerebral hyperemia as a consequence of repressurization in hypotensive vascular beds.
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PMID:Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. The Columbia University Arteriovenous Malformation Study Project. 872 37

Remifentanil hydrochloride is a new opioid rapidly metabolized by blood and tissue esterases. The swift degradation accounts for the elimination half-life (t1/2 beta) of < 10 min. An anesthetic agent allowing more rapid postoperative assessment of the neurosurgical patient would be beneficial. This study examined the effect of remifentanil on cerebral blood flow (CBF) reactivity to changes in the arterial pressure of carbon dioxide (PaCO2). Cerebral blood flow was measured with intravenous 133-Xenon during remifentanil/ nitrous oxide (N2O) anesthesia in 10 patients undergoing craniotomy. Cerebrovascular reactivity was determined by repeating CBF measurements after the addition of carbon dioxide (CO2) to the inspired gas mixture. The CBF increased from 21 +/- 6 to 31 +/- 7 ml/100 g/min as the PaCO2 increased from 27 +/- 4 to 36 +/- 3 mm Hg. The relative CBF reactivity was 3.6 +/- 1.2%/mm Hg CO2. During the CBF determinations, the doses of remifentanil administered were not significantly different (0.38 +/- 0.18 microgram/kg/min at hypocapnia vs. 0.34 +/- 0.16 microgram/kg/min at normocapnia). Electroencephalographic monitoring showed a spectral edge frequency of 26 +/- 1 Hz before induction, 25 +/- 1 Hz during maintenance of the remifentanil/N2O anesthetic (0.32 +/- 0.15 microgram/kg/ min), 24 +/- 1 Hz during hypocapnic CBF determination, and 24 +/- 2 Hz during normocapnic CBF determination. At the completion of the procedure, the patients responded to commands within 3.6 +/- 2.5 min and were extubated 7.2 +/- 4.5 min after the remifentanil/N2O was discontinued. In conclusion, absolute CBF values during remifentanil/N2O are similar to previously reported CBF values during fentanyl/N2O and isoflurane/N2O anesthesia, and cerebrovascular reactivity to CO2 remains intact.
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PMID:Intact cerebral blood flow reactivity during remifentanil/nitrous oxide anesthesia. 910 Jan 82

Nitrous oxide (N2O) use during anesthesia for intracranial procedures has been a subject of controversy in the past. To date, the isolated influence of N2O on mean cerebral blood flow velocity in the middle cerebral artery (VMCA) has not been investigated during hypocapnia in patients with brain tumors. We compared VMCA during normocapnic (ETCO2: 40 mm Hg) and hypnocapnic (ETCO2: 25 mm Hg) inhalation of air and 50% nitrous oxide in oxygen N2O/O2 in eight patients with unilateral brain tumors on both the tumor side and the healthy side. Six patients completed the study. Mean VMCA increased during normocapnic inhalation of N2O/O2 (tumor side: 86 +/- 16 cm sec-1; healthy side: 74 +/- 17 cm sec-1) when compared with air (tumor side: 72 +/- 18 cm sec-1; healthy side: 62 +/- 14 cm sec-1, p < 0.01), whereas during hyperventilation VMCA decreased on both sides (p < 0.001). Mean VMCA values were quite similar during hypocapnic inhalation of 50% N2O/O2 (tumor side: 50 +/- 12 cm sec-1; healthy side: 45 +/- 13 cm sec-1) and air (tumor side: 51 +/- 14 cm sec-1; healthy side: 45 +/- 12 cm sec-1). The data of our study suggest that in patients with cerebral tumors the N2O-induced increase in mean VMCA can be completely reversed by hyperventilation.
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PMID:Effects of normo- and hypocapnic nitrous-oxide-inhalation on cerebral blood flow velocity in patients with brain tumors. 910 Jan 83

Hyperventilation may reverse increases in cerebral blood flow velocity caused by inhalation of nitrous oxide (N2O). This study sought to determine whether inhalation of 50% nitrous oxide after the induction of hyperventilation increases cerebral blood flow velocity as measured by transcranial Doppler ultrasonography. Seven volunteers breathed air/O2 through a modified Circle system at normocapnia followed by air/O2 with hyperventilation, and then N2O/O2 with hyperventilation. Expired gas concentrations were measured in the expiratory limb of the circuit distal to a one-way valve. Hyperventilation reduced end-tidal carbon dioxide from 38+/-1 mmHg to 26+/-1 mmHg. Hypocapnia was maintained during inhalation of N2O (EtCO2=28+/-1 mmHg). Mean cerebral blood flow velocity decreased 34% with hyperventilation (38+/-4 cm/second versus 59+/-9 cm/second, p < 0.05) and returned to baseline with the addition of nitrous oxide (58+/-7 cm/second), despite persistent hypocapnia. The addition of nitrous oxide to the inspired gas mixture after induction of hypocapnia reversed reductions in cerebral blood flow velocity associated with hyperventilation. Potential benefits of induced hypocapnia in patients with intracranial pathology may be offset by the administration of N2O.
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PMID:Effect of nitrous oxide on cerebral blood flow velocity after induction of hypocapnia. 968 1

Sevoflurane and propofol have been widely used as anesthetic agents for neurosurgery. Recent evidence has suggested that the influence of these anesthetics on cerebral oxygenation may differ. In the present study, the authors investigated jugular bulb oxygen saturation (SjO2) during propofol and sevoflurane/nitrous oxide anesthesia under mildly hypothermic conditions. After institutional approval and informed consent, 20 patients undergoing elective craniotomy were studied. Patients were randomly divided to the group S/N2O (sevoflurane/nitrous oxide/fentanyl anesthesia) or the group P (propofol/fentanyl anesthesia). After induction of anesthesia, the catheter was inserted retrograde into the jugular bulb and SjO2 was analyzed. During the operation, patients were cooled and tympanic membrane temperature was maintained at 34.5 degrees C. SjO2 was measured at normocapnia during mild hypothermia and at hypocapnia during mild hypothermia. There were no statistically significant differences in demographic variables between the groups. During mild hypothermia, SjO2 values were significantly lower in group P than in group S/N2O. The incidence of SjO2 less than 50% under mild hypothermic-hypocapnic conditions was significantly higher in group P than in group S/N2O. These results suggest that hyperventilation should be more cautiously applied during mild hypothermia in patients anesthetized with propofol and fentanyl versus sevoflurane/nitrous oxide/fentanyl.
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PMID:Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients. 1467 62

Cerebral blood flow response to changes in PaCO2 was studied in the edematous cerebral cortex of 19 patients with malignant supratentorial tumors using laser Doppler flowmetry technology. General anesthesia for craniotomy was induced with thiopental, 3-5 mg/kg i.v., and N2O, 60% in O2. In random sequence, 8 patients were assigned to receive fentanyl, 6 +/- 1.6 (SEM). mug/kg i.v.; the other 11 received isoflurane, 0.56% end-tidal + 0.07 (SEM). After a craniotomy bone flap was turned and the dura was opened, laser flowmetry probes were placed over surgically undisturbed cortex that was known to be edematous from preoperative CT and MRI scans. Flow index measurements were first made at hypocarbia (PaCO2 = 24.2 +/- 0.9 and 21.5 +/- 2.1 mm Hg for the fentanyl and isoflurane groups, respectively). Minute ventilation was then decreased and cortical flow index was remeasured with PaCO2 = 34.2 +/- 0.6 and 33.0 +/- 0.8 mm Hg for the fentanyl and isoflurane groups, respectively. Hypocarbia during fentanyl-supplemented N2O-O2 anesthesia resulted in a cortical flow index that was 70 +/- 8% of the flow index at near normocarbia (p <0.05). During isoflurane N2O-O2 anesthesia, however, there was a wide variety of responses to hypocarbia, including three patients whose flow indices increased markedly. The mean flow index during hypocarbia was significantly (p <0.05) lower during fentanyl-N2O anesthesia than it was during isoflurane-N2O anesthesia. There was no predictable relationship between the type of brain tumor and the CBF response to hypocapnia during isoflurane-N2O anesthesia. It is concluded that, in edematous brain, cerebral cortical blood flow response to hypocarbia is more likely to be preserved during fentanyl-supplemented N2O-O2 anesthesia than it is during isoflurane-supplemented N2O-O2 anesthesia. In neuropathologic states where hyperventilation is thought to be necessary to reduce cerebral blood flow and decrease brain bulk, isoflurane may be less satisfactory than fentanyl as a supplement to N2O-O2 anesthesia.
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PMID:Cerebrovasculr response to CO2 in edematous brain during either fentanyl or isoflurane anesthesia. 1581 11


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