Hypocapnia Attenuates, and Nitrous Oxide Disturbs the Cerebral Oximetric Response to the Rapid Introduction of Desflurane

The aim of this study was to develop a nonlinear mixed-effects model for the increase in cerebral oximetry (rSO2) during the rapid introduction of desflurane, and to determine the effect of hypocapnia and N2O on the model. Twelve American Society of Anesthesiologist physical status class 1 and 2 subjects were allocated randomly into an Air and N2O group. After inducing anesthesia, desflurane was then increased abruptly from 4.0 to 12.0%. The PET(CO2), PET(DESF) and rSO2 were recorded at 12 predetermined periods for the following 10 min. The maximum increase in rSO2 reached +24-25% during normocapnia. The increase in rSO2 could be fitted to a four parameter logistic equation as a function of the logarithm of PET(DESF). Hypocapnia reduced the maximum response of rSO2, shifted the EC50 to the right, and increased the slope in the Air group. N2O shifted the EC50 to the right, and reduced the slope leaving the maximum rSO2 unchanged. The N2O-effects disappeared during hypocapnia. The cerebrovascular reactivity of rSO2 to CO2 is still preserved during the rapid introduction of desflurane. N2O slows the response of rSO2. Hypocapnia overwhelms all the effects of N2O.

Role of nitric oxide and ATP-sensitive K+ channels in regulation of basal blood flow and hypercapnic vasodilatation of cerebral blood vessels in rabbit

The mechanisms underlying cerebral hypercapnic vasodilatation are not fully understood. To investigate the role of nitric oxide [NO] and ATPsensitive potassium [KATP] channels in basal blood flow regulation and hypercapnia-induced vasodilatation in rabbit cerebral blood vessels. The change in cerebral blood flow was measured by a laser Doppler flowmeter in 18 New Zealand white rabbits, in two groups, under general anesthesia with sodium pentobarbital. Nomega- nitro-L-arginine methyl ester [L-NAME] and glibenclamide were administered locally and systemically before and during induction of hypercapnia. The change in cerebral blood flow was not significant following local and systemic L-NAME administration, showing a nonsignificant role of local and systemic NO in regulation of rabbit basal cerebral blood flow. Hypercapnia increased cerebral blood flow by 17.3 +/- 4.4% before and 17.3 +/- 5.8% after local, and 5.8 +/- 3.2% [p<0.05] after systemic L-NAME administration. The change in cerebral blood flow was not significant after local and systemic administration of glibenclamide indicating a lack of KATP channel role in basal blood flow regulation. Hypercapnia increased cerebral blood flow by 27.2 +/- 8.7% before and 24.7 +/- 6.4% after local, and 49.3 +/- 9.7% after systemic administration of glibenclamide [p: NS in both cases]. Regional NO production had no role in basal cortical blood flow regulation and systemic NO contributed to 66% increment in cerebral blood flow during hypercapnia. Also, the KATP channels did not mediate the effect of NO or other vasodilators responsible for increasing cerebral blood flow during hypercapnia

Effect of severity of pulmonary disease on nitrous oxide washin and washout characteristics.

The influence of chronic obstructive pulmonary disease (COPD) on the nitrous oxide (N2O) washin and washout characteristics was evaluated in 90 (ASA II-III) males undergoing elective peripheral surgery under general anaesthesia with controlled ventilation. Patients were classified by preoperative bedside pulmonary function testing into three groups. Group I (n = 30), patients without COPD (FEV1/FVC > 80% predicted values; control group); Group II (n = 30), patients with mild COPD (FEV1/FVC = 65-79% of predicted values); and Group III (n = 30), patients with moderate COPD (FEV1/FVC = 50-64% of predicted values). The anaesthetic technique was standardized for all patients. The Datex Capnomac Ultima monitor was used to measure the inspired and expired concentrations of nitrous oxide (N2O), carbon dioxide (CO2), and isoflurane. The duration of both N2O washin (time from start of N2O administration to equilibrium of inspired and expired N2O concentrations) and 5 per cent washout (time from discontinuation of N2O to an expired N2O concentration of 5 per cent of the equilibrium value) were recorded. The duration of N2O washin and washout were significantly prolonged in Groups II and III (P < 0.001) as compared to the control group (Group I). The end-tidal CO2 concentration decreased significantly during N2O washout without causing oxygen desaturation (SpO2 < 90%). We conclude that the duration of N2O washin and washout were significantly prolonged in anaesthetized patients with COPD which may delay the induction and recovery from N2O anaesthesia.

Difusión del óxido nitroso e los globos de los tubos endotraqueales / Nitrous oxide difusion in endotracheal cuffs

Con objeto de analisar las variables de presión de los globos endotraqueales durante la anestesia, se llevó a cabo un estudio en 20 pacientes adultos, programados para cirugía traumatológica. El estado físico ASA fue I y II. Se dividieron en dos grupos de 10 pacientes, y se manejaron con anestesia general balanceada a base de O2-N2O, Halotano-Fentanyl. Los tubos endotraqueales utilizados fueron Rush N§ 34, 36 y 38. El grupo I se insufló el globo con aire y el grupo 2 con solución salina. Se hicieron mediciones a los 20, 40, 60, 90 y 120 min., después de la intubación. En el grupo I la presión inicial en mmHg fue de 130.8 ñ 5.6 y después de 120 minutos se incrementó hasta 144 mmHg. En el grupo II la presión inicial fue de 131.4 ñ 13 mmHg y después de 120 minutos aumentó a 163.2 mmHg