Fujio Karasawa

Effects of propofol on cerebral blood flow and the metabolic rate of oxygen in humans

Background: Effects of propofol on human cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and blood flow‐metabolism coupling have not been fully evaluated. We therefore assessed the effects of propofol on total‐CBF and CMRO2 in patients without noxious stimuli and neurologic disorders.

Profile Soft-seal Cuff, a New Endotracheal Tube, Effectively Inhibits an Increase in the Cuff Pressure Through High Compliance Rather than Low Diffusion of Nitrous Oxide

We assessed the nitrous oxide (N2O) gas-barrier properties of a new endotracheal tube cuff, the Profile Soft-Seal Cuff (PSSC) (Sims Portex, Kent, UK). The tracheas of randomly selected patients were intubated with the Trachelon (Terumo, Tokyo, Japan), Profile Cuff (PC) (Sims Portex), or PSSC (n = 15 for each) endotracheal tube. Cuffs were inflated with air, and intracuff pressure was measured during anesthesia with 67% N2O. The concentration of N2O in cuffs was measured at the end of anesthesia. Postoperative sore throat was assessed. The volume-pressure relationship and thickness of the cuff were also measured. Cuff pressure, which increased gradually during anesthesia, was significantly less in the PSSC and PC groups than in the Trachelon group. The PSSC had smaller pressure than the PC 120 min after the start of anesthesia (P <0.05). There were no significant differences in the N2O concentration in cuffs among the groups, although the PSSC had the thinnest cuff with the highest compliance. The incidence of postoperative sore throat in the Trachelon group was significantly higher than in the other two groups. In summary, the PSSC effectively inhibits an increase in cuff pressure during anesthesia with N2O. The underlying mechanism is probably the higher compliance of the thinner cuff, rather than a reduction in N2O diffusion into the cuff. Implications A new material with nitrous oxide (N2O) gas barrier properties produces a thin and highly compliant cuff without increasing N2O diffusion, thereby reducing the increase of intracuff pressure and postoperative sore throat. Because the increase in the cuff pressure is time dependent, the Profile Soft-Seal Cuff (Sims Portex, Kent, UK) might be better than the Profile Cuff (Sims Portex) for anesthesia of a long duration.

Effects of sevoflurane on cerebral blood flow and cerebral metabolic rate of oxygen in human beings: a comparison with isoflurane

Background and objective: Isoflurane is commonly used for neurosurgery but the effects of sevoflurane on human cerebral blood flow and cerebral metabolic rate of oxygen have not been fully evaluated. We therefore assessed the effects of sevoflurane and isoflurane on global cerebral blood flow and cerebral metabolic rate of oxygen in patients without noxious stimuli or neurological disorders. Methods: General anaesthesia was induced with midazolam (0.2 mg kg−1) and fentanyl (5 μg kg−1) in 20 ASA I patients undergoing knee joint endoscopic surgery. Epidural anaesthesia was also performed to avoid noxious stimuli during surgery. Cerebral blood flow and cerebral arteriovenous oxygen content difference was measured using the Kety-Schmidt method with 15% nitrous oxide as a tracer before and after administration of either sevoflurane or isoflurane (1.5 minimum alveolar concentration, 60 min) and cerebral metabolic rate of oxygen was then calculated. Results: Sevoflurane and isoflurane both increased cerebral blood flow (17%, P < 0.05; 25%, P < 0.05, respectively) and decreased cerebral metabolic rate of oxygen (26%, P < 0.01; 38%, P < 0.01, respectively). There were no significant differences in cerebral blood flow and cerebral metabolic rate of oxygen between sevoflurane and isoflurane. Conclusions: Sevoflurane and isoflurane similarly increased cerebral blood flow and decreased cerebral metabolic rate of oxygen in human beings anaesthetized with midazolam and fentanyl.

The effect on intracuff pressure of various nitrous oxide concentrations used for inflating an endotracheal tube cuff.

UNLABELLED We sought to determine the optimal concentration of nitrous oxide (N(2)O) for inflating endotracheal tube cuffs, to avoid overinflation and air leaks. Female patients undergoing endotracheal intubation (inner diameter 7.5 mm) during anesthesia with 67% N(2)O were randomly assigned to five groups of 25 subjects each, in which cuffs were inflated with 0% (Air), 30% (N30), 40% (N40), 50% (N50), or 67% (N67) N(2)O. The cuff pressure and the N(2)O concentration in the cuff were measured. In an additional 15 patients (N40-a group), pilot balloons were replaced with metal tubes, and the mouths and noses of the patients were wrapped with tape, to minimize N(2)O efflux into the air. Postoperative sore throats were evaluated in double-blinded interviews. Cuff pressures increased significantly in the Air and N30 groups but decreased in the N67 group. Cuff pressures were <22 mm Hg in the N40 and N50 groups, but the N50 group had air leaks. The N(2)O concentration in the cuff in the N40 group was significantly smaller than that in the N40-a group, suggesting N(2)O rediffusion. The incidence of sore throats (40% in the Air group) was reduced significantly in the N40 and N50 groups. Therefore, 40% N(2)O is optimal for filling the cuff during anesthesia with 67% N(2)O. IMPLICATIONS Nitrous oxide (N(2)O) diffuses into the cuff, equilibrating at a smaller concentration than the gas mixture with which patients are ventilated. Our data indicate that inflation of the cuff with 40% N(2)O is recommended to prevent both excessive endotracheal cuff pressure and air leaks during anesthesia with 67% N(2)O, reducing postoperative sore throats.

Propofol injection pain is not alleviated by pretreatment with flurbiprofen axetil, a prodrug of a nonsteroidal antiinflammatory drug

AbstractPurpose. The effects of nonsteroidal antiinflammatory drugs (NSAIDs) on pain from propofol injection are controversial, partially because NSAIDs themselves cause injection pain. We evaluated the effects of flurbiprofen axetil (LFP), a prodrug of an NSAID, on pain induced by intravenous propofol injection, because LFP produces little pain on injection. Methods. A randomized, double-blind, controlled trial was undertaken in patients who were assigned to one of three groups (n = 50 in each). Patients received either 5 ml of saline followed approximately 10 min later by propofol mixed with 0.4 ml of saline, LFP (50 mg, 5 ml) i.v. followed by propofol mixed with 0.4 ml of saline, or 5 ml of saline followed by propofol mixed with lidocaine (40 mg, 0.4 ml). Verbal rating scores for injection pain were assessed every 10 s during propofol administration at a rate of 0.05 mg·kg−1·s−1. Results. None of the patients complained of pain during injection of LFP or saline. Admixture of lidocaine, but not of LFP, significantly reduced the incidence of pain and the severity of pain scores during propofol injection (P = 0.0017 and P < 0.001, respectively). Conclusion. Lidocaine, but not LFP, is effective for controlling pain induced by propofol injection. This result suggests that NSAIDs have little effect on pain from propofol injection.

Deflationary phenomenon of the nitrous oxide-filled endotracheal tube cuff after cessation of nitrous oxide administration.

After cessation of nitrous oxide (N2O) administration, intracuff pressure of the endotracheal tube may decrease through rediffusion of N2O. There may then be an increased risk for air leaks, aspiration of gastric contents, or both. In this study, the time required for intracuff pressure to decrease by 50% (T1/2) after substituting oxygen for N2O inspired was estimated with the least-squares method. Fifty patients were randomly assigned to five groups, and their tracheas were intubated with the Hi-Contour, Sheridan, Rush, Reinforce, or Profile Soft-Seal Cuff endotracheal tubes. Cuffs were inflated with 40% N2O, and cuff pressure was measured during anesthesia with 67% N2O. After 120 min, N2O inspired was replaced with 100% oxygen, and cuff pressure was measured until the cuff pressure decreased by about 30%. In the five groups, stable cuff pressures were achieved during 120 min of anesthesia with N2O. The cuff pressures at 120 min were not different among groups (P = 0.098). After cessation of N2O administration, the intracuff pressure decreased exponentially. T1/2 in the Hi-Contour group was 27.8 ± 8.5 min, which was significantly shorter than in the Profile Soft-Seal Cuff group (49.7 ± 18.5 min;P < 0.01). Therefore, our results demonstrate that pressure of the N2O-filled cuff decreases quickly when N2O-inspired concentrations are reduced, and we suggest that intracuff pressure should be checked frequently to avoid air leaks or aspiration of gastric contents during delayed extubation or transportation of patients with tracheal intubations. IMPLICATIONS A recently developed method for maintaining stable cuff pressure (N2O-filled cuffs) enables us to assess the decrease in cuff pressure after cessation of N2O administration. Our results confirm the limitations of N2O-filled cuffs when N2O-inspired concentrations are reduced.

The Brandt tube system attenuates the cuff deflationary phenomenon after anesthesia with nitrous oxide.

The Brandt tube system can limit excessive cuff pressure during nitrous oxide (N(2)O) anesthesia, but there is a lack of data assessing whether the Brandt tube system avoids cuff deflation after cessation of N(2)O administration. In this study, we recorded air-filled cuff pressures of the Mallinckrodt Brandt or Hi-Contour (control) tracheal tubes (Mallinckrodt, Athlone, Ireland) during 67% N(2)O anesthesia and the cuffs were aspirated if the cuff pressure exceeded 22 mm Hg; 180 min later, O(2) was substituted for N(2)O. The cuff pressure of both groups significantly decreased after N(2)O anesthesia but the time required for the cuff pressure to return to the initial pressure was longer in the Brandt group than in the control group (76.5 +/- 35.2 min and 36.5 +/- 18.1 min, respectively; P = 0.03). The incidence of air leaks was more frequent in the control group than in the Brandt group (P = 0.015); changes in intracuff N(2)O were small in the Brandt group (6.6 +/- 1.2% to 3.4 +/- 0.9%) compared with those in the control group (46.2 +/- 3.8% to 18.6 +/- 5.6%). Therefore, the Brandt tube system attenuates the cuff deflationary phenomenon after N(2)O anesthesia, whereas repeated cuff deflation during N(2)O anesthesia causes cuff deflation after cessation of N(2)O, resulting in a possible risk of air leaks.

Nitrous oxide concentrations in maternal and fetal blood during Caesarean section

Background and objective: There are little data on nitrous oxide (N2O) concentrations in neonatal blood at delivery. We investigated the effects of the time elapsing between the induction of anaesthesia and delivery (the I-D interval) on umbilical blood N2O concentrations. Methods: Maternal and neonatal blood N2O concentrations were measured in 27 patients undergoing Caesarean section under N2O 67% anaesthesia. The duration of N2O administration (range 2-50 min) was arbitrarily divided into three groups (each n = 9): short (2-9 min), medium (9.1-14 min) and long duration (14.1-50 min). Results: Compared with a rapid increase in the maternal arterial N2O concentration (48.9 ± 4.7%), the umbilical venous N2O concentration (17.9 ± 8.3%) rose slowly in the short duration group, whereas the N2O concentrations became more similar (61.6 ± 4.3 and 43.2 ± 10.0%, respectively) in the long duration group. The ratio of umbilical vein to maternal artery N2O concentrations correlated with the duration of N2O anaesthesia (r = 0.739), resulting in ratios of 0.37 ± 0.18, 0.61 ± 012 and 0.70 ± 0.13 for the short, medium and long duration groups, respectively. The Apgar score at 1 min correlated inversely with the duration of anaesthesia and with the umbilical vein N2O concentration (r = −0.457 and −0.423, respectively). Conclusions: The data suggest that placental N2O transfer during Caesarean section is time-dependent and slower compared with maternal N2O uptake. They also suggest that the Apgar score is less affected by N2O administration when the I-D interval is shorter.

Repeated deflation of a gas-barrier cuff to stabilize cuff pressure during nitrous oxide anesthesia.

Although a nitrous oxide (N2O) gas-barrier cuff effectively limits the increase of cuff pressure during N2O anesthesia, there are few data assessing whether an N2O gas-barrier cuff is more beneficial for stabilizing intracuff pressure than standard endotracheal tubes when cuffs are repeatedly deflated to stabilize pressure during N2O anesthesia. In the present study, the pressure of air-filled standard-type cuffs (Trachelon; Terumo, Tokyo, Japan) and N2O gas-barrier type endotracheal tube cuffs (Profile Soft-Seal Cuff [PSSC]; Sims Portex, Kent, UK) was measured during 67% N2O anesthesia (n = 8 in each), during which the cuffs were repeatedly deflated every 30 min (Trachelon) or 60 min (PSSC) for the first 3 or 4 h. After aspirating the cuffs for 3 h, the cuff pressure exceeded 22 mm Hg in more than half of the patients in both groups. However, aspiration of the cuffs for 4 h decreased the maximal cuff pressure between deflation intervals in both groups (P < 0.01 for each), and increased the intracuff N2O concentration (P < 0.0001 for each). After deflating the cuffs over 4 h, the cuff pressure in both groups never exceeded 22 mm Hg during the subsequent 3 h, and intracuff N2O concentrations did not significantly change. Therefore, deflation of cuffs for 4 h during N2O anesthesia sufficiently stabilized cuff pressure and equilibrated the intracuff N2O concentrations in both groups. The use of the PSSC endotracheal tube might be more practical because of the smaller number of cuff deflations required, but the PSSC does not reduce the duration of cuff deflations to stabilize the pressure.

Effects of alpha adrenoreceptor antagonists, prazosin and. yohimbine, on intrathecal lidocaine-induced antinociception in mice.

Background: The precise mechanisms involved in the spinal analgesic effect of lidocaine are not yet clear. We previously found that lidocaine releases noradrenaline, a modulator of nociception, in rat spinal cord. Here, we attempted to clarify whether or not the noradrenaline release contributes to spinal analgesia by lidocaine.