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K Nishina

Publications and source records attributed to K Nishina.

At least 55 records · Page 3Linked to original sources
PubMed1998

Effects of oral clonidine premedication on plasma glucose and lipid homeostasis associated with exogenous glucose infusion in children.

BACKGROUND: Oral clonidine may influence plasma glucose and lipid homeostasis by modulating endocrinologic responses to surgical stress. The effect of oral clonidine premedication on plasma glucose and lipid homeostasis associated with exogenous glucose infusion were investigated in children undergoing minor surgery. METHODS: Otherwise healthy children (n, 120; aged 3-13 yr) were assigned randomly to six groups according to the glucose concentration of the intravenous solution (0%, 2%, or 5%, at a rate of 6 ml kg(-1) x h(-1)) and the preoperative medications (4 microg/kg clonidine or placebo given 100 min before anesthesia) they were to receive. The plasma concentrations of glucose, nonesterified fatty acid, ketone bodies, epinephrine, norepinephrine, and cortisol were determined. RESULTS: Infusion of 5% glucose caused hyperglycemia (mean glucose concentration >200 mg/dl) in six children receiving placebo and two receiving clonidine. Although the mean plasma glucose concentration increased in three placebo groups, it was unchanged and the plasma concentrations of total ketone bodies and nonesterified fatty acid were increased in children receiving clonidine and glucose-free solution. The plasma epinephrine, norepinephrine, and cortisol levels in children receiving placebo increased in response to surgery. Clonidine attenuated the increase in catecholamines and cortisol. CONCLUSIONS: Oral clonidine premedication attenuated the hyperglycemic response, probably by inhibiting the surgical stress-induced release of catecholamines and cortisol. Infusion of 2% of glucose maintained plasma glucose concentrations within physiologic ranges in children receiving clonidine.

Administration, Oral↗
PubMed1998

Intravenous lidocaine attenuates acute lung injury induced by hydrochloric acid aspiration in rabbits.

BACKGROUND: Neutrophils play a crucial role in the pathogenesis of acid-induced acute lung injury. Lidocaine inhibits the function of neutrophils. This study aimed to determine whether lidocaine attenuates acute lung injury induced by hydrochloric acid (HCl) instillation. METHODS: In study 1, rabbits were divided into four groups (n = 7 each). Lung injury was induced by intratracheal HCl (0.1 N, 3 ml/kg) in two groups. The other two groups received saline intratracheally. Lidocaine given intravenously (2 mg/ g bolus + 2 mg x kg(-1) x h(-1) infusion) was started 10 min before intratracheal instillation in one HCl and one saline group, and saline was given intravenously in the other two groups. In study 2, rabbits (four groups of seven animals each) received HCl (0.1 N, 3 ml/kg) intratracheally. Treatment with intravenous lidocaine was started 10 min before, 10 min after, or 30 min after acid instillation, or saline was given intravenously 10 min before instillation. RESULTS: In study 1, HCl caused deterioration of the partial pressure of oxygen (PaO2), lung leukosequestration, decreased lung compliance, and increased the lung wet-to-dry weight ratio and albumin, interleukin-6 (IL-6), and IL-8 levels in bronchoalveolar lavage fluid. Lidocaine pretreatment attenuated these changes. Hydrochloric acid increased superoxide anion production by neutrophils and caused morphologic lung damage, both of which were lessened by lidocaine. In study 2, lidocaine given 10 min after acid instillation was as effective as pretreatment in PaO2, lung mechanics, and histologic examination. However, PaO2 changes in lidocaine 30 min after injury were similar to those in saline given intravenously. CONCLUSIONS: Intravenous lidocaine started before and immediately after acid instillation attenuated the acute lung injury, in part by inhibiting the sequestration and activation of neutrophils.

Anesthetics, Local↗
PubMed1998

Aminoguanidine attenuates endotoxin-induced acute lung injury in rabbits.

OBJECTIVE: To assess the effect of aminoguanidine, a selective inducible nitric oxide synthase inhibitor, on endotoxin-induced acute lung injury in rabbits. DESIGN: Prospective, blinded, controlled laboratory study. SETTING: University research laboratory. SUBJECTS: Twenty-eight male rabbits. INTERVENTIONS: The animals were randomly assigned to receive one of four treatments (n = 7 for each group): infusion of saline only (S-S group), infusion of saline and aminoguanidine (S-AG group), infusion of Escherichia coli endotoxin (5 mg/kg over 60 mins) (E-S group), and infusion of endotoxin and aminoguanidine (E-AG group). Fifteen minutes before infusion of endotoxin (E-S and E-AG groups) or saline (S-S and S-AG groups), the animals received an intravenous injection of 1 mg/kg of aminoguanidine (S-AG and E-AG groups) or saline (S-S and E-S groups). The same dose of aminoguanidine or saline was given 1 hr after the end of endotoxin or saline infusion. The lungs of the rabbits were ventilated with 40% oxygen. MEASUREMENTS AND MAIN RESULTS: Hemodynamics, peripheral leukocyte counts, and PaO2 were recorded during the ventilation period (6 hrs). After these observations were made, lung mechanics, cell fraction of bronchoalveolar lavage fluid, and concentrations of thromboxane A2 and prostacyclin metabolites in bronchoalveolar lavage fluid were determined. The wet weight/dry weight ratio of the lung and albumin concentrations in bronchoalveolar lavage fluid were analyzed as indices of pulmonary edema. Endotoxin decreased the lung compliance and PaO2 and increased the wet weight/dry weight ratio, neutrophil counts, and albumin concentrations in bronchoalveolar lavage fluid. The bronchoalveolar lavage fluid concentrations of thromboxane B2 in bronchoalveolar lavage fluid were increased by infusion of endotoxin. Aminoguanidine attenuated these changes. Endotoxin caused extensive morphologic lung damage, which was lessened by aminoguanidine. CONCLUSIONS: Aminoguanidine given intravenously before and after endotoxin attenuated endotoxin-induced lung injury in rabbits. These findings suggest that inducible nitric oxide synthase inhibition may be useful in the treatment of endotoxin-induced lung injury. However, further studies are required to determine the optimal dosage of aminoguanidine, when the inhibitor is given alone as therapy after lung injury.

Animals↗
PubMed1997

Prostaglandin E1, lidocaine, and prostaglandin E1-lidocaine combination for attenuating cardiovascular responses to extubation.

PURPOSE: Tracheal extubation produces haemodynamic changes that may cause myocardial ischaemia in patients with coronary arterial disease. Intravenous infusion of prostaglandin E1 (PGE1) attenuated the hypertensive response to tracheal extubation but failed to blunt the tachycardia, which was attenuated by intravenous lidocaine. Thus, we investigated whether a combination of PGE1 and lidocaine can overcome the drawbacks of treatment with PGE1 alone. METHODS: One hundred adult patients (ASA 1) undergoing elective minor surgery were randomly assigned to receive one of four treatments: saline (as a control), 1 mg-kg-1 lidocaine, infusion of 0.1 microgram-1.kg-1.min-1 PGE1, or infusion of 0.1 microgram-1.kg-1.min-1 PGE1 plus injection of 1 mg-1.kg-1 lidocaine. Lidocaine was injected two minutes before tracheal extubation. The PGE1 was infused from completion of surgery until five minutes after tracheal extubation. Anaesthesia was maintained with sevoflurane 1.0%-2.5% and nitrous oxide 60%. Heart rate (HR) and blood pressure (BP) were measured before and after tracheal extubation. RESULTS: Lidocaine alone and PGE1-lidocaine combination attenuated the increases in BP and HR observed in the control group: PGE1 alone was effective in attenuating hypertensive response but ineffective for tachycardia. The suppressive effect of the PGE1-lidocaine combination on BP increase was superior to that of each drug alone, and the combined effect on HR increase was similar to that of lidocaine alone. CONCLUSION: The combination of PGE1 infusion and lidocaine is a more effective method of attenuating hypertension and tachycardia associated with tracheal extubation than either drug alone.

Adult↗
PubMed1997

Dose-response of flurbiprofen on postoperative pain and emesis after paediatric strabismus surgery.

PURPOSE: Intravenous flurbiprofen, a non-steroidal antiinflammatory drug (NSAID), has been used recently for postoperative pain relief in adults. The drug is also likely to have antiemetic property. The present study was undertaken to investigate the effect of flurbiprofen on postoperative pain and emesis in children undergoing strabismus surgery, which is well known to produce postoperative nausea and vomiting. METHODS: In a prospective, randomised, controlled clinical trial, 90 children aged 2-11 yr received saline (control), flurbiprofen 0.5 mg.kg-1, or flurbiprofen 1 mg.kg-1. Saline and flurbiprofen were administered i.v. immediately after induction of anaesthesia. Anaesthesia was induced and maintained with sevoflurane and nitrous oxide in oxygen. Postoperative pain was assessed by a blinded observer using an objective pain scale (OPS). No opioids or antiemetics were administered throughout the study. The incidence and frequency of vomiting were compared among groups. RESULTS: Flurbiprofen 1 mg.kg-1 provided lower OPS (highest) scores during the eight hours after surgery and a reduced requirement for postoperative supplementary analgesic (diclofenac suppository) compared with the other two regimens. The two doses of flurbiprofen failed to decrease the incidence and frequency of vomiting. CONCLUSION: These data suggest that preoperative flurbiprofen 1 mg.kg-1 iv is a simple and effective approach to postoperative pain relief but not to the prevention of emesis following paediatric strabismus surgery.

Analgesics↗
PubMed1997

ONO-5046, an elastase inhibitor, attenuates endotoxin-induced acute lung injury in rabbits.

Endotoxin causes acute lung injury resembling acute respiratory distress syndrome. Elastase, as well as reactive oxygen species released from activated neutrophils, are thought to play pivotal roles in the pathogenesis of this lung injury. This study investigated whether ONO-5046, a specific elastase inhibitor, can attenuate acute lung injury induced by endotoxin in rabbits. Thirty-two male anesthetized rabbits were randomly assigned to receive one of four treatments (n = 8 for each group): infusion of saline without ONO-5046 treatment (Group S-S), infusion of saline with ONO-5046 (Group S-O), infusion of Escherichia coli endotoxin (100 micrograms/kg over 60 min) without ONO-5046 (Group E-S), and infusion of endotoxin with ONO-5046 (Group E-O). Fifteen minutes before the infusion of endotoxin (Groups E-O and E-S) or saline (Groups S-S and S-O), the animals received a bolus injection of ONO-5046 (10 mg/kg) followed by continuous infusion (10 mg.kg-1.h-1: Groups S-O and E-O) or saline (Groups S-S and E-S). The lungs of the rabbits were ventilated with 40% oxygen. Hemodynamics, peripheral leukocyte and platelet counts, and PaO2 were recorded during the ventilation period (6 h). Lung mechanics, cell fraction of the bronchoalveolar lavage fluid (BALF), activated complement, cytokines, and arachidonic acid metabolite concentrations in the BALF were measured at 6 h. The wet- to dry (W/D)-weight ratio of the lung and albumin concentrations in BALF were analyzed as indices of pulmonary edema. Endotoxin decreased lung compliance and PaO2, and increased the W/D weight ratio, neutrophil counts, and albumin concentration in the BALF. Concentrations of activated complement C5a, interleukin-6, interleukin-8, and thromboxane B2 in the BALF were increased by the infusion of endotoxin. ONO-5046 treatment attenuated these changes. Endotoxin caused extensive morphologic lung damage, which was lessened by ONO-5046. In conclusion, intravenous ONO-5046 pretreatment attenuated endotoxin-induced lung injury in rabbits. This beneficial effect of ONO-5046 may be due, in part, to a reduction in the levels of mediators that activate neutrophils, in addition to the direct inhibitory effect on elastase.

Airway Resistance↗
PubMed1997

Optimal dose of granisetron for prophylaxis against postoperative emesis after gynecological surgery.

UNLABELLED: We previously reported that 20 and 40 microg/kg of granisetron given during anesthesia prevented postoperative emesis with no severe complications. The aim of the current study was to determine the optimal dose of granisetron for the prevention of postoperative nausea and vomiting (PONV) after gynecological surgery. Two hundred female patients (ASA physical status I) were randomly allocated to one of five groups (n = 40 for each): saline (as a control), granisetron 2 microg/kg, granisetron 5 microg/kg, granisetron 10 microg/kg, and granisetron 20 microg/kg. Saline or granisetron was given intravenously immediately after induction of anesthesia. PONV was assessed 24 h after surgery. The percentage of emesis-free patients was significantly greater in the 5- to 20-microg/kg granisetron groups than in the control and 2-microg/kg granisetron groups (18%, 23%, 68%, 78%, and 75% of patients receiving saline or granisetron 2 microg/kg, 5 microg/kg, 10 microg/kg, and 20 microg/kg, respectively). Granisetron doses of 5 microg/kg or larger were also superior to the saline and 2-microg/kg granisetron treatment for the prevention of nausea over the 24-h study period (nausea visual analog scales 24 h after surgery: 49, 41, 18, 16, and 14 mm in the control and granisetron 2 microg/kg, 5 microg/kg, 10 microg/kg, and 20 microg/kg groups, respectively). A smaller proportion of patients received "rescue" antiemetic in the 5-microg/kg or larger granisetron groups than in the control and 2-microg/kg granisetron groups (48%, 40%, 18%, 13%, and 10% of patients in the control and granisetron 2 microg/kg, 5 microg/kg, 10 microg/kg, and 20 microg/kg groups, respectively). The antiemetic effect of granisetron was similar among the groups who received 5-microg/kg or larger doses. In conclusion, we suggest that the optimal dose of granisetron is 5 microg/kg for the prevention of PONV after gynecological surgery. IMPLICATIONS: Nausea and vomiting postoperatively after gynecologic surgery is a significant problem. The authors found that granisetron, a selective antagonist of serotonin, markedly decreases the incidence of postoperative nausea and vomiting at doses of 5 microg/kg or larger.

Adult↗
PubMed1997

Attenuation of cardiovascular responses to tracheal extubation: comparison of verapamil, lidocaine, and verapamil-lidocaine combination.

UNLABELLED: We recently showed that verapamil attenuated hemodynamic responses to tracheal extubation. The aim of the current study was to compare the efficacy of a combination of intravenous (I.V.) verapamil (0.1 mg/kg) and I.V. lidocaine (1 mg/kg) with that of each drug alone in suppressing the cardiovascular changes during tracheal extubation and emergence from anesthesia. One hundred adult patients (ASA physical status I) who were to undergo elective minor surgery were randomly assigned to one of four groups (n = 25 each): Group S = saline plus saline (control), Group V = verapamil 0.1 mg/kg I.V. plus saline, Group L = lidocaine 1 mg/kg I.V. plus saline, and Group V-L = verapamil 0.1 mg/kg I.V. plus lidocaine 1 mg/kg I.V. These medications were given 2 min before tracheal extubation. Anesthesia was maintained with 1.0%-2.0% sevoflurane and 60% nitrous oxide (N2O) in oxygen. Muscle relaxation was achieved with vecuronium, and a residual neuromuscular blockade was reversed with neostigmine 0.05 mg/kg (combined with atropine 0.02 mg/kg). Changes in heart rate (HR) and arterial blood pressure (AP) were measured during and after tracheal extubation. In the control group, the HR and systolic and diastolic AP increased significantly during tracheal extubation. Verapamil, lidocaine, and their combination attenuated the increases in these variables. The beneficial effect was the greatest with the combination of verapamil and lidocaine. These findings suggest that verapamil 0.1 mg/kg and lidocaine 1 mg/kg given I.V. concomitantly 2 min before tracheal extubation is a simple and more effective prophylaxis than verapamil or lidocaine alone for attenuating the cardiovascular changes associated with tracheal extubation. IMPLICATIONS: Tachycardia and hypertension associated with tracheal extubation, which may lead to myocardial ischemia, represent a potential risk for patients with coronary arterial disease. To seek effective pharmacological prophylaxis against these complications, we compared the attenuation of hemodynamic changes among verapamil, lidocaine, and a verapamil/lidocaine combination using ASA physical status I patients and found the combination to be effective.

Adult↗
PubMed1997

Oral clonidine premedication reduces minimum alveolar concentration of sevoflurane for tracheal intubation in children.

BACKGROUND: Sevoflurane is a useful anesthetic for inhalational induction in children because of its low solubility in blood and relatively nonpungent odor. Clonidine has sedative and anxiolytic properties and reduces the requirement for inhalation agents. Nitrous oxide (N2O) also decreases the requirement of inhaled anesthetics, but the effect is variable. The minimum alveolar concentration for tracheal intubation (MAC(TI)) of sevoflurane was assessed with and without N2O and clonidine premedication. METHODS: Seventy-two patients, aged 3-11 yr, were assigned to one of six groups (n = 12 each). They received one of three preanesthetic medications (two groups for each premedication): placebo (control), 2 microg/kg oral clonidine or 4 microg/kg oral clonidine. In one group of each premedication, anesthesia was induced with sevoflurane in oxygen; in the other group, anesthesia was induced with sevoflurane in the presence of 60% N2O. Each concentration of sevoflurane at which tracheal intubation was attempted was predetermined according to Dixon's up-and-down method and held constant for at least 20 min before the trial RESULTS: The MAC(TI) of sevoflurane in the absence of N2O (mean +/- SEM) was 3.2 +/- 0.2%, 2.5 +/- 0.1%, and 1.9 +/- 0.2% in the control, 2-microg/kg clonidine, and 4-microg/kg clonidine groups, respectively. Nitrous oxide (60%) decreased the MAC(TI) of sevoflurane by 26%, 24%, and 27% in the control, 2-microg/kg clonidine, and 4-microg/kg clonidine groups. CONCLUSIONS: Oral clonidine premedication decreased the MAC(TI) of sevoflurane. Nitrous oxide also decreased the MAC(TI). The combination of clonidine and N2O lessened the MAC(TI) of sevoflurane more than did either drug alone.

Administration, Oral↗
PubMed1997

Inhaled nitric oxide does not prevent endotoxin-induced lung injury in rabbits.

BACKGROUND: Neutrophils, platelets, and cytokines are thought to play a pivotal role in the pathogenesis of endotoxin-induced lung injury which resembles features of acute respiratory distress syndrome (ARDS). For initiation of this pathological process, neutrophils and platelets are activated and adhere to pulmonary endothelium. Nitric oxide (NO) inhibits adhesion and activation of these cells and decreases the cytokine level in bronchoalveolar lavage (BAL) fluid obtained from patients with ARDS. Limited data are available on the effect of NO treatment before and after endotoxin on the development and advance of ARDS. The aim of the current study was to determine whether NO inhalation prevents acute lung injury. METHODS: Thirty-two male anaesthetized rabbits were randomly assigned to receive one of four treatments (n = 8 each); Group S-N received saline with nitrogen (N2), Group S-NO received saline infusion with NO (20 p.p.m.) inhalation, Group E-N received an infusion of Escherichia coli endotoxin 100 micrograms/ kg over 60 min with inhalation of N2, and Group E-NO received endotoxin with NO (20 p.p.m.) inhalation. The lungs of the rabbits were ventilated with 40% oxygen until 6 h after the start of endotoxin or saline administration. Haemodynamics and PaO2 were recorded during the ventilation period. After observation, the lung wet-to dry-(W/D) weight ratio, lung mechanics, and cell fraction, activated complements, cytokines, arachidonic acid metabolites, and albumin concentrations in the BAL fluid were measured and analysed. Light microscopic findings were compared among the four groups. RESULTS: Pulmonary hypertension and deterioration of oxygenation by endotoxin were less pronounced in rabbits receiving NO. The lung compliance after endotoxin was similar in Groups E-NO and E-N. The W/D weight ratio and neutrophils and albumin concentrations in the BAL fluid increased in Groups E-NO and E-N. The BAL fluid concentrations of interleukin-8, thromboxane A2, and prostacyclin were similar in the two endotoxin-treated groups. Endotoxin caused extensive morphologic lung damage regardless of NO inhalation. CONCLUSIONS: The increase in pulmonary arterial pressure and deterioration of oxygenation were less in endotoxin-exposed rabbits receiving NO inhalation compared with those receiving N2. Accumulation of neutrophils and platelets in the lung, morphological lung damage, and the release of cytokines and prostanoids were observed in the E-NO group. However, we are unable to extrapolate these results directly to the human clinical setting because of the short observation period, the use of only one dose of NO, and the species difference.

Administration, Inhalation↗
PubMed1997

Inhibitory effect of local anaesthetics on reactive oxygen species production by human neutrophils.

BACKGROUND: Reactive oxygen species (ROS) generated from neutrophils accumulated in various major organs are thought to play a pivotal role in the pathogenesis of host auto-injury. Lidocaine has been shown to reduce the injury. We investigated the effect of local anaesthetics (lidocaine, mepivacaine and bupivacaine) on ROS production by neutrophils using an in vitro system. METHODS: We measured the production of superoxide (ferricytochrome c method), hydrogen peroxide (H2O2: scopoletin fluorescence technique), and hydroxyl radical (OH.: ethylene gas method) by neutrophils isolated from human adult volunteers in the absence and presence of lidocaine (2-200 micrograms/mL), mepivacaine (3-300 micrograms/mL), and bupivacaine (3-300 micrograms/mL). We also measured the ROS generation in a cell-free (xanthine-xanthine oxidase) system. RESULTS: Lidocaine and mepivacaine at higher levels significantly decreased the production of ROS by neutrophils. However, these local anaesthetics at clinically relevant blood concentrations had no effect on the levels of ROS. Furthermore, lidocaine and mepivacaine failed to reduce ROS generated by the cell-free system. Bupivacaine did not decrease ROS generation by either generating system. CONCLUSION: In conclusion, in the present in vitro system, only concentrations of lidocaine and mepivacaine 100-fold higher than clinically feasible ones reduced ROS production by human neutrophils. However, the local anaesthetics at clinically relevant blood concentrations had no suppressive effect. Further studies using in vivo systems are required to elucidate the inhibitory effects of local anaesthetics on ROS generation in clinical settings.

Adult↗
PubMed1996

Prostaglandin E1 attenuates the hypertensive response to tracheal extubation.

PURPOSE: Tracheal extubation causes hypertension and tachycardia, which may cause imbalance between myocardial oxygen demand and supply in patients at risk of coronary artery disease. We conducted a randomized, controlled study to evaluate the effects of 0.05 or 0.1 microgram.kg-1.min-1 prostaglandin E1 (PGE1) iv on haemodynamic variables occurring during tracheal extubation and emergence from anaesthesia and compared them in patients receiving either lidocaine or saline. METHODS: Eighty ASA physical status 1 patients undergoing elective surgery were enrolled in the current study. Anaesthesia was maintained with sevoflurane 1.0%-2.5% (ET concentration) and nitrous oxide 60% in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to receive one of four treatments (n = 20 each): saline (control), 0.05 microgram.kg-1.min-1 PGE1, 0.1 microgram.kg-1.min-1 PGE1, or 1 mg.kg-1 lidocaine. PGE1 was infused from completion of surgery until five minutes after tracheal extubation. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation. RESULTS: In the control group, the HR, systolic BP, and diastolic BP increased during tracheal extubation. Administration of 0.1 microgram.kg-1.min-1 PGE1 and 1 mg.kg-1 lidocaine attenuated the increases in BP although 0.05 microgram.kg-1.min-1 PGE1 failed to do so. The inhibitory effect of the 0.1 microgram.kg-1.min-1 PGE1 on BP was similar to that of lidocaine 1 mg.kg-1 iv. The increase in HR was attenuated by lidocaine but not by PGE1. CONCLUSION: The intravenous infusion of 0.1 microgram.kg-1.min-1 PGE1 given during emergence from anaesthesia and tracheal extubation is a useful method for attenuating the hypertension associated with noxious stimuli during this period.

Adult↗
PubMed1996

Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation.

We have compared the efficacy of three calcium channel blockers, nicardipine, diltiazem and verapamil, in attenuating the cardiovascular responses to laryngoscopy and intubation in 60 normotensive patients (ASA I) undergoing rapid sequence induction of anaesthesia with thiopentone and fentanyl. We also examined whether or not these blockers inhibited catecholamine release induced by intubation. The patients were allocated to one of four groups (n = 15 for each): saline (control), nicardipine 30 micrograms kg-1, diltiazem 0.2 mg kg-1 or verapamil 0.1 mg kg-1. Verapamil and the three other drugs were administered 45 s and 60 s before the start of direct laryngoscopy, respectively, in a double-dummy design. Anaesthesia was induced with thiopentone 4 mg kg-1 i.v. and fentanyl 2 micrograms kg-1 i.v. Tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% isoflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after administration of thiopentone and vecuronium. Patients receiving saline exhibited significant increases in systolic and diastolic arterial pressures (AP), heart rate (HR) and plasma concentrations of catecholamines associated with tracheal intubation. The increase in AP was attenuated in patients treated with any calcium channel blocker. The greatest effect was elicited by verapamil, which attenuated the increase in HR, although nicardipine seemed to enhance tachycardia. All three drugs failed to suppress the increase in plasma catecholamine concentrations in response to tracheal intubation. These findings suggest that bolus injection of verapamil 0.1 mg kg-1 was a more effective method of controlling hypertension and tachycardia associated with intubation than diltiazem 0.2 mg kg-1 or nicardipine 30 micrograms kg-1, and that these prophylactic effects were not caused by inhibition of the catecholamine response.

Adult↗
PubMed1996

Oral clonidine premedication reduces postoperative pain in children.

Clonidine is an effective preanesthetic medication in children, providing a preoperative sedative effect. The analgesic properties of the drug have been well documented in adults. The current study was designed to investigate the effect of oral clonidine given preoperatively on postoperative pain in children undergoing minor surgery. In a prospective, randomized, controlled clinical trial, 90 children aged 5-12 yr undergoing elective ophthalmic, urologic, and otologic surgery received placebo (control), clonidine 2 micrograms/kg, or clonidine 4 micrograms/kg. These drugs were administered 105 min before the estimated time of induction of anesthesia and followed by treatment with oral atropine 0.03 mg/kg 60 min before anesthesia. Anesthesia was induced and maintained with halothane and nitrous oxide in oxygen. Postoperative pain was assessed by a blinded observer using an objective pain scale (OPS). Clonidine 4 micrograms/kg provided lower OPS (highest) scores during 12 h after surgery and reduced requirement for postoperative supplementary analgesic (diclofenac suppository) compared with the other two regimens. These data suggest that oral clonidine premedication (4 micrograms/kg) is a possible approach to facilitating postoperative analgesia in children undergoing minor surgery.

Administration, Oral↗
PubMed1996

A comparison of lansoprazole, omeprazole, and ranitidine for reducing preoperative gastric secretion in adult patients undergoing elective surgery.

Acid aspiration syndrome of induction of anesthesia is a life-threatening complication whose severity is affected by both pH and volume of the aspirated gastric juice. We compared the effects of two proton pump inhibitors (PPIs), lansoprazole and omeprazole, and an H2 blocker, ranitidine, on gastric secretion in a prospective, randomized, double-blind fashion in 200 adult patients of ASA physical status I undergoing elective surgery. The patients were divided into eight groups (n = 25 each) according to their premedication. The patients received lansoprazole-lansoprazole (Group L-L), lansoprazole-placebo (Group L-P), placebo-lansoprazole (Group P-L), omeprazole-omeprazole (Group O-O), omeprazole-placebo (Group O-P), placebo-omeprazole (Group P-O), placebo-ranitidine (Group P-R), or placebo-placebo (Group P-P), as the first and second medications. The dose of the study drug was 30 mg for lansoprazole, 150 mg for ranitidine, and 80 mg for omeprazole. The first medication was administered orally at 9:00 PM on the night before surgery and the second at 5:30 AM in the morning on the day of the surgery. Each patient fasted overnight and took the drug with 20 mL of water. After tracheal intubation, gastric fluid was aspirated via an orogastric tube and the volume and pH of the aspirate were measured. The pH of the aspirated gastric fluid was higher in Groups P-R, L-L, P-L, O-O, and O-P than in Group P-P (P < 0.05). The volume of the gastric contents was similar in Groups P-0 and P-P, and the other groups had smaller gastric volume than Group P-P (P < 0.05). Gastric fluid from patients in Group P-R was the least acidic (pH 6.1 +/- 1.2) and had the least volume (0.09 +/- 0.06 mL/kg). Group L-L was comparable with Group P-R in both pH and volume, whereas Groups P-L and O-O were similar to Group P-R only in volume. The proportion of patients at risk according to the traditional criteria (pH < 2.5 and volume 0.4 mL/kg) was significantly lower in Groups L-L (0%), P-L (4%), O-O (4%), and P-R (0%) than in Group P-P (48%) (P < 0.05). We concluded that two consecutive doses of lansoprazole or a morning dose of ranitidine seemed to be the most effective preanesthetic medication for reducing gastric acidity and volume.

2-Pyridinylmethylsulfinylbenzimidazoles↗