Hideaki Yaku

Efficacy of Oral Clonidine Premedication in Children

BackgroundClonidine, an α2-adrenoceptor agonist, has been shown to be effective as a preanesthetic medication in adults. The current study was designed to investigate the efficacy of two doses of oral clonidine as a premedicant preceding oral atropine in children. MethodsIn a prospective, randomized, double-blind, controlled clinical trial, 105 children, aged 4–12 yr, undergoing elective ophthalmologic surgery received 0.4 mg/kg diazepam, 2 μg/kg clonidine, or 4 μg/kg clonidine orally. These agents mixed with apple juice were administered 105 min before the estimated time of induction of anesthesia, and were followed by treatment with 0.03 mg/kg oral atropine 60 min before anesthesia. A blinded observer noted the childrens level of sedation, quality of separation from parents, and degree of acceptance of mask application during inhalation of nitrous oxide used for establishment of venous access. Anesthesia was induced with 5 mg/kg thiamylal, and tracheal intubation was facilitated with 0.2 mg/kg vecuronium. Hemodynamic changes after tracheal intubation were compared among the three groups. ResultsClonidine produced significant sedation, and the effect was dose related. Clonidine, 4 μg/kg, provided better quality of separation and acceptance of mask than the two other regimens. This dose of clonidine attenuated the increases in blood pressure and heart rate after tracheal intubation. No clinically significant perioperative hypotension or bradycardia was observed. ConclusionsThese data indicate that, even in pediatric surgery, the combination of 4 μg/kg and 0.03 mg/kg oral clonidine is an effective premedication. However, the safety and optimal dose of clonidine in this setting remain to be determined.

Effect of Lidocaine Pretreatment on Endotoxin-induced Lung Injury in Rabbits

Background:It is well known that endotoxin causes acute lung injury resulting in adult respiratory distress syndrome. Numerous cellular and humoral factors such as macrophages, neutrophils, platelets, and inflammatory mediators (e.g., activated complements, cytokines, and arachidonic acid metabolites) are thought to play a pivotal role in the pathogenesis of endotoxin-induced lung injury. Furthermore, pulmonary edema in acute lung injury is associated with an increase in vascular permeability that may arise from a perturbation of the endothelial cell surface membrane. Lidocaine has been shown to inhibit function of these cells and stabilize cell membranes. The aim of the current study was to determine whether pretreatment with intravenous lidocaine could attenuate acute lung injury induced by endotoxin in rabbits. Methods:Twenty-seven anesthetized male rabbits were randomly assigned to receive one of three treatments (n=9 for each group); infusion of saline (as a control), infusion of Escbericbia coli endotoxin (30 µg kg-1 over a 60–min period) without treatment with lidocaine, and infusion of endotoxin with treatment with lidocaine. A single dose of intravenous lidocaine 2 mg·kg-1 was administered 10 min before infusion of endotoxin and thereafter infused at a rate of 2 mg·kg-1· h-1 until 6 h after the start of endotoxin administration, when the animals were killed. The lungs of the rabbits were ventilated with 40% oxygen. Hemodynamics, peripheral leukocytes counts, and arterial oxygen tension were recorded during the ventilation period. After the observation, lung mechanics, cell fraction of bronchoalveolar lavage fluid (BALF), activated complements, cytokines, and arachidonic acid metabolites concentrations in BALF were measured and analyzed. The lung wet- to dry-weight ratio and albumin concentrations in BALF were analyzed as an indices of pulmonary edema. The cypridina luciferin analog-dependent chemiluminescence (representing superoxide production) by neutrophils isolated from the pulmonary artery and light microscopic findings were compared among the three groups. Results:Endotoxin caused decreases in peripheral leukocyte counts, lung compliance, and arterial oxygen tension, and increases in the lung wet- to dry-weight ratio, polymorphonuclear cell counts in BALF, and albumin, C3a, C5a, tumor necrosis factor α, interleukin-1β2, and thromboxane B2 concentrations in BALF. Lidocaine pretreatment attenuated these changes. The cypridina luciferin analog—dependent chemiluminescence was greater in rabbits receiving endotoxin than in the control. Lidocaine pretreatment attenuated the increase in chemiluminescence. Endotoxin caused extensive morphologic lung damage, which was lessened by lidocaine. Conclusions:These results suggest that intravenous lidocaine pretreatment has a prophylactic effect on endotoxin-induced lung injury in rabbits. However, further studies are required to investigate the therapeutic (as an early posttreatment) effect of the drug given after lung injury because rabbits in the current study received lidocaine before endotoxemia.

Effects of Exogenous Intravenous Glucose on Plasma Glucose and Lipid Homeostasis in Anesthetized Children

Whether or not intravenous glucose administration during pediatric anesthesia is necessary remains a controversial issue. The current study was designed to investigate the effect of glucose infusion on concentrations of plasma glucose, nonesterified fatty acids (NEFA), triglycerides, ketone bodies, and insulin and to determine whether the use of solutions containing less than 5% glucose would maintain physiologic plasma glucose concentrations during tympanoplasty lasting about 6 h. Forty-five children aged between 1.5 and 9 yr were divided randomly into three groups of 15 patients each to receive the following intravenous solutions: LR groups, lactated Ringers solution (LR) alone; D2LR group, 2% glucose in LR; and D5LR group, 5% glucose in LR. All fluids were infused at a rate of 6 ml.kg-1.h-1 until 1 h after anesthesia. In the LR group, the plasma glucose concentrations remained unchanged perioperatively compared with basal values, whereas in the D2LR group they showed a gradual increase during surgery but remained normoglycemic. On the other hand, in the D5LR group, the plasma glucose concentrations increased markedly both during and after the operation. Furthermore, 3 of 15 patients showed hyperglycemia of more than 300 mg.dl-1 during anesthesia. There was no evidence of lipid mobilization or impaired secretion of insulin, since plasma NEFA, triglycerides, ketone bodies, and insulin remained within normal concentration ranges throughout the sample period in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Pregnant Patient with Primary Pulmonary Hypertension: General Anesthesia and Extracorporeal Membrane Oxygenation Support for Termination of Pregnancy

PRIMARY pulmonary hypertension (PPH) is a progressive and fatal disease characterized by elevation of the pulmonary vascular resistance and right heart failure. 1,2 PPH often becomes evident during pregnancy and may lead to maternal death during pregnancy, labor, or in the postpartum period. We describe a case of a pregnant woman with severe PPH and heart failure who underwent Cesarean section for termination of pregnancy under general anesthesia with the assistance of extracorporeal membrane oxygenation (ECMO).

The Effect of Halothane and Sevoflurane on Fatigue-induced Changes in Hamster Diaphragmatic Contractility

The purpose of this study was to examine the effect of halothane and sevoflurane on fatigue-induced changes in diaphragmatic contractility. Forty-two hamster diaphragm strips were randomly allocated according to anesthetics (no anesthesia control, 1%-3% halothane, 2%-6% sevoflurane) and stimulated directly in an organ bath. Under the influence of the anesthetics, muscle fatigue was induced by repetitive tetanic contraction, and diaphragmatic contractilities (i.e., peak twitch and tetanic tension, twitch contraction time, and half-relaxation time) were measured before and after fatigue. Neither halothane nor sevoflurane changed tension generation before or after fatigue, but each anesthetic significantly enhanced fatigue-induced prolongations of the contraction time and half-relaxation time after fatigue. Specifically, the half-relaxation times after fatigue in the 3% halothane, 4% sevoflurane, and 6% sevoflurane groups (225.6 +/- 37.6, 236.0 +/- 76.5, and 287.3 +/- 55.5 ms, respectively) were more than twice as long as those of the control group (104.7 +/- 19.7 ms, P < 0.05). We conclude that halothane and sevoflurane augment fatigue-induced prolongations of the contraction and relaxation times. Diaphragmatic function may deteriorate when there is a fatiguing task during the clinical administration of halothane or sevoflurane anesthesia. Implications: This study implicates diaphragmatic fatigue during anesthesia. An in vitro hamster diaphragm muscle preparation was used to study the effect of halothane and sevoflurane on fatigue-induced change in contractility. Our findings suggest that increased load on the diaphragm during volatile anesthesia may lead to impaired diaphragmatic contractility. (Anesth Analg 1998;86:392-7)

Attenuation of hypertensive response to tracheal intubation with nitroglycerin

STUDY OBJECTIVE To evaluate the efficacy and safety of intravenous (IV) nitroglycerin in attenuating the hypertensive response to laryngoscopy and intubation as a new application of the drug. DESIGN Controlled, randomized, double-blind study. SETTING University hospital. PATIENTS Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each. INTERVENTIONS Anesthesia was induced with thiopental sodium 5 mg/kg i.v., and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Either 1.5 micrograms/kg of nitroglycerin, 2.5 micrograms/kg of nitroglycerin, or saline (control) was administered IV simultaneously with the start of laryngoscopy (lasting 30 seconds), which was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in nitroglycerin-treated patients compared with those in the control group (p < 0.05). CONCLUSION A single, rapid IV dose of nitroglycerin is a simple, practical, effective, and safe method to attenuate the hypertensive response to laryngoscopy and tracheal intubation.

Effects of Nilvadipine on the cardiovascular responses to tracheal intnhation

STUDY OBJECTIVE To evaluate the efficacy of nilvadipine given orally in attenuating the hypertensive response to laryngoscopy and intubation. DESIGN Controlled, randomized, double-blind study. SETTING Induction of anesthesia for elective surgery at a university hospital. PATIENTS Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each. INTERVENTIONS Either 2 mg of nilvadipine, 4 mg of nilvadipine, or a placebo (control) was administered orally 90 minutes before induction of anesthesia. Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide (N2O) in oxygen. Laryngoscopy lasting 30 seconds was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS Patients receiving the placebo showed a significant increase in mean arterial pressure (MAP) and heart rate associated with tracheal intubation. The increase in MAP following tracheal intubation was significantly lower in nilvadipine-treated patients than in the control group (p less than 0.05). However, neither dose of nilvadipine attenuated the tachycardic response to intubation. CONCLUSIONS Oral administration of nilvadipine before induction of anesthesia is a simple and practical method for attenuating pressor response to laryngoscopy and tracheal intubation after standard elective induction under additional 1% enflurane-N2O anesthesia.

Partial attenuation of the cardiovascular responses to tracheal intubation with oral nisoldipine.

STUDY OBJECTIVE To evaluate the efficacy and safety of nisoldipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation. DESIGN Randomized, double-blind, placebo-controlled study. SETTING Induction of anesthesia for elective surgery at a university hospital. PATIENTS Thirty normotensive patients (ASA physical status I) undergoing elective surgery were assigned to one of three groups; placebo, nisoldipine 5 mg, or nisoldipine 10 mg. Each group consisted of ten patients. INTERVENTIONS Either 5 mg of nisoldipine, 10 mg of nisoldipine, or a placebo was administered orally 2 hours before induction of anesthesia. Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 seconds was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS Patients receiving the placebo showed a significant increase in mean arterial pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving nisoldipine 10 mg compared with patients receiving the placebo (p less than 0.05). CONCLUSIONS Oral administration of nisoldipine before induction of anesthesia is a simple, practical, and safe method for attenuating pressor response to laryngoscopy and tracheal intubation.

Prostaglandin E1 and tracheal intubation : relationship between the cardiovascular responses and plasma catecholamine concentrations

A study was carried out on 30 normotensive patients (American Society of Anesthesiologists physical status 1) to investigate whether or not a suppressive effect of 0.3 or 0.6 μg/kg prostaglandin E1 on the hypertensive response to tracheal intubation was due to inhibition of the increase in plasma catecholamine concentrations following the stressful stimulation. A total of 30 patients in three groups underwent elective surgery. Anaesthesia was induced with 5 mg/kg sodium thiopentone given intravenously and tracheal intubation was facilitated by 0.2 mg/kg vecuronium. Either saline (group A) or 0.3 (group B) or 0.6 μg/kg (group C) prostaglandin E1 was administered intravenously 15 s before direct laryngoscopy (lasting 30 s) which was attempted 2 min after administering thiopentone and vecuronium. All groups exhibited significant (P < 0.05) increases in mean arterial pressure, heart rate, rate – pressure product and plasma noradrenaline concentrations following tracheal intubation, but the increases in mean arterial blood pressure and rate – pressure product were significantly (P < 0.05) less in groups B and C than in group A. Prostaglandin E1, however, enhanced the increase in plasma noradrenaline concentrations following intubation. Data suggest that attenuation of the pressor response to intubation by prostaglandin E1, may not be due to inhibition of the noradrenaline release stimulated by intubation but to inhibition of noradrenaline-induced vasoconstriction.

Improvement of gas exchange following endobronchial instillation of an exogenous surfactant in an infant with respiratory failure by postoperative pulmonary haemorrhage.

We administered surfactant to a 5-month-old infant with respiratory failure due to right pulmonary haemorrhage accompanied by oedema following abdominal surgery. These pathological conditions were probably precipitated by disseminated intravascular coagulation and intra-operative excessive administration of fluids, respecitively. Endobronchial instillation of the exogenous surfactant (120 mg) after selective intubation of the right bronchus produced a dramatic improvement of gas exchange 30 min after treatment and of chest X-ray findings at 6 h post-treatment. This case on an infant indicates that administration of surfactant may be one of promising therapeutic approaches to respiratory failure due to pulmonary haemorrhage.