Search PubMed⌕ Search

Biomedical subjects

K Nishina

Publications and source records attributed to K Nishina.

At least 91 records · Page 5Linked to original sources
PubMed1995

Oral clonidine premedication blunts the heart rate response to intravenous atropine in awake children.

BACKGROUND: Clonidine, which is known to have analgesic and sedative properties, has recently been shown to be an effective preanesthetic medication in children. The drug may cause side effects, including bradycardia and hypotension. This study was conducted to evaluate the ability of intravenous atropine to increase the heart rate (HR) in awake children receiving clonidine preanesthetic medication. METHODS: We studied 96 otherwise healthy children, 8-13 yr old, undergoing minor surgery. They received, at random, oral clonidine 2 or 4 micrograms.kg-1 or placebo 105 min before scheduled induction of anesthesia. Part I (n = 48, 16 per group): When hemodynamic parameters after insertion of a venous catheter had been confirmed to be stable, atropine was administered in incremental doses of 2.5, 2.5, and 5 micrograms.kg-1 every 2 min. The HR and blood pressure were recorded at 1-min intervals. Part II (n = 48, 16 per group): After the recording of baseline hemodynamic values, successive doses of atropine (5 micrograms.kg-1 every 2 min, to 40 micrograms.kg-1), were administered until HR increased by 20 beats.min-1. The HR and blood pressure were recorded at 1-min intervals. RESULTS: Part I: The increases in HR in response to a cumulative dose of atropine 10 micrograms.kg-1 were 33 +/- 3%, 16 +/- 3%, and 8 +/- 2% (mean +/- SEM) in children receiving placebo, clonidine 2 micrograms.kg-1, and clonidine 4 micrograms.kg-1, respectively (P < 0.05). Part II: The HR in the control group increased by more than 20 beats.min-1 in response to atropine 20 micrograms.kg-1 or less. In two patients in the clonidine 4 micrograms.kg-1 group, HR did not increase by 20 beats.min-1 even after 40 micrograms.kg-1 of atropine. CONCLUSIONS: Oral clonidine premedication (4 micrograms.kg-1) blunted the increase in HR after intravenous atropine in awake children, although clonidine 2 micrograms.kg-1 did not. A larger dose of atropine was required to increase the HR by 20 beats.min-1 in children receiving the premedicant in the larger dose.

Administration, Oral↗
PubMed1995

Does early posttreatment with lidocaine attenuate endotoxin-induced acute injury in rabbits?

BACKGROUND: It is well known that endotoxin causes acute lung injury, resulting in adult respiratory distress syndrome. Lidocaine pretreatment has recently been shown to attenuate endotoxin-induced lung injury in rabbits. The aim of the current study was to determine whether early postinjury treatment with intravenous lidocaine could attenuate acute lung injury induced by endotoxin in rabbits. METHODS: Thirty-two male anesthetized rabbits were randomly assigned to receive one of four treatments (n = 8 for each group): infusion of saline (group S-S), infusion of saline with lidocaine treatment (group S-L), infusion of Escherichia coli endotoxin (100 micrograms.kg-1 over a 60-min period) without lidocaine treatment (group E-S), or infusion of endotoxin with lidocaine treatment (group E-L). Ten minutes after the end of infusion of endotoxin (groups E-L and E-S) or saline (groups S-S and S-L), the animals received a bolus injection followed by continuous infusion of lidocaine (2 mg.kg-1 + 2 mg.kg-1.h-1 in groups S-L and E-L) or saline (groups S-S and E-S). The rabbits' lungs were ventilated with 40% O2. Hemodynamics, peripheral leukocyte and platelet counts, and arterial O2 tension (PaO2) were recorded during the ventilation period (6 h). After the observation, lung mechanics; the cell fraction of bronchoalveolar lavage fluid (BALF); and concentrations of activated complement components C3a and C5a, cytokines, and arachidonic acid metabolites in BALF were measured and analyzed. The ratio of lung wet weight to dry weight (W/D weight ratio) and albumin concentrations in BALF were analyzed as indexes of pulmonary edema. The Cypridina luciferin analogue-dependent chemiluminescence (representing O2 production) by neutrophils isolated from the pulmonary artery and light-microscopic findings of the lung were compared among the four groups. RESULTS: Endotoxin caused decreases in peripheral leukocyte and platelet counts, lung compliance, and PaO2. It caused increases in lung W/D weight ratio; polymorphonuclear cell counts in BALF; and albumin, C3a, C5a, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, and thromboxane B2 concentrations in BALF. Lidocaine attenuated the changes in W/D weight ratio and morphologic lung damage. The change in compliance, decrease in PaO2, and albumin concentrations in BALF were slightly but significantly less in rabbits receiving lidocaine after injury. The Cypridina luciferin analogue-dependent chemiluminescence by neutrophils was greater in rabbits receiving endotoxin without lidocaine than in those receiving endotoxin with lidocaine. CONCLUSIONS: These results indicate that early treatment with lidocaine attenuates endotoxin-induced lung edema in rabbits without affecting chemical mediators in BALF. However, the improvement is slight and likely to be of little clinical significance.

Animals↗
PubMed1995

Effects of exogenous intravenous glucose on plasma glucose and lipid homeostasis in anesthetized infants.

BACKGROUND: Whether intravenous glucose administration to infants during anesthesia is necessary remains to be resolved. The current study was designed to investigate the effect of exogenous glucose infusion on plasma glucose and lipid homeostasis in infants undergoing minor surgery. METHODS: Sixty infants (inpatients, ASA physical status 1) between 1 and 11 months of age were divided randomly into three groups as follows: LR group, lactated Ringer's solution (LR) alone; D2LR group, 2% glucose in LR; and D5LR group, 5% glucose in LR. Anesthesia was induced and maintained with halothane and nitrous oxide in oxygen. All fluids were infused at a rate of 6 ml.kg-1.h-1 until 1 h after surgery. Plasma concentrations of glucose, nonesterified fatty acids, ketone bodies, insulin, and cortisol were determined at induction of anesthesia, at the end of surgery, and 1 h after surgery. RESULTS: No infants in the three groups had hypoglycemia (< 50 mg.dl-1) throughout the study. In the LR group, plasma glucose concentration remained unchanged perioperatively compared with the basal values (at induction), whereas in the D2LR group, it increased during surgery but remained normoglycemic. In the D5LR group, plasma glucose concentration increased markedly both during and after surgery. In 6 of 20 infants, plasma glucose was greater than 200 mg.dl-1 at the end of surgery. In 8 of 20 infants receiving glucose-free infusion, plasma glucose concentrations decreased at the end of surgery. In contrast, the plasma glucose concentration increased in infants receiving glucose infusion. In the LR group, plasma concentrations of nonesterified fatty acids and ketone bodies increased at the end of and after surgery, suggesting lipid mobilization. The base excess decreased in the LR groups as concentration of the ketone bodies increased. Plasma insulin concentrations increased in the D2LR and D5LR groups and decreased after surgery in infants receiving a glucose-free solution. No intergroup differences in plasma cortisol concentrations existed at any sample point. CONCLUSIONS: These data indicate that, in otherwise healthy infants undergoing minor surgery, intravenous infusion of 2% glucose may be sufficient to maintain plasma glucose concentrations within physiologic ranges and to prevent a compensatory increase in lipid mobilization (lipolysis) when fluids are infused at a rate of 6 ml.kg-1.h-1. However, there are limitations in extrapolating the results to neonates.

Anesthesia↗
PubMed1995

The accuracy of references in Anaesthesia.

We reviewed all the references quoted in Volume 45 (1990) (n = 3967) and half the references quoted in Volume 49 (1994) (n = 2183) of Anaesthesia. The references were numbered sequentially and 100 references from each year were randomly selected. Citations of non-journal articles were omitted leaving 197 citations for careful scrutiny. The authors' names, article title, journal title, volume number, page numbers, and year were examined in each selected reference. A reference was deemed correct if each element of the citation was identical to its source. Of the references examined, 32% and 41% contained one or more errors in 1990 and 1994, respectively. The elements most likely to be inaccurate were, in descending order of frequency, article title, author, and page number. There was no significant difference in the error rate between the 2 years. It is the responsibility of contributors to ensure that all references are carefully checked.

Anesthesia↗
PubMed1995

Attenuation of hyperoxic lung injury in rabbits with superoxide dismutase: effects on inflammatory mediators.

BACKGROUND: Superoxide dismutase (SOD) has been shown to attenuate hyperoxic lung injury. This effect is thought to be exhibited by scavenging superoxide released from neutrophils and other aerobic cells. The aim of the current study was to investigate the effect of pre-treatment with SOD on the chemical mediators in hyperoxic lung injury. METHODS: Thirty male anesthetized rabbits were allocated to receive one of three treatments (n = 10 for each group): ventilated with 100% oxygen for 36 h with or without recombinant human SOD (rhSOD) treatment, and ventilated with air for 36 h without rhSOD. In the rhSOD-treated group, a single intravenous dose of rhSOD 10,000 U kg BW-1 was administered immediately after the start of exposure to 100% oxygen and thereafter infused at a rate of 340,000 U kg BW-1 day-1 for 36 h until the animals were sacrificed. The lungs of all rabbits were ventilated with 100% oxygen or air. Haemodynamics, PaO2, and lung mechanics were recorded during the ventilation period. After exposure to 100% oxygen, lung mechanics, cell fraction of bronchoalveolar lavage fluid (BALF), activated complements, cytokines, and arachidonic acid metabolite concentrations in BALF were measured and analyzed. The lung wet-to-dry (W/D) weight ratio and albumin concentrations in BALF were determined as indices of pulmonary oedema. RESULTS: Exposure to the high concentration of oxygen for 36 h caused no significant changes in haemodynamics but decreased compliance and increased A-aDo2. In the rhSOD-treated group, the decrease in compliance was not observed. At the end of the 36 hr-exposure period, however, hyperoxia significantly increased the lung W/D weight ratio, influx of neutrophils into the lung, BALF concentrations of C3a, C5a, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, thromboxane B2, and albumin. Pre-treatment with rhSOD attenuated these increases. Exposure to 100% oxygen caused extensive morphologic lung damage (alveolar haemorrhage and hyaline membrane formation), which was lessened by rhSOD. CONCLUSION: These results indicate that intravenous rhSOD prevented hyperoxic lung injury (decreases in PaO2 and compliance, increased pulmonary vascular permeability, histopathological damage) in rabbits. This prophylactic effect of rhSOD amy be due, in part, to decreased chemical mediators such as activated complements, cytokines, and arachidonic acid metabolites.

Animals↗
PubMed1995

The accuracy of reference lists in Acta Anaesthesiologica Scandinavica.

To determine the accuracy of bibliographic citation in Acta Anaesthesiologica Scandinavica, we reviewed all 1990 volumes and part of 1994 volumes of the journal and sequentially numbered all references appearing in those years (n = 2701 and 2158 in 1990 (No. 1-No. 8) and 1994 (No. 1-No.5), respectively). We randomly selected 100 references from each year. After citations of nonjournal articles were excluded, the remaining 195 citations were carefully scrutinized. Authors' names, article title, journal title, volume number, page numbers, and year were examined in each selected reference. A reference was deemed correct if each element of the citation was identical to its source. Of the examined references, 40% and 45% contained one or more errors in 1990 and 1994, respectively. The elements most likely to be inaccurate were, in descending order of frequency, article title, author, and page number. No significant differences existed in the error rate between the two years. We have found many citation errors in the reference lists of Acta Anaesthesiologica Scandinavica and no improvement in these latest four years. All contributors to Acta Anaesthesiologica Scandinavica should thoroughly check the accuracy of reference lists.

Anesthesiology↗
PubMed1995

Fentanyl attenuates cardiovascular responses to tracheal extubation.

We carried out a controlled, randomized, double-blind study to examine the effects of intravenous fentanyl (1 or 2 micrograms kg-1) on hemodynamic changes during tracheal extubation and emergence from anesthesia in 60 ASA physical status I or II patients undergoing elective gynecological surgery. Anesthesia was maintained with 0.5%-1.5% isoflurane and 60% nitrous oxide (N2O) in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to three group (each, n = 20), and fentanyl (1 or 2 micrograms kg-1), or saline (as a control) was given at the time of peritoneal closure. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation. Adverse effects, including postoperative sedation and respiratory depression, were also assessed. The HR, systolic BP, and diastolic BP increased significantly during tracheal extubation in the control group (P < 0.05). Fentanyl 2 micrograms kg-1 attenuated the increases in these variables more effectively than fentanyl 1 microgram kg-1. The time interval from the study drug to extubation was similar in each group. Postoperative somnolence and respiratory depression were not observed in any patients in any of the three groups. We concluded that a bolus dose of intravenous fentanyl 2 micrograms kg-1 given at the time of peritoneal closure was of value in attenuating the cardiovascular changes associated with tracheal extubation and emergence from anesthesia, and that this treatment did not prolong the recovery. However, further studies are required to assess this technique in patients with cardiovascular or cerebrovascular diseases.

Adult↗
PubMed1994

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, respectively. 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.

Biliary Atresia↗
PubMed1994

Omeprazole reduces preoperative gastric fluid acidity and volume in children.

To explore the effects of oral omeprazole on preoperative gastric fluid pH and volume in children, 104 healthy in-patients aged 4-9 yr were randomly allocated to four groups (n = 26). Subjects in the Omeprazole-Omeprazole Group received two doses of omeprazole (20 mg per dose), those in the Placebo-Placebo Group, two doses of placebo, those in the Placebo-Omeprazole and Omeprazole-Placebo Groups, one dose each of the two preparations by mouth. For each treatment regimen, the first medication was administered at 9:00 p.m. on the night before surgery and the second at 5:30 a.m. on the morning of the day of surgery (three hours preoperatively). Children undergoing elective surgery were offered 10 ml.kg-1 of apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. The administration of omeprazole at bedtime before surgery increased gastric pH (3.3 +/- 1.3 vs 2.0 +/- 0.6, P < 0.05) in comparison with placebo, as did two doses of omeprazole (pH = 4.8 +/- 1.6, P < 0.05). A single dose of omeprazole administration on the morning of the day of surgery failed to increase gastric pH. There was a reduction in the number of children with a pH < 2.5 and a volume > 0.4 ml.kg-1 in the Omeprazole-Omeprazole and Omeprazole-Placebo Groups, compared with the Placebo-Placebo or Placebo-Omeprazole Groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Inhibitory effect of prostaglandin E1 on human neutrophil function.

Neutrophils accumulated in the lung are thought to play a pivotal role in the pathogenesis of host auto-injury such as adult respiratory distress syndrome (ARDS). We investigated the effect of prostaglandin E1 (PGE1) on several aspects of human neutrophil function. PGE1 significantly decreased reactive oxygen species (ROS), (O2-, H2O2, OH.) generation by neutrophils as well as neutrophil phagocytosis and chemotaxis. In contrast, the drug did not affect the levels of ROS generated by a cell-free ROS generating system. In addition, intracellular calcium concentrations ([Ca2+]i) in neutrophils stimulated by f-Met-Leu-Phe were decreased in the presence of PGE1. These data suggest that the reduction in ROS production and neutrophil phagocytosis and chemotaxis by PGE1 may contribute to the effectiveness of the drug in host auto-injury including ARDS. The suppression of the increase in [Ca2+]i may at least be responsible for inhibition of these neutrophil functions by PGE1.

Adult↗
PubMed1994

Effects of oral nizatidine on preoperative gastric fluid pH and volume in children.

We have studied the effect of oral nizatidine 6 mg kg-1 in total on preoperative gastric fluid pH and volume in children. One hundred and four healthy children, aged 4-11 yr, were allocated randomly to four groups (n = 26): placebo administered at 21:00 and 06:30 the night before and on the day of surgery, respectively (placebo-placebo: control); nizatidine 6 mg kg-1 at 21:00 and placebo at 06:30 (nizatidine-placebo); placebo at 21:00 and nizatidine 6 mg kg-1 at 06:30 (placebo-nizatidine); and nizatidine 3 mg kg-1 at 21:00 and 06:30 (nizatidine-nizatidine). Each child ingested a large volume of apple juice 3 h before estimated induction of anaesthesia. After induction of anaesthesia, pH and volume of gastric fluid obtained via an orogastric tube were measured. Mean pH in the placebo-nizatidine and nizatidine-nizatidine groups was significantly higher than that in the placebo-placebo group (5.7 (SEM 0.3), 6.0 (0.3) vs 1.8 (0.2), respectively) (P < 0.05). Mean pH in the nizatidine-placebo group was similar to that in the control group (2.3 (0.3) vs 1.8 (0.2)). The number of children with pH < 2.5 and volume > 0.4 ml kg-1 in the nizatidine-nizatidine (0%) and placebo-nizatidine (4%) groups was reduced compared with the control (46%) or nizatidine-placebo (38%) group.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

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 Escherichia coli endotoxin (30 micrograms 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 alpha, interleukin-1 beta, 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.

Animals↗
PubMed1994

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

We conducted a placebo-controlled, randomized, and double-blinded study to evaluate the efficacy of manidipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation. Thirty normotensive patients (ASA physical status 1) undergoing elective surgery were allocated to one of three groups (n = 10 for each); placebo, 5 mg manidipine, and 10 mg manidipine groups. These tablets were orally administered 3 h before induction of anaesthesia. Anaesthesia was induced with thiopentone 5 mg.kg-1 iv, and tracheal intubation was facilitated with vecuronium 0.2 mg.kg-1. Laryngoscopy lasting 30 sec was attempted 2 min after induction of anaesthesia. Patients receiving placebo showed a significant increase in systolic and diastolic blood pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving manidipine 10 mg compared with patients receiving placebo or manidipine 5 mg (P < 0.05). Oral administration of manidipine 10 mg before induction of anaesthesia is a simple and effective method for attenuating pressor response to laryngoscopy and tracheal intubation. We stressed that the potential beneficial effect of a reduced haemodynamic reaction to intubation might be obtained at the expense of hypotension later on.

Administration, Oral↗
PubMed1994

Clonidine decreases the dose of thiamylal required to induce anesthesia in children.

Clonidine is a useful drug to give preoperatively because it produces anxiolysis, sedation, and hemodynamic stability, and reduces intravenous and volatile anesthetic requirements. Several premedicants, including midazolam and diazepam, have been shown to reduce the induction dose of intravenous anesthetics, such as thiopental, ketamine, or propofol. A randomized, double-blind controlled study was conducted to evaluate the effect of premedication with oral clonidine on thiamylal requirement for the induction of anesthesia and on associated hemodynamic changes in children. Sixty children (ASA grades I-II, 7-12 yr old) were assigned randomly to receive one of three treatments (n = 20, for each group): placebo (control), clonidine 2 micrograms/kg, or clonidine 4 micrograms/kg 105 min before the induction of anesthesia. Thiamylal was injected at a dose of 1 mg/kg every 15 s until loss of the eyelash reflex and the dose was recorded. Blood pressure (BP), heart rate (HR), and arterial oxygen saturation were recorded every minute from the beginning of injection of thiamylal for 5 min. Significant decreases in thiamylal dose were observed in patients receiving clonidine. The induction dose of thiamylal (mean +/- SD) was 5.4 +/- 0.9, 4.5 +/- 1.1, and 3.4 +/- 0.9 mg/kg for patients receiving placebo, clonidine 2 micrograms/kg, and clonidine 4 micrograms/kg, respectively (P < 0.05). Systolic BP decreased by 6.8%, 5.6%, and 6.6% and HR increased by 5.7%, 4.8%, and 4.1% after administration of thiamylal in the control (placebo) group and the clonidine 2 micrograms/kg and clonidine 4 micrograms/kg groups, respectively (P > 0.05). Premedication with oral clonidine reduced the dose of intravenous thiamylal required for the induction of anesthesia in children.

Anesthesia, Intravenous↗