Biomedical subjects

K Nishina

Publications and source records attributed to K Nishina.

115 records · Page 7Linked to original sources

PubMedDate not supplied

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.

Administration, Oral↗

PubMedDate not supplied

The effects of sarpogrelate on superoxide production by human neutrophils.

BACKGROUND AND OBJECTIVES: Superoxide anion (O2-) released from neutrophils plays an important role in antibacterial host defense system and tissue auto-injury. Sarpogrelate, a serotonin-receptor antagonist, has been successfully used for management of chronic pain caused by arterial occlusive or ischemic vascular diseases, or by microcirculation disturbances. Suppression of O2- generation may be detrimental to infection or contribute to the therapeutic approach to these diseases, the pathogenesis of which probably includes neutrophil activation. No data regarding the effects of sarpogrelate on neutrophil functions are available despite the possible clinical concern. The purpose of this study was to determine whether sarpogrelate reduces O2- production by human neutrophils using an in vitro system. In addition, we examined changes in concentrations of the intracellular calcium ion ([Ca2+]i), which is responsible for one of the mechanisms of the neutrophils' O2- production. METHODS: The O2- production by human neutrophils or the xanthine-xanthine oxidase system and [Ca2+]i were measured in the absence and the presence (at clinically relevant concentrations: 0.1x, 10x, and 100x these concentrations) of sarpogrelate. RESULTS: Sarpogrelate inhibited O2- production of neutrophils in a dose-dependent manner. The drug at a clinically relevant concentration suppressed this neutrophil function. In contrast, sarpogrelate failed to inhibit O2-generation by the cell-free (xanthine-xanthine oxidase) system. Elevation of [Ca2+]i in neutrophils stimulated by a chemotactic factor was dose-dependently attenuated with sarpogrelate. CONCLUSIONS: These findings suggest that sarpogrelate (even at clinically relevant concentrations) is able to inhibit O2- production by neutrophils. However, the drug failed to quench an excessive amount of O2- (similar to the level produced by neutrophils). There is a possibility that the inhibitory effect of the drug on [Ca2+]i response in neutrophils may contribute to impairment of the neutrophils' O2- production. Further studies using in vivo systems are required to elucidate the inhibitory effects of sarpogrelate on O2- in clinical settings.

Calcium↗

PubMedDate not supplied

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 microgram/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 micrograms/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 less than 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 less than 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.

Adult↗

PubMedDate not supplied

Use of prostaglandin E1 to treat peri-anaesthetic pulmonary hypertension associated with mitral valve disease.

Severe pulmonary hypertension (PH) can be a critical problem during and after cardiac surgery, since it increases right ventricular afterload resulting in decreased cardiac output. A case of pulmonary hypertension associated with mitral valve disease and resistant to glyceryl trinitrate therapy during surgery is reported. The case was treated successfully with prostaglandin E1 (PGE1), indicating that PGE1 can be used peri-operatively in a patient with refractory PH resistant to glyceryl trinitrate treatment.

Alprostadil↗

PubMedDate not supplied

Effect of superoxide dismutase on endothelium-dependent relaxation of aorta from endotoxin-treated rabbits.

To assess the protective effect of superoxide dismutase (SOD) on the endothelium of aorta in endotoxaemia, we investigated the production of endothelium-derived relaxing factor in aorta obtained from endotoxin-treated rabbits concomitantly receiving SOD or not. Thirty-two male Japanese white rabbits were randomly divided into four groups (n = 8 for each group): one group receiving saline as a placebo, a second receiving 5 mg/kg endotoxin intravenously, a third receiving 5 mg/kg endotoxin intravenously plus SOD, and a fourth receiving SOD alone. SOD was injected intravenously at a dose of 10,000 U/kg before the endotoxin and was infused continuously at a rate of 15,000 units/kg/h throughout the experiment. The tension of the aorta was recorded in vitro 6 h after the start of in vivo treatment with endotoxin or saline. In the aorta of rabbits receiving endotoxin alone, acetylcholine-induced relaxation was reduced by 50%. The SOD fully restored the reduction of acetylcholine-induced relaxation by endotoxin. Histological studies using photomicroscopy revealed endothelial damage in the endotoxin-treated aorta, which was attenuated in the SOD-treated group. These data suggest that intravenous SOD may be an effective treatment for unstable haemodynamics in endotoxaemia.

Acetylcholine↗

PubMedDate not supplied

Inhibitory effect of gabexate mesilate on human neutrophil function.

Neutrophils accumulated in the lung are thought to play a key role in the pathogenesis of adult respiratory distress syndrome and interstitial pneumonia following bone-marrow transplantation. The effects of gabexate mesilate on several aspects of human neutrophil function have been investigated. Gabexate mesilate significantly decreased both the generation of reactive oxygen species (O2-, H2O2, OH.) by neutrophils and neutrophil chemotaxis. In contrast, the drug did not affect the levels of reactive oxygen species generated by a cell-free reactive-oxygen-species generating system. Intracellular calcium concentrations in neutrophils stimulated by f-Met-Leu-Phe were decreased in the presence of gabexate mesilate. These data suggest that the reduction in reactive-oxygen-species production and neutrophil chemotaxis by gabexate mesilate may contribute to the effectiveness of the drug in adult respiratory distress syndrome and interstitial pneumonia after bone-marrow transplantation. The suppression of the increase in intracellular calcium concentration may at least be responsible for the inhibition of these neutrophil functions by gabexate mesilate.

Calcium↗

PubMedDate not supplied

Acceleration of phagocytosis in human neutrophils incubated with gabexate mesilate.

It has recently been shown that gabexate mesilate inhibited human neutrophil functions including chemotaxis and reactive oxygen species production. In the present study, the effects of gabexate mesilate on phagocytosis by human neutrophils in vitro were investigated. Gabexate mesilate significantly enhanced neutrophil phagocytosis in a dose-dependent manner. This characteristic of gabexate mesilate may facilitate protection against infecting micro-organisms, although the inhibition of reactive oxygen species production by neutrophils may be a disadvantage for host-defense against infection.

Analysis of Variance↗