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Biomedical subjects

Shosuke Takahashi

Publications and source records attributed to Shosuke Takahashi.

27 records · Page 2Linked to original sources
PubMed2002

Involvement of rho-kinase in agonists-induced contractions of arteriosclerotic human arteries.

Coronary artery spasm plays an important role in the pathogenesis of a wide variety of ischemic heart diseases. We have recently demonstrated that Rho-kinase plays a key role in the spasm in our porcine model. However, it remains to be elucidated whether Rho-kinase-mediated pathway also contributes to vasoconstriction of human arteries. From 15 patients who underwent coronary artery bypass operation, segments of isolated left internal thoracic arteries were obtained, and the endothelium was gently removed. Serotonin and histamine caused contractions, which were markedly inhibited by a specific Rho-kinase inhibitor, hydroxyfasudil. Western blot analysis showed that, during the serotonin-induced contractions, the extent of phosphorylation of myosin-binding subunit of myosin phosphatase (MBS, one of the major substrates of Rho-kinase) was significantly increased in the specimens. Hydroxyfasudil again significantly suppressed the serotonin-induced increase in MBS phosphorylation. There was a significant positive correlation between the extent of MBS phosphorylation and that of the serotonin-induced contractions and between hydroxyfasudil-sensitive components of the contractions and the extent of arteriosclerosis. These results indicate that Rho-kinase plays an important role in vascular smooth muscle contractions of arteriosclerotic human arteries, suggesting that Rho-kinase could be regarded as an important target for the treatment of arteriosclerotic vascular diseases in humans.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2002

Propofol prevents endothelial dysfunction induced by glucose overload.

Surgical operations often induce acute hyperglycemia, which is known to affect endothelial functions. In this study, we examined the effects of propofol, a commonly used general anaesthetic, on bovine aortic endothelial cell (BAEC) dysfunction induced by glucose overload. 2 D-glucose overload (23 mM) induced an accumulation of superoxide anion (O2-), assessed by MCLA chemiluminescence, to a similar extent as that generated by 233 microU ml(-1) xanthine oxidase (XO) and 100 micro M xanthine. Propofol inhibited this accumulation with an IC50 of 0.21 micro M, whereas much higher concentrations of propofol were required to scavenge O2- generated by 250 microU ml(-1) XO and 100 microM xanthine (IC50: 13.5 micro M). 3 D-glucose overload attenuated ATP-induced NO production which was detected using diaminofluorescence-2 (DAF-2). The inhibition was reversed by propofol with an EC50 of 0.60 microM. In contrast, inhibitions caused by xanthine/XO were not altered by propofol (1 microM). 4 D-glucose overload suppressed ATP-induced Ca2+ oscillations and capacitative Ca2+ entry (CCE), which were both restored by superoxide dismutase, indicating that O2- was responsible. Propofol restored these attenuated Ca2+ oscillations and CCE with EC50 of 0.31 and 1.0 microM, respectively. 5 D-glucose overload (23 mM) increased the intracellular glucose concentration 4 fold, compared with cells exposed to 5.75 mM glucose, and 1 micro M propofol reduced this increase to 2.8 fold. 6 We conclude from these results that anaesthetic concentrations of propofol prevent the impairment of Ca2+-dependent NO production in BAEC induced by glucose overload. This effect is mainly due to the reduction of O2- accumulation, and involves, at least in part, the inhibition of cellular glucose uptake.

Animals↗
PubMed2002

Sevoflurane and bradykinin-induced calcium mobilization in pulmonary arterial valvular endothelial cells in situ: sevoflurane stimulates plasmalemmal calcium influx into endothelial cells.

Kinins locally synthesized in the cardiovascular tissue are believed to contribute to the regulation of cardiovascular homeostasis by stimulating the endothelial cells to release nitric oxide, prostacyclin, or a hyperpolarizing factor via autocrine-paracrine mechanisms. This study was designed to investigate the action of sevoflurane on bradykinin-induced Ca2+ mobilization in endothelial cells in situ. Utilizing fura-2-loaded rat pulmonary arterial valve leaflets, the effects of sevoflurane were examined on bradykinin-induced increases in intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ. In the presence of extracellular Ca2+ (1.5 mM), bradykinin (3-30 microM) produced an initial phasic and a subsequent tonic increase in [Ca2+]i in a concentration-dependent manner. However, it produced only the phasic increase in [Ca2+]i in the absence of extracellular Ca2+. Sevoflurane (5%, 0.67 mM) inhibited both the phasic and tonic responses to bradykinin. In these experiments, sevoflurane (3-5%) generated sustained increases (approximately 20-40% of the bradykinin-induced maximal increase in [Ca2+]i) in the resting [Ca2+]i level. Sevoflurane still increased [Ca2+]i after depletion of the intracellular Ca stores with ionomycin (0.1 microM ). However, the sevoflurane-induced increase in [Ca2+]i was eliminated by removal of the extracellular Ca and attenuated by NiCl (1-3 mM). In conclusion, in the pulmonary arterial valvular endothelial cells, sevoflurane inhibits both bradykinin-induced Ca2+ release from the intracellular stores and bradykinin-induced plasmalemmal Ca2+ influx. In addition, sevoflurane appears to stimulate the plasmalemmal Ca2+ influx and thereby increase the endothelial [Ca2+]i level. Sevoflurane might influence the pulmonary vascular tone through its direct action on the pulmonary arterial valvular endothelial cells.

Anesthetics, Inhalation↗
PubMed2002

[Acute renal failure in an infant attributable to arterial cannula malposition during cardiopulmonary bypass via ministernotomy].

A 6-month-old female (4.9 kg) with multiple congenital heart lesions underwent intracardiac repair with the aid of cardiopulmonary bypass (CPB) through a lower half sternotomy. Aortic cannulation, venous cannulation, and cardioplegia cannula insertion were all accomplished through the ministernotomy. During the CPB, in spite of a high perfusion flow rate (182 ml.kg-1.min-1), the systemic arterial pressure was persistently low (mean values = 25-35 mmHg) and the urine output was greatly reduced (< 1 ml.hr-1). In addition, inappropriate increases in the arterial inflow line pressure were recognized. Since abutment of the cannula tip against the aortic intima was suspected, several attempts were made to correct its malpositioning. During the CPB, hemolysis was also found in the mixed venous blood. Since the oliguria and resultant hyperkalemia persisted after weaning from the CPB, peritoneal dialysis was introduced immediately after the surgery. Her renal function gradually recovered postoperatively, and she was finally weaned from the peritoneal dialysis on the 13th postoperative day. Although the ministernotomy has been proposed to be a safe approach for most of cardiac surgeries, it appears to increase the risk for arterial cannula malposition as compared to the standard full-length sternotomy in small pediatric patients.

Acute Kidney Injury↗
PubMed2002

[Distribution of an explanatory note concerning the risks of anesthesia prior to preanesthetic evaluation].

To make the public aware of the risks of anesthesia, we prepared an explanatory note composed of 634 Japanese characters or of 248 English words. The incidences of fatal anesthetic complications over a five-year period in 2,358,642 anesthetics in 741 Certified Training Hospital belonging to the Japanese Society of Anesthesiologists were cited in the explanatory note. Patients were asked to read and sign the explanatory note prior to agreeing to surgery. After patients having received this general information about surgical and anesthesia risks, surgeons then apply to the Department of Anesthesiology for their anesthetic management. Thereafter, responsible anesthesiologists visit and evaluate patients, and explain common as well as specific anesthesia risks to each patient. A survey by mailing questionnaires regarding this explanatory note and anesthesia risks sent to patients, who had read and signed the explanatory note, revealed that the patients were generally satisfied with the content of the explanatory note. This system may help patients, surgeons and anesthesiologists to recognize anesthesia risks on the same basis.

Anesthesia↗
PubMed2002

[Intraoperative monitoring of pressure within saline-filled, endotracheal tube cuff in adult patients undergoing CO2 laser laryngomicrosurgery].

In laser laryngomicrosurgery, saline is injected into the endotracheal tube cuff to prevent airway fire. Utilizing regression analyses, we investigated the relation between the saline volume required to obtain optimal intracuff pressure and tracheal diameters in patients undergoing laser laryngomicrosurgery as well as in model tracheas. Although excellent linear correlations were found between the saline volume and the diameter of model tracheas, no significant linear or non-linear correlation was found between the saline volume and the patient's tracheal diameter. In the model tracheas, a rate of rise in the intracuff pressure caused by increments in the injected volume was far steeper when saline was injected into the cuff than when air was injected into the cuff. Addition of only 0.2 ml saline could result in large (> 50 mmHg) increases in the intracuff pressure. Also in patients, addition of 1 ml could result in notable (> 50 mmHg) increases in the intracuff pressure. These results suggest that the saline volume necessary to obtain optimal intracuff pressure is difficult to be predicted from the patient's tracheal diameter, and that slight increases in the saline volume may cause excessive increases in the intracuff pressure. The intracuff pressure should be tightly monitored in patients undergoing laser laryngomicrosurgery.

Adult↗
PubMed2002

[Changes in acid-base balance and blood lactate levels during radio frequency ablation conducted for the treatment of hepatocellular carcinomata in patients with liver cirrhosis].

BACKGROUND: Radio frequency ablation (RFA) has recently received increasing attention as an effective minimally invasive approach for the treatment of hepatocellular carcinomata (HCCs). However, we experienced a patient with liver cirrhosis (LC, Child-Pugh class B) in whom severe lactic acidosis developed during RFA conducted for the treatment of a HCC (-4.5 cm in diameter). This case prompted us to reevaluate possible injurious effects of RFA on non-tumorous liver tissues in the vicinity of its target in LC patients. METHODS: Intraoperative changes in acid-base balance and blood lactate levels, and postoperative changes in serum transaminases were investigated in LC (Child-Pugh class A) patients undergoing either laparotomic RFA (for the treatment of HCCs [diameter < 3 cm]) or partial hepatectomy (with the aid of the Pringle's manuever), and non-LC patients undergoing pancreatectomy. RESULTS: During the intraoperative period, significant lactic acidosis developed only in the patients undergoing hepatectomy. Core temperature significantly increased following the RFA. Postoperative increases in the transaminases observed in the patients undergoing hepatectomy were far larger than those observed in the patients undergoing either RAF or pancreatectomy. CONCLUSION: RFA, conducted for the treatment of smaller HCCs, appears to be minimally invasive even in the presence of LC (Child-Pugh class A).

Acid-Base Equilibrium↗
PubMed2002

[Development of severe lactic acidosis during radio frequency ablation conducted for the treatment of hepatocellular carcinomata in a patient with liver cirrhosis].

A 60-year-old male with liver cirrhosis (Child-Pugh class B) underwent laparotomic radio frequency ablation for the treatment of a solitary hepatocellular carcinoma (-4.5 cm in diameter). Severe lactic acidosis (base excess < -12 mEq.l-1, lactate > 150 mg.dl-1) developed during the intraoperative period, when neither his hemodynamics nor arterial oxygenation was significantly impaired. The blood loss was small (-200 g), and the serum hemoglobin level was maintained -10 g.dl-1 during the procedure. There was no evidence for impairment of either peripheral perfusion or renal function. In addition, there was no evidence for development of either splanchnic ischemia or diabetic ketoacidosis. Thus, the acidosis appeared to be caused by significant impairment of liver function possibly resulting from the ablation (total ablation time = -60 min). The core temperature increased rapidly (-1.5 degrees C/60 hr) immediately after the ablation was started, suggesting that a large amount of heat was produced in the ablated area and/or that the vicinity of the ablated area was richly supplied by blood flow. As a result, intact liver cells in the vicinity of the tumor probably suffered from thermal injuries. In conclusion, depending on preoperative liver function, ablated area, and/or blood flow in the vicinity of ablated area, the ablation may become significantly invasive.

Acidosis, Lactic↗