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S Kawana

Publications and source records attributed to S Kawana.

At least 19 recordsLinked to original sources
PubMed1998

Role of nitric oxide production through M2-cholinergic receptors in cultured rat ventricular myocytes.

We previously reported that carbachol (CCh) caused the enhancement of NO production coinciding with negative chronotropy in cultured rat ventricular myocytes. In this study, we examined which subtype of muscarinic cholinergic receptor mediated these effects of CCh by measuring the NOx production with an HPLC-Griess reaction system and monitoring the beating with a Fotonic Sensor. The enhancement of NO production and negative chronotropy by 10(-4) M CCh stimulation were significantly inhibited by 10(-6) M atropine, 10(-6) M methoctramine, 3 x 10(-4) M L-NMMA, and 10(-5) M methylene blue. On the other hand, 10(-6) M pirenzepine and 10(-6) M HHSiD had no influence on the negative chronotropy by 10(-4) M CCh stimulation. Both 10(-6) M pirenzepine and 10(-6) M HHSiD suppressed the enhancement of NO production by 10(-4) M CCh stimulation slightly though not statistically. In addition, the m2 cholinergic receptor gene was expressed in our cell preparations, as demonstrated by reverse-transcriptase/PCR analysis. We concluded that M2-cholinergic receptor-mediated negative chronotropy may be due in part to activation of the NO-signaling pathway in cultured rat ventricular myocytes.

Animals↗
PubMed1998

Ca2+ channel modulation alters halothane-induced depression of ventricular myocytes.

PURPOSE: This study examined the direct myocardial depressant effect of halothane and determined whether an L-type Ca2+ channel agonist and antagonists altered the myocardial depression induced by halothane in cultured rat ventricular myocytes. METHODS: Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 6 to 7 days. The myocytes were stabilized in a serum-free medium, and the spontaneous beating rate and amplitude were measured. To assess the halothane-induced conformational changes in L-type Ca2+ channel, receptor binding study was performed using a dihydropyridine derivative, [3H] PN 200-110, in cardiac membrane preparation. RESULTS: Halothane (1%, 2%, 3%, 4%) decreased the beating rate and amplitude in a concentration-dependent manner (P < 0.05). The myocardial depressant effects of halothane were potentiated by nifedipine or verapamil (P < 0.05). Bay K 8644, an L-type Ca2+ channel agonist, completely prevented the halothane-induced depression in amplitude (P < 0.05), but affected the beating rate less. Adding halothane (2%) decreased (P < 0.05) the maximum binding site density for [3H] PN 200-110 (from 198.6 +/- 23.7 fmol.mg-1 protein to 115.3 +/- 21.6 fmol.mg-1 protein) but did not affect binding affinity (from 0.461 +/- 0.077 nM to 0.307 +/- 0.055 nM). CONCLUSION: The reduction of Ca2+ current via sarcolemmal L-type Ca2+ channel, probably due to conformational changes in dihydropyridine binding sites, plays an important role in halothane-induced myocardial depression in living heart cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1998

Comparative myocardial depression of sevoflurane, isoflurane, and halothane in cultured neonatal rat ventricular myocytes.

UNLABELLED: In this study, we compared the direct myocardial depressant effects of sevoflurane, isoflurane, and halothane and determined whether an L-type Ca2+ channel agonist, Bay K 8644, could attenuate the myocardial depression induced by these anesthetics in cultured neonatal rat ventricular myocytes. Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 6-7 days. The myocytes were stabilized in serum-free medium, and the spontaneous beating rate and contractile amplitude were measured by using a fiberoptic sensor. Each anesthetic decreased the beating rate and amplitude in a concentration-dependent manner (1%-4% vol/vol) (P < 0.001), with halothane decreasing the beating rate and amplitude the most (P < 0.01). Isoflurane caused larger decreases in the beating rate than sevoflurane at 3% and 4% (P < 0.05). Potency for suppression of contractile amplitude was in the order of halothane > > isoflurane > sevoflurane. However, the myocardial depressant effects of the anesthetics were not different when their concentrations were corrected for minimum alveolar anesthetic concentration values. Bay K 8644 significantly prevented the anesthetic-depressed amplitude (P < 0.05). We conclude that sevoflurane, isoflurane, and halothane have direct myocardial depressant effects on cultured neonatal rat ventricular myocytes and that the reduction of sarcolemmal L-type Ca2+ channel current levels mediates the myocardial depression observed in these immature hearts. IMPLICATIONS: Sevoflurane, isoflurane, and halothane have a direct cardiodepressant effect on cardiac excitation-contraction coupling in the immature heart, which is mediated by an interaction with the L-type Ca2+ channel.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Drug eruption induced by cyanamide (carbimide): a clinical and histopathologic study of 7 patients.

BACKGROUND: In some countries, cyanamide is used as an alcohol intake inhibitor with few harmful side effects. So far 3 cases of allergic contact dermatitis and only 1 of lichenoid drug eruption due to cyanamide have been reported. OBJECTIVES AND METHODS: We describe the clinical manifestations, course, histopathologic and immunohistochemical findings of 7 cases of cyanamide-induced drug eruption. RESULTS: Of the 7 patients, 6 developed exfoliative dermatitis and 1 a lichen-planus-like eruption. Three patients with exfoliative dermatitis showed high fever, severe itching, anorexia, insomnia and general malaise, suggesting the diagnosis of hypersensitivity reaction. In all cases, mononuclear cell infiltration in the upper dermis with epidermotropism and dyskeratosis of the epidermal cells were observed histopathologically. The infiltrating cells consisted mainly of T4-positive lymphocytes. CONCLUSION: The cyanamide-induced skin reaction may be included in the spectrum of lichenoid drug eruptions, and its incidence may be much higher than previously reported.

Alcohol Deterrents↗
PubMed1997

[Evaluation of postoperative hypoxemia after spinal anesthesia with a pulse oximeter].

We investigated postoperative hypoxemia after spinal anesthesia in 24 adult patients by monitoring SPO2 with a pulse oximeter for 5 hours in the ward. The patients received spinal anesthesia with 0.5% hyperbaric tetracaine and sedated with midazolam during operation. Twelve patients inhaled 3 l.min-1 oxygen via a mask for initial 3 hours, and the other breathed room air all the time. In two of the patients breathing room air, SPO2 decreased to less than 94%. In patients inhaling oxygen, SPO2 was maintained above 98% but decreased significantly after stopping oxygen inhalation (below 94% in five patients). The postoperative SPO2 value correlated significantly with BMI (body mass index) and preanesthetic SPO2, but not with the dose of midazolam or supplemental pentazocine, and postoperative conscious states. In conclusion, there are some incidences of postoperative hypoxemia after spinal anesthesia irrespectively of the dose of midazolam used intraoperatively. Inhalation of 3 l.min-1 oxygen via a mask is sufficient to prevent such postoperative hypoxemia.

Adolescent↗
PubMed1997

[Severity and prognosis of congenital diaphragmatic hernia from the viewpoint of perioperative respiratory function].

We studied severity and prognosis of congenital diaphragmatic hernia (CDH) by using preductal arterial blood gas analysis (BGA) and pulmonary function tests (PFTs) in 29 newborn infants. CDH was diagnosed within 24 hours of life, and surgical repair was performed through an abdominal approach after a period of stabilization. The infants were classified into the following three groups based on the highest preoperative alveolar-arterial oxygen tension difference (A - aDO2) and the lowest arterial carbon dioxide pressure (PaCO2) values; Group A (n = 15) : A - aDO2 < 500 mmHg, PaCO2 < 40 mmHg, Group B (n = 7) : A - aDO2 > or = 500 mmHg, PaCO2 < 40 mmHg, Group C (n = 7) : A - aDO2 > or = 500 mmHg, PaCO2 > or = 40 mmHg. Furthermore, the patients were classified into the following three groups based on the preoperative respiratory system compliance (Crs) and forced vital capacity (FVC) values; Group D (n = 8) : Crs < 0.5 ml.cmH2O-1.kg-1, FVC < 10 ml.kg-1, Group E (n = 4) : Crs < 0.5 ml.cmH2O-1.kg-1, FVC > or = 10 ml.kg-1, Group F (n = 17) : Crs > or = 0.5 ml.cmH2O-1.kg-1, FVC > or = 10 ml.kg-1. The mortality in the Group C was significantly higher than in the Group A and B, and the preoperative Crs and FVC values in the Group C were significantly lower than the other groups. The mortality in the Group D and E were significantly higher than the Group F. In conclusion, it is suggested that the preoperative Crs value less than 0.5 ml.cmH2O-1.kg-1 indicates severe pulmonary hypoplasia and is critical for survival.

Blood Gas Analysis↗
PubMed1997

[Two cases of anaphylactic shock induced by chlorhexidine].

We reported two patients who developed skin eruptions and severe hypotension immediately after scrubbing their wound in the leg using 4% chlorhexidine solution. Both patients were successfully treated by epinephrine administration. Patient-1 (a 42-year-old man) had his wound scrubbed using this antiseptic several times before the operation. He showed a positive skin scratch test for chlorhexidine. Patient-2 (a 74-year-old man) had no prior treatment with chlorhexidine. Positive lymphocyte transformation test was not demonstrated in these patients. It has been reported that more than 10% of patients with anaphylactic shock induced by chlorhexidine use had previous exposure to it and 80% of them had it used for mucosa or wound washing. From these results, we should keep it in mind that chlorhexidine is not likely to be a safe antiseptic and can possibly induce anaphylactic shock.

Adult↗
PubMed1996

Cardiac arrest during removal of a pulmonary artery catheter.

PURPOSE: This case report describes an asystolic cardiac arrest that occurred during removal of a pulmonary artery (PA) catheter. CLINICAL FEATURES: A 70-yr-old man underwent elective hepatectomy because of hepatic carcinoma with a combination of thoracic epidural blockade and general anaesthesia. After the conclusion of the operation, the PA catheter was removed and immediately after, the patient developed profound sinus bradycardia and hypotension followed by asystolic cardiac arrest. Two minutes after the onset of asystole, cardiac rhythm was detected following the administration of epinephrine and atropine. He had no further episodes of bradycardia or neurological deficit. CONCLUSION: Removal of a PA catheter has the potential of inducing asystole requiring cardiac resuscitation and availability of emergency drugs.

Aged↗
PubMed1996

Alpha 1- and beta-adrenergic and muscarinic-cholinergic regulation in the spontaneous beating and Ca2+ oscillations in cultured neonatal rat cardiac myocytes.

alpha 1- and beta-adrenergic and muscarinic-cholinergic regulation in spontaneous beating and Ca2+ oscillations in neonatal rat cardiac myocytes at day 6 of culture was investigated. The spontaneous beating in myocytes decreased in the presence of 10 microM norepinephrine (NE). This negative chronotropic action was antagonized by prazosin. Carbachol (CCh) also showed negative chronotropic action which was inhibited by atropine. On the other hand, isoproterenol (ISP) increased the beating rate which was antagonized by propranolol. NE increased inositol phosphate formation whereas CCh and ISP did not. NE and CCh suppressed the frequency of the spontaneous Ca2+ oscillations but ISP increased. The present results suggest that alpha 1-adrenergic and muscarinic receptors regulate chronotropism to be negative whereas beta-adrenoceptor regulates chronotropism to be positive in cultured neonatal rat cardiac myocytes.

Adrenergic Agents↗
PubMed1996

The membrane attack complex of complement alters the membrane integrity of cultured endothelial cells: a possible pathophysiology for immune complex vasculitis.

Recently, the possibility of direct involvement of the membrane attack complex of complement in the endothelial damage of immune complex vasculitis has been pointed out. However, no studies have so far elucidated this mechanism. The present study investigated the effects of complement on the membrane integrity of endothelial cells, using the fluorescein diacetate and ethidium bromide staining method. Cultured human umbilical vein endothelial cells were maintained in medium containing 10% zymosan-activated normal human serum. Cell detachment began to occur after 3 h of incubation, and the number of fluorescein diacetate-positive adherent cells decreased significantly, whereas that of ethidium bromide-positive detached cells increased significantly. Heat inactivation of the serum or replacement of the complement source with non-activated normal human serum or C5-, C7- or C9-deficient serum resulted in complete inhibition of these effects. These results suggest that complement induces detachment of endothelial cells by altering the cell membrane integrity and support the contention that the membrane attack complex of complement plays a significant role in the mechanisms of endothelial cell damage in immune complex vasculitis.

Antigen-Antibody Complex↗
PubMed1996

[Evaluation of postoperative hypoxemia with a pulse oximeter].

We investigated postoperative hypoxemia by monitoring of SPO2 with a pulse oximeter for the first 5 hours in the ward. Forty-eight adults were divided into the general anesthesia along (G) group and the combination of epidural and general anesthesia (E) group. The patients were randomly administered either 3 l. min(-1) oxygen with face mask for the initial 3 hours or room air. Postoperative Spo2 values in the patients who breathed room air in both groups were less than 94% in 33% of G group and 50% of E group. 3 l. min(-1) oxygen inhalation through the face mask was enough to avoid postoperative hypoxemia in both groups; the mean values of Spo2 were 99% in G group and 97.9% in E group. Spo2 rapidly and significantly decreased after stopping the oxygen inhalation to under 94% in 25% of G group and 58% of E group. Significant correlations were found between Spo2 levels and both age (R = 0.75) and preanesthetic Spo2 (R = 0.66) in G group. Spo2 was significantly lower in the patients whose anesthesia was stopped after 5 p.m. than in those who were weaned before 5 p.m. In conclusion, there is a high incidence of postoperative hypoxemia for several hours in the ward, which can be relieved by 3 l. min(-1) oxygen inhalation with face mask.

Adolescent↗
PubMed1995

Comparison of haemodynamic changes induced by sevoflurane and halothane in paediatric patients.

The purpose of this study is to investigate the haemodynamic effects of 1 MAC and 2 MAC of sevoflurane in children in comparison with halothane. Thirty-eight children (aged from one to six years, average age; 3.6 +/- 0.2 yr) were randomly assigned to four groups, depending on the dose and agent (1 and 2 MAC of sevoflurane: S1 and S2; 1 and 2 MAC of halothane: H1 and H2, respectively). After collecting control data during 0.2 MAC of either anaesthetic, end-expired anaesthetics were kept at 1 MAC or 2 MAC for 15 min. Mean blood pressure (mBP) and stroke volume index (SVI), measured by impedance cardiometry, decreased in all groups without differences between groups. Heart rate (HR) increased in groups S1, S2 and H2 but not in group H1. The HR in S2 was higher than that in H2. The cardiac index (CI), a product of SVI and HR, tended to decrease but not significantly in all groups. These results suggested that the haemodynamic depressant effects of sevoflurane in children were similar to those of equipotent halothane concentration except for HR.

Analysis of Variance↗
PubMed1995

Pustular psoriasis and aseptic purulent arthritis: possible role of leukotrienes B4 and C4 in a flare of synovitis.

BACKGROUND: Arthritis is a frequent complication of pustular psoriasis. However, the mechanism of onset of this arthritis still remains unclear. OBJECTIVES: The present study was conducted to determine whether leukotriene (LT) B4 or LTC4 is one of the proinflammatory mediators that possibly enhance exacerbation of the arthritis lesions. METHODS: We investigated the condition of the arthritis and autopsy findings of two cases of generalized pustular psoriasis with the severe complication of aseptic purulent arthritis. We also measured the synovial fluid levels of LTB4 and LTC4 by radioimmunoassay. RESULTS: The collected synovial fluid was purulent, but nonbacterial, and the synovium of the knee joint showed histopathologic evidence of polymorphonuclear leukocyte (PMN) invasion, edema and dilatation of small vessels showing similarity to a histologic reaction in the skin lesions. The immunoreactive (i-) LTB4 and i-LTC4 in the samples significantly exceeded the amount measured in osteoarthritis patients used as the controls. CONCLUSION: Thus, i-LTB4 and i-LTC4 appear to be generated in the arthritis lesions of pustular psoriasis, the former attracting PMNs to the joints and the latter causing exudation of synovial fluid.

Aged↗
PubMed1995

Effects of 2-deoxyglucose, a metabolic inhibitor, on spontaneous contraction and adrenoceptor responsiveness in cultured rat ventricular myocytes.

Although it is well known that myocardial ischemia induces the depletion of myocardial ATP and sustained myocardial dysfunction, the mechanisms causing impaired myocardial function have not been elucidated completely. To clarify the relationship between ATP depletion and myocardial contractility, we investigated the influence of myocardial ATP depletion on spontaneous beating in cultured rat ventricular myocytes. Furthermore, because catecholamines have been used to improve myocardial contraction in the ischemic heart, we attempted to determine whether the ATP depletion per se alters the contractile responses to alpha 1- and beta-adrenoceptor stimulation. After 24 hr of culture in the presence of a metabolic inhibitor, 2-deoxyglucose (2DG, 5mM), myocardial contractility decreased to 19% of the vehicle level, and returned to normal after the removal of 2DG. The beating rate did not show any alterations in the vehicle, in the presence of 2DG (2DG [+/+]) or after the removal of 2DG (2DG [+/-]). Norepinephrine (NE) caused significant decreases in beating rate and increases in contractility in all groups. Isoproterenol (ISP) caused significant increases in beating rate and contractility in all groups. In the 2DG (+/+) group, the contractility was significantly lower as compared to other groups during NE or ISP stimulation. However, the percent change of contractility was similar to those of other groups after NE or ISP stimulation in the 2DG (+/+) group. These results suggest that decreased myocardial ATP causes the decreased contractility and does not affect the alpha 1- or beta-adrenoceptor-mediated responses.

Adenosine Triphosphate↗