Search PubMed⌕ Search

Biomedical subjects

O Kemmotsu

Publications and source records attributed to O Kemmotsu.

At least 37 records · Page 2Linked to original sources

Diminished function and expression of the cardiac Na+-Ca2+ exchanger in diabetic rats: implication in Ca2+ overload.

1. The present work was carried out in order to determine whether a decrease in cardiac Na+-Ca2+ exchanger (NCX) activity observed in diabetes is caused by a reduction in NCX protein and mRNA levels and to elucidate the significance of this decrease in alterations in [Ca2+]i homeostasis in diabetic cardiomyocytes. 2. The NCX current was significantly reduced in ventricular myocytes freshly isolated from streptozotocin-induced diabetic rat hearts, and its current density was about 55 % of age-matched controls. 3. Diabetes resulted in a 30 % decrease in cardiac protein and mRNA levels of NCX1, a NCX isoform which is expressed at high levels in the heart. 4. The reduced NCX current and the decreased protein and mRNA levels of NCX1 in diabetes were prevented by insulin therapy. 5. Although both diastolic and peak systolic [Ca2+]i were not different between the two groups of myocytes, increasing external Ca2+ concentration to high levels greatly elevated diastolic [Ca2+]i in diabetic myocytes. Inhibition of NCX by reduction in extracellular Na+ by 50 % could produce a marked rise in diastolic [Ca2+]i in control myocytes in response to high Ca2+, as seen in diabetic myocytes. However, cyclopiazonic acid, an inhibitor of sarcoplasmic reticulum Ca2+ pump ATPase, did not modify the high Ca2+-induced changes in diastolic [Ca2+]i in either control or diabetic myocytes. 6. Only in papillary muscles from diabetic rats did the addition of high Ca2+ cause a marked rise in resting tension signifying a partial contracture that was possibly due to an increase in diastolic [Ca2+]i. 7. In conclusion, the diminished NCX function in diabetic myocytes shown in this study results in part from the decreased levels of cardiac NCX protein and mRNA. We suggest that this impaired NCX function may play an important role in alterations in Ca2+ handling when [Ca2+]i rises to pathological levels.

Animals↗

Out-of-hospital cardiac arrest increases soluble vascular endothelial adhesion molecules and neutrophil elastase associated with endothelial injury.

OBJECTIVES: To investigate the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes in markers of endothelial activation, neutrophil activation, and endothelial injury. DESIGN: Prospective, cohort study. SETTING: General intensive care unit of a tertiary care center. PATIENTS AND PARTICIPANTS: Forty-four out-of-hospital cardiac arrest patients were classified into two groups, those who achieved return of spontaneous circulation (ROSC) (n = 23) and those without ROSC (n = 21). Eight normal healthy volunteers served as control subjects. MEASUREMENTS AND RESULTS: Serial levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin) as markers of endothelial activation, neutrophil elastase as a marker of neutrophil activation, and soluble thrombomodulin as a marker of endothelial injury were measured during and after cardiopulmonary resuscitation (CPR). In patients with ROSC, cardiac arrest and CPR led to increases in the levels of three vascular endothelial adhesion molecules, neutrophil elastase, and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. In patients without ROSC, only neutrophil elastase showed moderate elevation during CPR. We could not find significant differences in all measured parameters between the two groups. CONCLUSIONS: As evidence of inflammatory responses in whole-body ischemia and reperfusion, our study demonstrates neutrophil-endothelium interaction with signs of endothelial injury in patients with out-of-hospital cardiac arrest. These inflammatory changes may have an important role in post-resuscitation syndrome after human cardiac arrest.

Cardiopulmonary Resuscitation↗

Differential gene transcriptional regulation of Gi isoforms and Gs protein expression in diabetic rat hearts.

Many cardiac diseases can be associated with alterations in the function and quantity of G proteins. We examined the gene expressions and protein levels of Gi-1alpha, Gi-2alpha, Gi-3alpha and G(s alpha) in ventricular myocardial preparations from rats 4-6 weeks after induction of diabetes with streptozotocin in comparison with those from age-matched control rats. Diabetic rat myocardium exhibited reductions in the protein levels of Gi-2alpha and Gi-3alpha by 22+/-2% and 57+/-2%, respectively. In diabetes, 22% and 53% reductions in myocardial mRNA levels of Gi-2alpha and Gi-3alpha were observed. Although a faint protein signal of Gi-1alpha was detectable, no apparent expression of mRNA for Gi-1alpha was found in either control or diabetic myocardium. The reduced protein and mRNA levels of Gi-2alpha and Gi-3alpha were prevented by insulin therapy. No change was found in the protein and mRNA levels of G(s alpha) in diabetic myocardium. In conclusion, diabetes leads to a differential regulation of protein expressions of G(i alpha) isoforms and G(s alpha) in ventricular myocardium. The reduced expression of Gi-2alpha and Gi-3alpha proteins can be explained, at least in part, by the decreases in the transcriptional levels.

Animals↗

An increase in macrophage migration inhibitory factor release in patients with cardiopulmonary bypass surgery.

To determine the macrophage migration inhibitory factor (MIF) responses to cardiopulmonary bypass (CPB) surgery as well as to investigate their roles in predicting patient outcome, a prospective, observational, pilot study was performed. Thirty patients undergoing cardiovascular surgery with CPB received 10mg/kg betamethasone immediately before the CPB. Ten normal healthy volunteers served as control subjects. Blood samples were serially obtained for 24h and assayed for MIF, cortisol, and tumor necrosis factor alpha (TNF-alpha). TNF-alpha release could not be detected during the study period. Compared with both the control and baseline values, the MIF and cortisol levels were elevated before CPB and peaked at the end of CPB (57.5 +/- 4.8 ng/ml, P < 0.0001), and at the end of the surgery (507.7 +/- 44.1 nmol/l, P < 0.0001), respectively. Peak MIF levels correlated with aortic cross-clamp time (r2 = 0.183, P = 0.0182, n = 30), but did not show a significant correlation with peak cortisol levels. The levels of MIF tended to be 40%-50% higher during CPB in patients with longer intensive care unit (ICU) stays and in those with organ dysfunction than in those with short ICU stays and no organ dysfunction. All patients were discharged from the ICU. In conclusion, our findings demonstrate that MIF production occurs in patients with CPB surgery. When high-dose steroids are administered, high MIF levels were found to only slightly affect the patient morbidity and outcome after CPB surgery.

Cardiopulmonary Bypass↗

The effect of calcium channel blockers on cerebral oxygenation during tracheal extubation.

UNLABELLED: Calcium channel blockers are effective in stabilizing systemic hemodynamics during tracheal extubation. However, they may increase cerebral blood flow (CBF) during tracheal extubation because of cerebral vasodilation, even if systemic arterial blood pressure decreases. In this study, we observed changes in cerebral oxygenation during tracheal extubation by using near-infrared spectroscopy and evaluated the effect of nicardipine and diltiazem on the resultant changes. We studied 45 women undergoing elective gynecologic surgery. After surgery, the patients were randomly allocated to three groups (n = 15 each): saline (control), 0.02 mg/kg nicardipine, and 0.2 mg/kg diltiazem. After 2 min, we started to aspirate secretions for 2 min and then, extubated the trachea. Changes in cerebral oxygenated hemoglobin (HbO(2)) and deoxygenated hemoglobin were measured during the extubation procedure for 9 min after drug treatment. Systemic hemodynamics, including mean arterial blood pressure, heart rate, end-tidal CO(2), end-tidal sevoflurane concentration, and peripheral arterial oxygen saturation were also monitored. During extubation, HbO(2) increased significantly, presumably caused by the increase in CBF. Changes in deoxygenated hemoglobin were minimal. Compared with the control, nicardipine and diltiazem significantly inhibited the increase in mean arterial blood pressure. On the contrary, they significantly enhanced the increase in HbO(2). In conclusion, calcium channel blockers may increase CBF during extubation, even if these drugs stabilize systemic hemodynamics. IMPLICATIONS: This study is a preliminary report evaluating the changes in cerebral oxygenation during the tracheal extubation. Cerebral oxygenated hemoglobin increased significantly, presumably caused by the increase in cerebral blood flow during extubation. In addition, these changes were enhanced by calcium channel blockers.

Blood Pressure↗

Impairment of cardiac beta-adrenoceptor cellular signaling by decreased expression of G(s alpha) in septic rabbits.

BACKGROUND: Abnormalities in the beta-adrenergic control of cardiac function play a role in the pathogenesis of several disease states. Because circulatory failure in patients with septic shock is known to be less responsive to catecholamines, we investigated whether the beta-adrenoceptor-linked signal transduction mechanisms are altered in the heart of a septic animal model METHODS: Rabbits were rendered endotoxemic by an intravenous injection of 100 microg/kg Escherichia coli lipopolysaccharide. Three and 6 h later, the myocardial tissues were used for the experiments. RESULTS: The positive inotropic response to isoproterenol was significantly impaired in papillary muscles isolated from septic rabbits compared with those from controls. The impaired inotropic responsiveness to isoproterenol was not prevented by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine, indicating no involvement of nitric oxide overproduction. Adenylate cyclase activity stimulated with isoproterenol and 5'-guanylyl imidodiphosphate was markedly reduced in septic myocardium. The contractile and adenylate cyclase responses to colforsin daropate, a direct adenylate cyclase activator, were unaffected by sepsis. Radioligand binding experiments with (-)[125I]iodocyanopindolol revealed no significant alteration in myocardial beta-adrenoceptor density or affinity in sepsis. Determination of cardiac G(s alpha) level by Western blotting showed a reduction of approximately 50% in sepsis. The relative content of G(s alpha) messenger RNA in septic myocardium also was reduced from the control level by about 50%, as determined by Northern blot analysis. Little change was found in protein and messenger RNA levels of G(s alpha) in septic myocardium. CONCLUSIONS: Impairment of myocardial functional responsiveness to beta-adrenoceptor stimulation appears in the early stage of sepsis. The impaired response to beta-adrenoceptor stimulation in the heart in this pathologic state may result in part from a decreased level of G(s alpha) protein which occurs at the level of gene expression.

Adenylyl Cyclases↗

Pentobarbital inhibits apoptosis in neuronal cells.

OBJECTIVE: Previous reports have demonstrated that barbiturates have a protective effect against cerebral ischemia, although the mechanisms are incompletely understood. Recently, it has been suggested that apoptosis is involved in ischemic neuronal death. This study examined the effect of pentobarbital on neuronal apoptosis. DESIGN: Randomized, controlled, prospective study. SETTING: University research laboratory. SUBJECTS: PC12 cells derived from rat pheochromocytoma as a model of neuronal tissue. INTERVENTIONS: Apoptosis was induced by depriving serum from the cell culture medium. Effect of pentobarbital (0.5, 5, 50 microg/mL) was evaluated. MEASUREMENTS AND MAIN RESULTS: First, electrophoresis of DNA and fluorescence microscopic examination were performed to ascertain whether apoptosis was really induced after serum deprivation in our cells. Second, the effect of pentobarbital on cytotoxicity (evaluated by a leakage assay of lactic dehydrogenase) was evaluated. Third, the percentage of apoptotic cells was calculated by measuring cellular DNA content with flow cytometry. Calculation of the percentage of apoptotic cells was based on cumulative frequency curves of the appropriate DNA histograms. DNA electrophoresis exhibited a typical ladder pattern from the first day after the induction of apoptosis. The cells with chromatin condensation and/or fragmentation increased day by day after depriving serum in fluorescence microscopic examination. Four days after the induction of apoptosis, cytotoxicity without pentobarbital was 53.9 +/- 24.3% (mean +/- SD). Pentobarbital significantly inhibited cell death in a dose-dependent fashion. The percentage of apoptotic cells without pentobarbital was 94.9 +/- 6.3% 4 days after the induction of apoptosis. The treatment with 50 microg/mL pentobarbital significantly decreased the percentage of apoptotic cells to 61.8 +/- 21.3%. CONCLUSIONS: Our data indicate that pentobarbital inhibits apoptosis induced by serum deprivation in PC12 cells.

Apoptosis↗

[Hypercapnea after minitracheotomy].

Minitracheotomy is a useful procedure for the respiratory management of patients with sputum retention observed frequently in chronic lung disease and postoperative respiratory failure. However, we experienced a case of hypercapnea after minitracheotomy. An 83-year-old woman was scheduled for gastrectomy. She had respiratory failure of Hugh-Jones 5 with fibroid lungs and the infection with atypical Mycobacterium and MRSA. Her sputum was adhesive and showed persistent increase during pre- and intra-operative periods. After the operation, minitracheotomy was carried out against the sputum retention by using Portex Mini-Trach II kit. Hypercapnea, however, was observed in spite of no evidence of the surgical complications such as bleeding or inadequate care for sputum from the inserted tube. Bronchofiberscope revealed adhesive sputum stuck to the space between the inserted tube and the trachea. In this case, hypercapnea was improved by opening the top of the inserted tube and frequent care for sputum. In cases with a large amount of adhesive sputum, sputum retention may easily occur not only at the peripheral bronchial branch but also between the inserted tube and the trachea and it can cause hypercapnea which may be overlooked.

Aged↗

[Accidental decrease in the air flow during air/oxygen sevoflurane anesthesia].

We describe our experience of an accidental decrease in the air flow during air/oxygen sevoflurane anesthesia. According to the malfunction of an air compressor system, dehydration of the compressed air was inadequate, and the wet air was delivered to the anesthesia machine. The moisture was formed at a flow control valve to cause a gradual decrease in the air flow. The low-pressure alarm did not work at that time, because the pressure of the air supply was normal. There are two types of medical air, one is produced from the ambient air by air compressor system and another is the synthetic air which is a mixture of oxygen and nitrogen. Although the synthetic air is always dry and clean, the former contains dust, bacteria, and moisture. There is a possibility that all of these particles cannot be excluded before use. Accordingly, we must check the air compressor system routinely when a source of the compressed air is used.

Air↗

[Patent blue-induced false-methemoglobinemia].

We experienced an anesthetic case, in which interference in oxygen saturation values by patent blue was mistaken for nitroglycerin-induced methemoglobinemia. A 40-year-old woman underwent mastectomy for breast cancer under general anesthesia. Nitroglycerin was infused to produce hypotensive anesthesia. Patent blue was locally injected around the cancer by a surgeon and surgery was started. A few minutes later, oxygen saturation by finger pulse oximeter suddenly decreased from 100% to 90%. And then, blood gas analysis was performed to confirm this change. The decrease of oxygen saturation and the increase of methemoglobin were also observed in the finding of blood gas analysis. At first, we judged these changes as methemoglobinemia by nitroglycerin infusion. Finally, however, we concluded that all these changes were attributable to the interference by patent blue on oxygen saturation value because we found that there had been some inconsistent findings as methemoglobinemia. The fact seems that nothing happened to the patient during the episode. This case showed us that anesthesiologists should understand the principle of hematological monitors and the meaning of the data obtained by monitors.

Adult↗

[Efficacy of patient-controlled epidural analgesia using a disposable PCA device].

We evaluated efficacy of patient-controlled epidural analgesia (PCEA) using a disposable PCA device (3.0 ml type). Twenty-two patients for elective gynecological surgery were randomized into two groups. Patients of the continuous epidural group received epidural fentanyl (15 micrograms.ml-1) with bupivacaine (1.25 mg.ml-1) from a disposable infusion pump (infusion rate: 2.1 ml.hr-1). Patients of the PCEA group received the same anesthetic solution from the same infusion pump serially connected to the disposable PCA device. There were no significant differences in postoperative visual analogue scale (VAS) scores at rest and with movement between the two groups. However, VAS scores significantly decreased from 6.8 +/- 1.6 to 1.0 +/- 1.3 when the PCA device was used for severe pain. This suggests that segmental analgesic effect might be obtained by diffusion of anesthetic solution in the epidural space after 3.0 ml PCEA bolus administration. The incidences of side effects were similar in both groups. Respiratory depression and sedative effects were not observed in both groups. We conclude that PCEA using a disposable PCA device (3.0 ml type) seems to be effective for postoperative pain relief.

Adult↗

[Asystole during electroconvulsive therapy in a patient with depression and myasthenia gravis].

A 44-yr-old woman presented with major depression. She was scheduled to receive electroconvulsive therapy under anesthetic care because of drug-induced leukopenia. Her significant past medical history was myasthenia gravis. She had been treated with thymectomy and pyridostigmine. She showed no evidence of muscle weakness while receiving the medication. After preanesthetic assessment, pyridostigmine was continued and routine anesthetics were chosen. Under 100% oxygen inhalation, thiamylal and suxamethonium were administered intravenously. Alternate current was delivered for 5 seconds, which induced seizure satisfactorily. However, asystole lasted for 10 seconds during the procedure. Spontaneous beating appeared followed by tachycardia and bigemina. Normal sinus rhythm returned four minutes later. She recovered smoothly, and showed no evidence of confusion nor muscle weakness. We speculated that pyridostigmine potentiated the ECT-induced vagal reflex and provoked asystole. In the following session, we pretreated her with intravenous atropine prior to thiamylal and suxamethonium. Although the current delivery increased RR-interval up to 1.2 seconds, neither asystole nor serious tachyarrhythmia occurred. Seven sessions of ECT relieved her psychiatric symptoms uneventfully. We presented a case of depression for which ECT was applied. Asystole with ECT seems associated with administration of pyridostigmine for the treatment of myasthenia gravis. Pretreatment with atropine can prevent asystole without inducing hazardous tachyarrhythmia.

Adult↗

[Perioperative management for emergency cesarean section of a patient with reexpansion pulmonary edema].

A 27-year-old woman with 39 week gestation was admitted because of cough and dyspnea accompanied by massive right-sided pleural effusion. Following the right thoracocentesis, about 2000 ml of bloody pleural effusion was drained. Just after the thoracocentesis, the fetal heart rate (FHR) temporarily showed a variable deceleration pattern but the rate was restored spontaneously. One hour later, cough and dyspnea became worse. Changes in FHR pattern indicated the premature separation of the normally implanted placenta. Accordingly, an emergency cesarean section was performed under general anesthesia. Massive foamy tracheal secretion was drained from the tracheal tube during surgery. As her chest X-ray showed signs of pulmonary edema in the right lung, her status was diagnosed as reexpansion pulmonary edema (RPE). She was transferred to the intensive care unit and treated with mechanical ventilation, prednisolone and diuretics. Extubation was performed on the 2nd day after the surgery. On reexpansion of the collapsed lung, it is always necessary to consider not only the hemodynamic changes just after reexpansion but also RPE following reexpansion.

Adult↗

[Propofol anesthesia for ambulatory surgery in adults].

We reported 131 cases of ambulatory surgery in adults mainly anaesthetized with propofol infusion. Without any premedication, anesthesia was induced with propofol and fentanyl. A laryngeal mask airway was inserted using intravenous injection of vecuronium. Anesthesia was maintained with continuous infusion of propofol and intermittent fentanyl administrations, and local anesthetic infiltration was combined. All patients received air and oxygen mixture (FIO2 0.4) throughout the procedure. During surgery, metoclopramide and flurbiprofen axetil were given to prevent postoperative pain, nausea and vomiting. After surgery, patients were observed at the daycare unit in ward. Average age was 42 years and ASA risk was 1.3. Operation time and anesthesia time and hospital stay were 43.4 minutes, 70.6 minutes and 332 minutes, respectively. In 25 patients (19%) analgesics were needed for postoperative pain. Although 3 patients (2.3%) were unsuccessful as ambulatory surgery due to excessive pain, all patients including these three could be discharged within 24 hours after surgery. We conclude that combined anesthesia with propofol, fentanyl and local anesthetic is suitable for ambulatory surgery in adults.

Adult↗

[Tracheal tube damage by Harmonic Scalpel during tonsillectomy].

We experienced a case in which a tracheal tube was damaged by a Harmonic Scalpel during tonsillectomy. A 33-year-old man with chronic tonsillitis underwent tonsillectomy under general anesthesia. The trachea was intubated by Polar Preformed Tracheal Tube (Polar tube). About 45 minutes after the start of surgery, sudden massive air leakage in the trachea occurred. Surgery was accomplished under oral suctioning. After extubation, we found that an inflation cuff tube was cut off by the Harmonic Scalpel. The cause of damage was the position of an inflation cuff tube which had been in the dorsal side of the tracheal tube (near the surgical field) in the Polar tube. Anesthesiologists should be aware of the characteristics of the surgical equipment newly introduced.

Adult↗

Tissue factor and tissue factor pathway inhibitor levels during and after cardiopulmonary resuscitation.

Disseminated intravascular coagulation frequently occurs after global ischemia and reperfusion due to cardiac arrest. The present study was performed to demonstrate the role of tissue factor for coagulation pathway activation, as well as to investigate the precise time course of tissue factor pathway inhibitor (TFPI) during and after cardiopulmonary resuscitation (CPR). Thirty-two of out-of-hospital cardiac arrest patients were classified into two groups, those who achieved return of spontaneous circulation (ROSC) (n=13) and those without ROSC (n=19). Ten normal healthy volunteers served as control subjects. Serial levels of tissue factor and TFPI were measured during and after cardiac arrest and CPR. In patients with ROSC, cardiac arrest and CPR led to persistent increases in the levels of tissue factor that peaked 6 hours after arrival at the Emergency Department. Tissue factor levels in patients without ROSC also showed marked elevations compared to those of the control subjects. In both groups, the levels of TFPI were significantly lower than those in the control subjects. However, we could not find differences in the levels of the two markers between the patients with ROSC and those without ROSC. In conclusion, we demonstrated persistent elevation of the tissue factor levels associated with low TFPI during and after CPR in patients with out-of-hospital cardiac arrest. These results indicate the activation of the extrinsic coagulation pathway without adequate TFPI generation, which may contribute to thrombin activation and fibrin formation after whole-body ischemia and reperfusion.

Adult↗

Diabetes-induced down-regulation of beta1-adrenoceptor mRNA expression in rat heart.

The present study addressed the question of whether the number of myocardial beta-adrenoceptors in rats with 4- to 6-week streptozotocin-induced diabetes is regulated in a transcriptional or translational manner. Radioligand binding experiments with [3H]CGP 12177 {4-(3-t-butylamino-2-hydroxypropoxy)-[5,7-3H]benzimidazol-2-one} showed that the density of beta-adrenoceptors fell by 50% with no change in affinity in diabetic rat ventricular myocardium compared with age-matched control myocardium. The relative content of beta1-adrenoceptor mRNA in diabetic myocardium also was reduced from the control level by 57%, as determined by northern blot analysis. The reductions in myocardial beta-adrenoceptor number and beta1-adrenoceptor mRNA observed in diabetes were prevented by insulin therapy. These data indicate that the diminished density of myocardial beta-adrenoceptors in diabetes occurred, at least in part, at the mRNA level.

Animals↗