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Biomedical subjects

O Kemmotsu

Publications and source records attributed to O Kemmotsu.

At least 19 recordsLinked to original sources
PubMed2002

Effects of mild and moderate hypothermia on apoptosis in neuronal PC12 cells.

BACKGROUND: There is still a possibility that mild hypothermic therapy may be useful as a neuroprotective tool during the intraoperative period, although the mechanism of cerebral protection by mild hypothermia is not well understood. We hypothesized that mild hypothermia may be protective against cerebral ischaemia by inhibiting post-ischaemia apoptosis. In this study, we used serum-deprived PC12 cells as the neuronal apoptotic model and examined the direct effects of mild and moderate hypothermia. METHODS: Apoptosis was induced by depriving the cell culture medium of serum, which is one of the most representative methods to induce apoptosis, but not necrosis, in PC12 cells. Effects of mild (35 and 33 degrees C) and moderate (31 and 29 degrees C) hypothermia on apoptosis were evaluated. Cytotoxicity (lactate dehydrogenase leakage) and the percentage of apoptotic cells (calculated by flow cytometry with propidium iodide) were evaluated 4 days after induction of apoptosis. As a control, cells without induction of apoptosis were incubated under the same conditions as the apoptosis group. RESULTS: Without induction at 37 degrees C, cytotoxicity and the percentage of apoptotic cells were over 60 and 90%, respectively. At each temperature examined below 35 degrees C, significant decreases in cytotoxicity and the percentage of apoptotic cells were observed. Mean cytotoxicity at 31 and 29 degrees C was 50.2 (SD 4.2)% and 47.9 (4.4)%, respectively. The percentage of apoptotic cells at 31 and 29 degrees C was 42.5 (7.4)% and 36.5 (7.3)%, respectively. In the control group, cytotoxicity and the percentage of apoptotic cells were significantly higher at 29 degrees C than at 37 degrees C. CONCLUSIONS: Mild and moderate hypothermia (29-35 degrees C) inhibited apoptosis, although hypothermia below 30 degrees C may induce apoptosis in intact cells.

Animals↗
PubMed2001

Systematic elucidation of effects of tranexamic acid on fibrinolysis and bleeding during and after cardiopulmonary bypass surgery.

The aim of this study was to systematically elucidate the effects of tranexamic acid on fibrinolysis and bleeding during and after cardiopulmonary bypass (CPB) surgery. Twenty-two patients undergoing CPB surgery were randomized to receive 100 mg/kg tranexamic acid or an equal volume of saline after anesthesia induction and prior to skin incision. Plasma levels of tissue plasminogen activator (t-PA) antigen and activity, crosslinked fibrin degradation products (D-dimer), alpha2-antiplasmin-plasmin complex, and plasminogen activator inhibitor-1 (PAI-1) antigen were measured. Blood samples were obtained after induction of anesthesia, before, during, and after CPB, at the end of surgery, and the next morning after surgery. Intraoperative and postoperative blood loss during 24 h after surgery was recorded. Patients' demographics were similar between the two groups. No patients suffered from thrombotic complications after surgery. In the tranexamic acid group, fibrinolytic activity and secondary fibrinolysis as measured by t-PA activity and D-dimer were markedly suppressed during CPB surgery (P=.042 and P=.015, respectively). Decreased fibrinolytic activity and fibrinolysis were accompanied by reduction of perioperative bleeding in the tranexamic acid group. We could also find a good positive correlation between the peak levels of t-PA activity and D-dimer (r(2)=.4203, P=.0011). No differences in the t-PA antigen, PAI-1 antigen release, and plasmin inhibition by alpha2-antiplasmin were apparent between the two groups. In a randomized, prospective trial of patients undergoing CPB surgery, we demonstrated that the synthetic antifibrinolytic drug tranexamic acid effectively suppresses fibrinolysis by inhibiting t-PA and plasmin activity with clear reduction of perioperative blood loss. While tranexamic acid had no effects on the other important fibrinolytic inhibitors like PAI-1 and alpha2-antiplasmin.

Antifibrinolytic Agents↗
PubMed2001

Tracheal lidocaine attenuates the cardiovascular response to endotracheal intubation.

PURPOSE: In order to examine the efficacy of tracheal lidocaine (TL) for attenuation of the cardiovascular responses to endotracheal intubation (EI), we compared the cardiovascular responses to TL alone and EI with TL, with those to EI without TL. METHODS: Seventy-five patients (ASA I-II) were studied. Anesthesia was induced with fentanyl 2 microg x kg(-1) iv, thiamylal 5 mg x kg(-1) iv and sevoflurane 1.0% in oxygen. Vecuronium 0.12 mg x kg(-1) was used to facilitate EI. In Group A (n=25), three minutes after induction, EI was performed. In Group B (n=25), three minutes after induction, the patients received TL (4% lidocaine, 4 mL). This was followed by immediate EI. In Group C (n=25), EI was performed two minutes after TL. Heart rate, arterial blood pressure and rate- pressure product (RPP) were measured from one minute before induction until five minutes after EI. RESULTS: The changes of RPP caused by TL alone in Group C (TL; +34.6 +/- 29.0%, mean +/- SD) were significantly (P <0.01) less than those caused by EI without TL in Group A (+77.3 +/- 42.6%). EI after TL in Group C did not cause significant changes in RPP (+5.4 +/- 15.2%). There were no significant differences between Groups A and B (+58.3 +/- 36.6%). CONCLUSION: We conclude that the cardiovascular responses to TL alone are half as great as those to EI without TL, and that TL is effective for attenuation of the cardiovascular responses to EI. EI should be performed more than two minutes after TL.

Adult↗
PubMed2001

Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome.

OBJECTIVE: To determine the relations between macrophage migration inhibitory factor (MIF), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and cortisol in patients with systemic inflammatory response syndrome (SIRS) and to determine whether their levels correlate with patient survival. DESIGN: Prospective, observational, cohort study. SETTING: General intensive care unit in a university hospital. PATIENTS AND PARTICIPANTS: The study included 17 consecutive patients who met the criteria for SIRS; the patients were classified into subgroups, survivors (n = 8) and nonsurvivors (n = 9); eight healthy volunteers served as control subjects. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Serum MIF, TNF-alpha, IFN-gamma, and cortisol levels were measured serially when the patients were first identified as having SIRS (day 0), and on days 1-4. Except for the high tendency of acute respiratory distress syndrome in nonsurvivors (44%) compared to survivors (13%), there were no differences in the clinical backgrounds of the patients between the two groups. All patients had multiple organ dysfunction syndrome. The values of MIF and TNF-alpha in the nonsurvivors were significantly more elevated than those cytokines measured in the survivors and control subjects. Peak MIF levels significantly correlated with peak TNF-alpha levels (r2 = 0.448, P = 0.002), but did not correlate with peak levels of cortisol and IFN-gamma. Although the levels of IFN-gamma and cortisol showed a marked increase compared to those of the control subjects, we could not find differences in these variables between the survivors and the nonsurvivors. CONCLUSIONS: High MIF and TNF-alpha levels are closely linked with poor outcome in patients with SIRS. MIF and TNF-alpha may act together and have pathogenic roles in SIRS.

Adult↗
PubMed2001

Serial measurement of arterial lactate concentrations as a prognostic indicator in relation to the incidence of disseminated intravascular coagulation in patients with systemic inflammatory response syndrome.

To demonstrate the prognostic value of measuring blood lactate concentrations and to investigate the mechanisms of lactate production in patients with systemic inflammatory response syndrome (SIRS), we conducted a prospective cohort study. Among 22 patients with SIRS, there were 9 survivors and 13 nonsurvivors. Serial arterial lactate concentrations were measured on the day of admission to the intensive care unit (day 0). then on days 1-4. The subjects of this study consisted of 14 patients with SIRS, 6 with severe sepsis, and 2 with septic shock. On admission, the lactate concentrations did not differ between the two groups, but remained high in the nonsurvivors throughout the study period, while they progressively decreased in the survivors. The incidence of disseminated intravascular coagulation (DIC) was significantly higher in the nonsurvivors than in the survivors. The nonsurvivors had persistently higher DIC scores and lower platelet counts than the survivors. The changes in lactate concentration over time were statistically different between the patients with DIC and those without DIC. The findings of this study clearly demonstrated that serial arterial lactate measurements can predict a poor outcome in patients with SIRS, severe sepsis, or septic shock. DIC might play an important role in the pathogenesis of lactate production in these newly defined critically ill patients.

Analysis of Variance↗
PubMed2001

Systemic macrophage migration inhibitory factor release following hepatic resection.

We set out to determine the responses of macrophage migration inhibitory factor (MIF) to hepatic resection and investigate its role in predicting short-term postoperative morbidity and outcome. Blood samples from 29 patients undergoing hepatic resection and eight healthy volunteers were obtained serially for 24h and assayed for serum MIF, cortisol, and tumor necrosis factor (TNF)-alpha. The MIF and cortisol levels showed a parallel increase and their peak levels were significantly correlated (r2 = 0.33, P = 0.0011). The TNF-alpha levels also increased during and after hepatic resection, but did not correlate with the MIF levels. The patients were classified into an extended hepatectomy group (n = 9); a lobectomy/segmentectomy group (n = 12); and a subsegmentectomy group (n = 8). There were no differences in the time courses of MIF (P = 0.8699), cortisol (P = 0.7485), and TNF-alpha (P = 0.3819) among the three groups. No patients developed organ dysfunction and all were discharged from the intensive care unit without any complications. Our findings demonstrate that MIF production occurs in patients undergoing hepatic resection. Surgical stress may play a more important role in MIF secretion than inflammatory stimulus by TNF-alpha in these patients. Therefore, MIF minimally affects short-term postoperative morbidity and outcome.

Analysis of Variance↗
PubMed2001

Increased sensitivity to vecuronium and prolonged duration of its action in patients with end-stage renal failure.

STUDY OBJECTIVES: To determine whether the duration of action of vecuronium is influenced by chronic renal failure. DESIGN: Prospective clinical comparison. SETTING: Operating room, Hokkaido University Hospital. PATIENTS: 7 adult ASA physical status II and III patients with impaired renal function undergoing living-related renal transplantation (Group A), 5 adult ASA physical status II and III patients with impaired renal function undergoing elective surgery other than renal transplantation (Group B), and 13 adult ASA physical status I and II patients with normal hepatorenal function undergoing elective surgery (Group C). INTERVENTIONS: Anesthesia was induced with thiamylal 5 mg x kg(-1) and fentanyl 100 microg IV and maintained with 60% nitrous oxide and 1% isoflurane. An initial dose of vecuronium was administered and patients' tracheas were intubated. MEASUREMENTS: Neuromuscular function was monitored by acceleration of thumb adduction with train-of-four stimulation. Vecuronium 60 microg x kg(-1) was administered as the initial dose via a central catheter, and if the first twitch was more than 3% of the control, another dose of vecuronium 20 microg x kg(-1) was given as necessary. Both onset time and duration of action until 25% recovery were measured. Plasma vecuronium and its metabolite, 3-desacetyl-vecuronium, levels were measured at onset and at 25% recovery in Groups A and C. MAIN RESULTS: The total dose of vecuronium and initial concentration of vecuronium showed no significant difference between Group A and Group C. Duration of action was significantly prolonged in Group A and Group B compared with Group C. CONCLUSIONS: Duration of action of vecuronium is prolonged in patients with end-stage renal failure mainly due to higher sensitivity to vecuronium.

Adult↗
PubMed2001

Another point of view on the mechanism of thrombin generation during cardiopulmonary bypass: role of tissue factor pathway inhibitor.

OBJECTIVE: To determine the role of tissue factor and tissue factor pathway inhibitor (TFPI) in coagulation activation during cardiopulmonary bypass (CPB). DESIGN: Prospective, observational study. SETTING: Operating room in a city hospital. PARTICIPANTS: Thirty-one patients undergoing cardiac surgery. MEASUREMENTS AND MAIN RESULTS: The plasma levels of tissue factor antigen (tissue factor), total and free TFPI, several markers of thrombin generation (prothrombin fragment F1+2, thrombin antithrombin complex, and fibrinopeptide A), and heparin concentration were measured. Blood samples were obtained after induction of anesthesia (baseline level), before and after CPB, and at the end of the surgery. Despite an average heparin concentration of 2.9 +/- 0.2 IU/ mL, markers of thrombin generation, fibrin formation and its degradation (D-dimer) were observed during CPB. Significant increases of total and free TFPI levels (p < 0.0001) were found during CPB associated with lower tissue factor concentration (p < 0.0001) compared with the baseline values. Heparin concentration correlated with levels of total TFPI (r2 = 0.613, p < 0.0001) and free TFPI (r2 = 0.689, p < 0.0001). Tissue factor concentration showed significant negative correlations with levels of total TFPI (r2 = 0.128, p = 0.0003) and free TFPI (r2 = 0.070, p = 0.0078). CONCLUSION: These data indicate that TFPI release by heparin probably has an important role in the suppression of the tissue factor-dependent coagulation pathway during CPB. These changes occur along with ongoing thrombin generation and its activation. Either insufficient prevention of thrombin generation by TFPI or indirect activation of the intrinsic coagulation pathway occurs during CPB.

Aged↗
PubMed2001

Tissue factor pathway inhibitor response does not correlate with tissue factor-induced disseminated intravascular coagulation and multiple organ dysfunction syndrome in trauma patients.

OBJECTIVE: To determine the precise relationship between tissue factor and tissue factor pathway inhibitor (TFPI) after trauma, as well as to test the hypothesis that low TFPI levels are not sufficient to prevent tissue factor-dependent intravascular coagulation, leading to multiple organ dysfunction syndrome (MODS). DESIGN: Prospective, observational cohort study. SETTING: Emergency room and intensive care unit in a university hospital. PATIENTS: Thirty-three trauma patients, 18 with disseminated intravascular coagulation (DIC) and 15 without DIC were studied. Ten normal, healthy volunteers served as control subjects. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Antigen concentration of tissue factor and TFPI, and global parameters of coagulation and fibrinolysis were measured on the day of admission, and on days 1-4 after admission. The number of systemic inflammatory response syndrome (SIRS) criteria that patients met and the DIC score were determined, simultaneously. The results of these measurements, incidence of MODS, and outcome were compared between the DIC patients and those without DIC. In the DIC patients, significantly higher tissue factor levels (p =.0049) and lower platelet counts (p =.0016) were found compared with the non-DIC patients and control subjects. However, the TFPI values remained at normal levels during the study period. No correlation was found between the peak levels of tissue factor and TFPI. The mean duration of SIRS and the maximum number of the SIRS criteria being met by the patients in the DIC group were statistically longer and higher than those in the non-DIC patients. The incidence of MODS and the number of the dysfunctioning organs were higher in the DIC patients compared with those in the non-DIC patients, and the DIC patients had a poor outcome. CONCLUSIONS: We systematically elucidated the relationship between tissue factor and TFPI in post-trauma patients. Highly activated tissue factor-dependent coagulation pathway is not sufficiently prevented by the normal TFPI levels in patients with DIC. The DIC associated with thrombotic and inflammatory responses causes MODS, and leads to poor outcome in post-trauma patients.

APACHE↗
PubMed2001

[Do all patients with mandibular hypoplasia present difficulty in endotracheal intubation?].

On 7 patients with Pierre-Robin syndrome (PR), 8 patients with first and second brachial arch syndrome (BA) and 7 patients with Treacher Collins syndrome (TC), we examined retrospectively the number of patients whom anesthesiologists found difficult to perform laryngoscopy and intubation, the number of attempt necessary for proper insertion of the tracheal tube, the number of patients in whom the endotracheal intubation with laryngoscopy was given up and the time necessary for endotracheal intubation. We compared these with those from 22 control patients. Our results suggest that the difficult laryngoscopy and intubation are more frequent in TC. On the other hand, most of PR and BA may not present difficulty in intubation.

Child↗
PubMed2001

Postoperative myocardial ischemia in thoracic aortic aneurysms.

BACKGROUND: To determine the incidence and predictors of postoperative myocardial ischemia in non-coronary risk patients undergoing surgery for thoracic aortic aneurysms. METHODS DESIGN: a prospective, observational study. SETTING: a general intensive care unit in a university hospital. PARTICIPANTS: twenty patients without ischemic heart disease, scheduled for elective surgical repair of thoracic or thoracoabdominal aortic aneurysms. INTERVENTIONS: all patients underwent aortic replacement with prosthetic graft and routine postoperative care. Patients who developed myocardial ischemia received an infusion of coronary vasodilators. RESULTS: ECG episodes of myocardial ischemia were defined as reversible ST-segment changes of either >1 mm of depression or >2 mm of elevation at the J point. All patients survived operation. Eleven patients (ischemia group) developed myocardial ischemia, and 9 patients did not (non-ischemia group). These episodes were transient in 8 cases, but lasted longer than 3 days in 3 cases. In univariate analysis of perioperative factors between the two groups, the use of total cardiopulmonary bypass (p<0.01), the cardiac index at ICU admission (p<0.05), and the incidence of pre-existent hypertension (p<0.05) were significantly different. Multiple regression analysis identified the use of total cardiopulmonary bypass as the only predictor of myocardial ischemia. CONCLUSIONS: The use of total cardiopulmonary bypass is predictive of perioperative myocardial ischemia in surgery for thoracic aortic aneurysms, probably due to the production of proinflammatory cytokines by systemic ischemia and reperfusion. Prophylactic use of coronary vasodilators may be validated in these cases.

Adolescent↗
PubMed2001

Pathological evaluation of venous emboli during total hip arthroplasty.

One of the possible causes of bone cement implantation syndrome during total hip arthroplasty is pulmonary embolism, as has been suggested by a characteristic image seen during transoesophageal echocardiography, the so-called 'Snow Flurry'. However, the nature of the embolic material has not been definitively determined. We studied seven patients undergoing cemented or uncemented total hip arthroplasty. 'Snow Flurry' images were detected in all patients. Blood was aspirated from the right atrium during 'Snow Flurries' and was subjected to pathological examination. Amorphous, eosinophilic, fine granular material was seen in all specimens. The material did not originate from cement. Fat and bone marrow were not detected. The material seen may consist of fine particles of bone ('bone dust') originating from reamed bone.

Adult↗
PubMed2001

Effects of Ca2+ sensitizers on contraction, [Ca2+]i transient and myofilament Ca2+ sensitivity in diabetic rat myocardium: potential usefulness as inotropic agents.

The purpose of the present study was to investigate the effects of Ca2+ sensitizers EMD 57033, MCI-154, and EGIS-9377 in cardiac preparations from streptozotocin-induced diabetic rats. In enzymatically dissociated ventricular myocytes loaded with the Ca2+ probe indo 1, these Ca2+ sensitizers caused an increase in cell shortening without a significant effect on the intracellular Ca2+ ([Ca2+]i) transient. The contractile responses were substantially similar in myocytes from diabetic and age-matched control rats. In contrast, the contractile and [Ca2+]i responses to pimobendan and isoproterenol were significantly less in diabetic myocytes. The Ca2+ sensitivity of tension in beta-escin-skinned trabeculae from diabetic hearts was not significantly different from that of controls. The effect of EMD 57033 on myofilament responsiveness to Ca2+ was identical in control and diabetic preparations. The slower time course of relaxation observed in diabetic papillary muscles was further prolonged in the presence of EMD 57033. However, the extent of the increase in relaxation produced by EMD 57033 did not differ between control and diabetic muscles, and the detrimental effect on resting tension was less pronounced in the two groups. In anesthetized rats, echocardiography showed that intra-duodenal administration of EMD 57033 increased left ventricular systolic function without affecting variables of diastolic filling in both groups. Taken together, the present results suggest that Ca2+ sensitizers, unlike conventional inotropic agents, have the potential to increase in force of contraction to the same extent in nondiabetic and diabetic myocardium, possibly without exaggerating extremely the impairment of diastolic function in diabetes.

Actin Cytoskeleton↗
PubMed2001

[Anesthesia for electroconvulsive therapy during pregnancy--a case report].

We experienced anesthetic management for ECT in a patient with psychiatric disease during the third trimester of pregnancy. The 24 year-old patient had been on oral antipsychotics prescribed to treat schizophrenia for ten years. Her signs and symptoms deteiorated during pregnancy in spite of increased doses of antipsychotics. With tocolytic agent administered intravenously, anesthesia was induced by intravenous thiamylal immediately followed by intravenous suxamethonium for muscle relaxation. Alternative current was applied on both side of the head after the sufficient anesthesia had been obtained. The patient received intermittent mandatory ventilation by breathing mask with 100% oxygen during the procedure. Along with monitoring of maternal hemodynamic variables and arterial oxygen saturation (Spo2), fetal heart rate and uterine contraction were recorded by cardiotocogram throughout the procedure. At the first two treatments, the patient showed neither significant uterine contraction nor fetal heart rate changes. At the third treatment, continuous uterine contraction refractory to tocolysis was recorded for six minutes, resulting in fetal bradycardia. At the sixth treatment, general anesthesia was induced and maintained by sevoflurane in oxygen followed by suxamethonium for muscle relaxation. The uterine contraction was remarkably diminished and fetal heart rate remained unchanged during the procedure. In conclusion, inhalation anesthesia is beneficial for ECT in the last stage of pregnancy to reduce uterine contraction by potential uterine relaxation effect of anesthetics.

Adult↗
PubMed2000

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↗
PubMed2000

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↗
PubMed2000

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↗