Biomedical subjects
Publications and source records attributed to Satoshi Furukawa.
This case report describes a patient with a symptomatic diaphragmatic hernia that developed after orthotopic heart transplantation and explantation of a left ventricular assist device. The hernia was repaired laparoscopically, and at 6-month follow-up, she is without evidence of recurrence.
STUDY OBJECTIVES: To characterize patients who acquired postoperative respiratory failure after lung transplantation (LT), and to identify risks associated with postoperative respiratory failure and poor surgical outcome. STUDY DESIGN: Retrospective clinical analysis in a tertiary care transplantation center. METHODS: We reviewed the records of 80 consecutive patients who underwent LT from April 1994 to May 1999, analyzing their records for a number of preoperative and perioperative variables and complications. RESULTS: Forty-four patients (55%) acquired postoperative respiratory failure and had a mortality rate of 45%. No difference was noted between patients with respiratory failure and those without in terms of age (mean +/- SD, 56 +/- 9 years vs 53 +/- 11 years), gender, baseline pretransplant arterial blood gas analysis (PaCO(2), 46 +/- 9 mm Hg vs 44 +/- 10 mm Hg), and cardiopulmonary exercise testing (maximum oxygen uptake, 0.76 +/- 0.44 L/min/m(2) vs 0.82 +/- 0.20 L/min/m(2)). Ischemic reperfusion lung injury (IRLI) [55%] and perioperative cardiovascular/hemorrhagic events (36%) were the major contributors to the development of respiratory failure. Preoperative pulmonary hypertension, right ventricular (RV) dysfunction, ischemic times, and need for bilateral LT and cardiopulmonary bypass (CPB) were higher in patients with respiratory failure (p < 0.05) compared to recipients without respiratory failure. However, the presence of preoperative moderate-to-severe RV dysfunction was the only independent factor (odds ratio, 21.9; 95% confidence interval, 1.6 to 309.0). CONCLUSION: Respiratory failure after LT is common and is associated with high morbidity and mortality. Respiratory failure often occurred in patients with operative technical complications, cardiovascular events, and postoperative IRLI, which were observed most in patients requiring CPB because of RV dysfunction.
Ca2+ influx through the L-type calcium channel (LTCC) induces Ca2+ release from the sarcoplasmic reticulum (SR) and maintains SR Ca2+ loading. Alterations in LTCC properties, their contribution to the blunted adrenergic responsiveness in failing hearts and their recovery after support with LV assist devices (LVAD) were studied. L-type Ca2+ current (I(Ca,L)) was measured under basal conditions and in the presence of isoproterenol (ISO), dibutyryl-cAMP (db-cAMP), Bay K 8644 (BayK), Okadaic acid (OA, a phosphatase inhibitor), and phosphatase 2A (PP2A) in nonfailing (NF), failing (F), and LVAD-supported human left ventricular myocytes (HVMs). Basal I(Ca,L) density was not different in the 3 groups but I(Ca,L) was activated at more negative voltages in F- and LVAD- versus NF-HVMs (V(0.5): -7.18+/-1.4 and -7.0+/-0.9 versus 0.46+/-1.1 mV). Both ISO and db-cAMP increased I(Ca,L) in NF- and LVAD- significantly more than in F-HVMs (NF >LVAD> F: ISO: 90+/-15% versus 77+/-19% versus 24+/-12%; db-cAMP: 235%>172%>90%). ISO caused a significant leftward shift of the I(Ca,L) activation curve in NF- and LVAD- but not in F-HVMs. After ISO and db-cAMP, the I(Ca,L) activation was not significantly different between groups. BayK also increased I(Ca,L) more in NF- (81+/-30%) and LVAD- (70+/-15%) than in F- (51+/-8%) HVMs. OA increased I(Ca, L) by 85.6% in NF-HVMs but had no effect in F-HVMs, while PP2A decreased I(Ca, L) in F-HVMs by 35% but had no effect in NF-HVMs. These results suggest that the density of LTCC is reduced in F-HVMs but basal I(Ca,L) density is maintained by increasing in LTCC phosphorylation.
OBJECTIVE: To describe an outbreak of mediastinitis in heart transplant recipients. DESIGN: Retrospective and contemporaneous cohort SETTING: Urban tertiary-care university hospital with a large cardiac transplantation program. PATIENTS: Heart transplant recipients. INTERVENTIONS: Modifications of donor harvest technique; procedures aimed at decreasing skin and mucosal bacterial colonization; strict aseptic technique in the intensive care unit; and aggressive policing of established infection control practices. RESULTS: In April 1999, mediastinitis rates among heart transplant recipients increased abruptly from a baseline of 6 cases per 100 procedures to sequential quarterly rates of 22, 31, and 50 cases per 100 procedures, whereas infection rates in other cardiac operations were unchanged. Bacteria causing these infections were multidrug-resistant "nosocomial" organisms. The epidemic occurred 2 months after a change in the United Network for Organ Sharing organ allocation algorithm. This change resulted in an increase in the duration of preoperative hospitalization from a median of 52 to 79 days (P = .008) and may have promoted prolonged hospitalization of patients with high illness severity. Aggressive multidisciplinary interventions were temporally associated with a return to preoperative mediastinitis rates without changing length of hospitalization prior to transplantation. CONCLUSIONS: Changes in organ allocation for transplant that prolong waiting time in the hospital and alter illness acuity may lead to increased rates of postoperative infection. Measures to limit bacterial colonization may be a helpful countervailing strategy.
Antibiotic therapy is an essential treatment for gram-negative bacterial infections. Antibiotic-induced endotoxin release and subsequent production of inflammatory cytokines reportedly depend on the type of antibiotic action. This study examined the effects of various beta-lactam antibiotics on cell death of human polymorphonuclear neutrophils (PMNs) cocultured with Escherichia coli (E. coli) in vitro. E. coli morphology after antibiotic treatment was determined. PMNs and E. coli were cocultured with antibiotics for 0, 4, or 12 h. Levels of endotoxin and cytokines (TNF-alpha, IL-1beta, and IL-6) in the supernatants were measured. The filtrates of antibiotic-treated E. coli supernatants were cocultured with PMNs for 0, 4, or 12 h. In all experiments, ampicillin (ABPC), cefazolin sodium (CEZ), cefoperazone sodium (CPZ), latamoxef sodium (LMOX), imipenem (IPM), and polymyxin B sulfate (PLB) were used at 30 microg/mL. PMNs were isolated from healthy volunteers. PMN cell death was assessed by flow cytometry and light microscopy. ABPC, CEZ, CPZ, and LMOX, which induce bacterial filament formation with lysis, caused PMN necrosis when cocultured with E. coli. In contrast, IPM, which induces bacterial spheroplast formation with lysis, caused PMN apoptosis. Levels of endotoxin, TNF-alpha and IL-6 in the supernatants with IPM and PLB were significantly lower than in those with other beta-lactam antibiotics. The filtrates of IPM- and PLB-treated E. coli supernatants induced PMN apoptosis, whereas those treated with other beta-lactam antibiotics increased PMN necrosis. Beta-lactam antibiotics have different impacts on the types of PMN cell death after E. coli killing. Underlying mechanisms and the clinical relevance of IPM-induced PMN apoptosis in severe gram-negative infection warrant further investigation.
Moderate chronic exercise attenuates the elevation of blood pressure in young spontaneously hypertensive rats. In order to elucidate the physiological process of the effects of exercise, we examined the involvement of nitric oxide, angiotensin II, and superoxide dismutase in this process. Rats were exercised by voluntary running in a wheel-cage for 10 weeks. Systolic blood pressure in the exercised rats (195+/-4 mmHg, n=27) was significantly (p<0.05) lower than in the post-control rats (212+/-3 mmHg, n=28). The concentration of total plasma nitrite was significantly higher in exercised rats (14.9+/-1.5 micromol l(-1)) than in the post-control rats (9.9+/-0.7 micromol l(-1), p<0.05). Superoxide dismutase activity in the exercised rats was significantly higher (p<0.05) than in the post-control rats (thoracic aorta: 4.6+/-0.3 U mg protein(-1) vs 3.6+/-0.3 U mg protein(-1), heart: 12.7+/-0.6 U mg protein(-1) vs 10.2+/-0.6 U mg protein(-1), p<0.05). The plasma angiotensin II concentration was higher in the post-control rats (74.4+/-14.0 pg mL(-1)) than in the exercised rats (45.0+/-6.4 pg mL(-1), p<0.05), and in the pre-control rats (47.2+/-6.0 pg mL(-1)). The results suggest that exercise acts to decrease the level of superoxide by increasing superoxide dismutase activity in the aorta and heart and to decrease levels of angiotensin II, both of which, in turn, increase the effective concentration of nitric oxide. We conclude that the combination of these effects with the increased NO formation resulted in the low blood pressure seen in the exercised rats.
We report 2 patients with acute cholecystitis for which percutaneous transhepatic gallbladder aspiration (PTGBA) was useful. In Case 1, the patient was a 75-year-old woman who experienced a sudden onset of back pain and upper abdominal pain at night. Abdominal ultrasound (US) showed enlargement of the gallbladder with thickening of the wall, a sonolucent layer, and a stone in the neck of the gallbladder, which led to a diagnosis of acute cholecystitis. Magnetic resonance imaging (MRI) demonstrated thickening of the gallbladder wall and 2 areas of low-intensity signal. The pain and fever persisted, for which we performed PTGBA, aspirating about 113 ml of infected bile. Subsequently, the pain and fever subsided, and abdominal US revealed a reduction in the enlargement of the gallbladder with the persistence of thickening of the wall. On the eighth day after PTGBA, open abdominal cholecystectomy was performed. In Case 2, the patient was a 56-year-old woman who had right hypochondriac pain after supper. The pain gradually increased in severity. Abdominal US showed enlargement of the gallbladder with a thickened wall, a sonolucent layer, and a gallstone in the neck of the gallbladder, which led to a diagnosis of acute cholecystitis. Magnetic resonance cholangiopancreatography (MRCP) showed enlargement of the gallbladder with no abnormalities in the common bile duct. After admission to hospital, the pain and fever persisted, for which we performed PTGBA, aspirating about 50 ml of infected bile. Subsequently, the pain and fever vanished. Abdominal US revealed a reduction in the enlargement of the gallbladder with the persistence of thickening of the wall. On the seventh day after PTGBA, laparoscopic cholecystectomy was performed. PTGBA seems useful for early alleviation of the symptoms of acute cholecystitis because of low invasiveness and ease of performance.
Indole-3-acetic acid (IAA), known as natural auxin, induces cleft palate in rodents. However, there has been no report about the neurodevelopmental toxicity of IAA in rats. In the present study, we found microencephaly in the fetuses from the rats exposed to IAA. The purpose of this work was to examine the effects of IAA administration in pregnant rats on neuroepithelial cells in the embryos/fetuses. IAA was administered at 500 and 1,000 mg/kg on gestation days (days) 12, 13, and 14, and then embryos/fetuses were harvested on days 14.5, 15, 16, and 21. Cleft palate was induced at 1,000 mg/kg. The brain in treated groups exhibited reduction in the size and weight on day 21 in a dose-dependent manner. Histopathologically, apoptotic cells were observed mainly in the medial and dorsal layer of the neuroepithelium at 500 and 1,000 mg/kg on day 14.5. On day 15, they were observed in the medial and dorsal layer of the neuroepithelium, and preplate at 1,000 mg/kg. On day 16, they existed in the dorsal layer of the neuroepithelium and intermediate zone in the embryos from 1 dam at 1,000 mg/kg. On day 21, an increase in cell proliferative activity was observed in the neuroepithelium at 500 and 1,000 mg/kg. The reduction of the cortical plate, the enlargement of the neuroepithelium and a slight increase in neuron density in the intermediate zone were observed at 1,000 mg/kg. These findings indicated IAA might induce the neuronal apoptosis in the S phase and lead to microencephaly.
We evaluated the effects of nutrient enriched medium and hemoglobin based oxygen carrier (HBOC) upon myocardial functional recovery after 15 minutes of warm ischemia in an isovolumic Langendorff rat heart model. Hearts (n = 8/group) were perfused at constant pressure (90 mm Hg) with Krebs-Henseleit buffer or HEPES modified cell culture medium (M199) in the absence and presence of HBOC. Hearts received 15 minutes of normothermic no flow ischemia followed by 60 minutes reperfusion. Hemodynamics, coronary flow, and tissue water content were measured, and microscopic evidence of injury including TUNEL assay was assessed. Preischemic left ventricular performance (left ventricular developed pressure and maximum rate of positive and negative change in systolic pressure) and coronary flow were similar among groups. At 60 minutes of reperfusion, M199 alone provided more stable and complete left ventricular systolic and diastolic functional recovery than any other perfusate. Coronary flow rates reflected left ventricular function observed under each perfusate condition. TUNEL assay showed arterial endothelial cell death in some hearts perfused with HBOC. Tissue water content did not reflect functional recovery. The combination of M199 and HBOC was associated with poor recovery and elevated perfusate methemoglobin. In this system, postischemic dysfunction is prevented by components in M199. Added HBOC does not improve functional recovery and negates the salutary effects of M199, possibly by augmenting methemoglobin formation.