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81.

Background

A pulmonary hypertensive crisis (PHC) can be a life-threatening condition. We established a PHC model by exposing rats with monocrotaline (MCT)-induced pulmonary hypertension to acute hypoxia, and investigated the effects of vasopressin, phenylephrine, and norepinephrine on the PHC.

Methods

Four weeks after MCT 60 mg kg?1 administration i.v., right ventricular systolic pressure (RVSP), systolic BP (SBP), mean BP (MBP), cardiac index (CI), and pulmonary vascular resistance index (PVRI) were measured. PHC defined as an RVSP exceeding or equal to SBP was induced by changing the fraction of inspiratory oxygen to 0.1. Rats were subsequently treated by vasopressin, phenylephrine, or norepinephrine, followed by assessment of systemic haemodynamics, isometric tension of femoral and pulmonary arteries, cardiac function, blood gas composition, and survival.

Results

PHC was associated with increased RV dilatation and paradoxical septal motion. Vasopressin increased MBP [mean (standard error)] from 52.6 (3.8) to 125.0 (8.9) mm Hg and CI from 25.4 (2.3) to 40.6 (1.8) ml min?1 100 g?1 while decreasing PVRI. Vasopressin also improved RV dilatation, oxygenation, and survival in PHC. In contrast, phenylephrine increased MBP from 54.8 (2.3) to 96.8 (3.2) mm Hg without improving cardiac pump function. Norepinephrine did not alter MBP. Vasopressin contracted femoral but not pulmonary arteries, whereas phenylephrine contracted both arterial beds. Hence, improvements with vasopressin in PHC might be associated with decreased PVRI and selective systemic vasoconstriction.

Conclusions

In this rat model of a PHC, vasopressin, but not phenylephrine or norepinephrine, resulted in better haemodynamic and vascular recovery.  相似文献   
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Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2) and glucose transporter 1 (GLUT1) after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o.) for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid) in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.  相似文献   
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Aim: The epidemiology of acute hepatitis B is unknown in many countries, and the clinical features of this disease remain unclear. In this study, we used the Diagnosis Procedure Combination (DPC) database to estimate the incidence of acute hepatitis B and investigate the clinical practices for acute hepatitis B in Japan. Methods: The DPC database is a nationwide discharge abstract and administrative claims database, covering 40% of all inpatient admissions to acute care hospitals between 1 July and 31 December each year in Japan. We identified cases with a diagnosis of acute hepatitis B between 2007 and 2008. Patient characteristics, length of stay, in‐hospital mortality and total charges were determined. Clinical practice patterns were examined, including drugs used and procedures performed during hospitalization. Results: We identified 890 cases with acute hepatitis B among 5.85 million inpatients in the database. The mean age was 40.0 years old and 76% were male. The incidence of acute hepatitis B was estimated to be approximately 2100–2400/year (17–19/1 million people per year). Of 890 cases, 53 (6.0%) developed fulminant hepatitis and 36 (4.0%) died. Nucleos(t)ide analogs were prescribed for 226 cases (25.4%). Only 194 cases (21.8%) were tested for HIV status. Conclusion: It is essential to monitor the trends of this communicable and preventable disease. The establishment and distribution of appropriate clinical evidence and guidelines are vital to improve the clinical practices for acute hepatitis B.  相似文献   
86.
In almost every type of artificial valve, structural failure has been described. We are reporting on a case of a sudden leaflet escape of an Edwards TEKNA mitral valve prosthesis 12 years after implantation. The patient had a sudden onset of dyspnea and severe pulmonary edema with subsequent cardiogenic shock. An emergency mitral replacement was successfully performed. A multi-detector computed tomography scanning and three-dimensional imaging showed two fragments that had embolized in the terminal aorta and the left common iliac artery. The patient presented visual field abnormality, and postoperative head computed tomography showed watershed cerebral infarction. The escaped leaflet that fractured transversely was removed, following the patient’s recovery, during cardiac surgery.  相似文献   
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