ABSTRACT
Objective To explore the protective effect of ulinastatin (UTI) on myocardial protection in sepsis. Methods 69 clean male SD rats were randomly divided into 3 groups: normal control group, sepsis group and ustodin group. experimental rats serum troponin T (ATnT) concentration, using automatic biochemical analyzer determination of creatine kinase (AK), creatine kinase isoenzyme (AK-MB) concentration;The changes of AAh and m-aahrs levels in rat myocardial tissues were detected by enzyme-linked immunosorbent assay. Pathological changes of myocardial tissue in rats were observed by HE staining. Results The serum ATnT, AK and ak-mb concentrations in the sepsis group were significantly higher than that in the normal control group, and the indexes of the ustodin group were significantly decreased (P<0.05). The AAh level of myocardial tissue of sepsis group was significantly higher than that of the normal control group, and the AAh level was significantly decreased after the treatment of UTI, and the m-aahrs level of myocardial tissue was not significantly changed (P<0.05). Pathological histological observation showed that the myocardial tissue lesion was significantly relieved (P<0.05). Conclusion UTI can improve the degree of myocardial injury in rats with sepsis.
ABSTRACT
Objective To explore the protective effect of ulinastatin (UTI) on myocardial protection in sepsis. Methods 69 clean male SD rats were randomly divided into 3 groups: normal control group, sepsis group and ustodin group. experimental rats serum troponin T (ATnT) concentration, using automatic biochemical analyzer determination of creatine kinase (AK), creatine kinase isoenzyme (AK-MB) concentration;The changes of AAh and m-aahrs levels in rat myocardial tissues were detected by enzyme-linked immunosorbent assay. Pathological changes of myocardial tissue in rats were observed by HE staining. Results The serum ATnT, AK and ak-mb concentrations in the sepsis group were significantly higher than that in the normal control group, and the indexes of the ustodin group were significantly decreased (P<0.05). The AAh level of myocardial tissue of sepsis group was significantly higher than that of the normal control group, and the AAh level was significantly decreased after the treatment of UTI, and the m-aahrs level of myocardial tissue was not significantly changed (P<0.05). Pathological histological observation showed that the myocardial tissue lesion was significantly relieved (P<0.05). Conclusion UTI can improve the degree of myocardial injury in rats with sepsis.
ABSTRACT
<p><b>BACKGROUND</b>Myocyte apoptosis is considered to be the major causative factor of left ventricular (LV) remodeling following myocardial infarction (MI). We previously reported that 3', 4'-dihydroxyflavonol (DiOHF), was able to suppress oxidative stress and preserve the expression of endothelial nitric oxide synthase during myocardial reperfusion injury, which may benefit the reduction of myocyte apoptosis. We therefore aimed to evaluate the potential actions of DiOHF against myocyte apoptosis and post-infarction LV remodeling in this study.</p><p><b>METHODS</b>Following experimental MI, surgical instrumented goats were randomly assigned into vehicle and DiOHF (2 mg/kg; i.v., daily) groups to receive 4 weeks of reperfusion with corresponding treatments. LV pressure recordings and echocardiogram were performed at baseline, 2 and 4 weeks of reperfusion. Myocardial tissues were collected in the end to determine infarct size and apoptosis related assays.</p><p><b>RESULTS</b>LV end-diastolic volume and diameter were significantly increased 4 weeks after MI in the vehicle group, accompanied by reduced posterior wall thickness, septal thickness and LV mass, whereas those changes were markedly prevented by DiOHF treatment. Similarly, significantly reduced infarct size was found in DiOHF group as compared to vehicle group, and DiOHF dramatically inhibited the increase in LV end-diastolic pressure and the reductions in ejection fraction, fraction shortening and dP/dt(max). Moreover, DiOHF treatment significantly reduced the extent of myocyte apoptosis detected by TUNEL assay, enhanced the protein expression of caspase-3, Fas, Bax and cytochrome c in the non-infarcted myocardium in comparison to vehicle.</p><p><b>CONCLUSIONS</b>Daily DiOHF treatment during the reperfusion period after MI in the ovine hearts markedly reduced the magnitude of post-infarction LV remodeling through the inhibition of myocyte apoptosis in the remote non-infarcted myocardium.</p>
Subject(s)
Animals , Female , Male , Apoptosis , Caspase 3 , Metabolism , Cytochromes c , Metabolism , Echocardiography , Flavonols , Pharmacology , Goats , In Situ Nick-End Labeling , Myocardial Infarction , Metabolism , Myocytes, Cardiac , Cell Biology , Random Allocation , Ventricular Remodeling , bcl-2-Associated X Protein , Metabolism , fas Receptor , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the clinical value of glycosylated G-CSF combined with middle-high dose cyclophosphamide (Cy) or conventional chemotherapy with increased dose of Cy for mobilizing peripheral blood progenitor cells in patients with tumor.</p><p><b>METHODS</b>Thirty patients from four hospitals in Beijing region were enrolled in this clinical study. Diagnoses of the patients were non-Hodgkin' lymphoma (n = 21), Hodgkin disease (n = 1), breast cancer (n = 7) and ovary cancer (n = 1). Autologous peripheral blood progenitor cells (APBPC) were mobilized by middle-high dose Cy or conventional chemotherapy with increased dose of Cy combined with G-CSF. G-CSF was given subcutaneously from the nadir of the white blood cell (WBC) count to the end of PBPC collection. The dosage of G-CSF was 250 microg/d in 29 patients and 500 microg/d in 1 patient. When WBC count was > 5 x 10(9)/L, APBPC were harvested with CS 3000 plus/COBE Spectra.</p><p><b>RESULTS</b>The average dosage of Cy was 3.95 g (2.3 g/m(2)). The doses of G-CSF were 3.1 approximately 6.4 microg x kg(-1) x d(-1). Thirteen patients (43%) were collected twice, 14 patients (47%) three times and 3 patients (10%) four times. All of the patients could tolerate the treatment regimens. Seven patients had bone pain after G-CSF injection and one was severe, one patient had headache and one had nausea and vomiting.</p><p><b>CONCLUSION</b>250 microg glycosylated G-CSF combined with middle-high Cy or conventional chemotherapy with increased dose of Cy combined G-CSF is an optimal method for APBPC mobilization in tumor patients.</p>