干姜附子汤对大鼠心肌缺血-再灌注损伤的保护作用

[目的]观察干姜附子汤对大鼠心肌缺血-再灌注引起的氧化应激损伤的保护作用。[方法]采用在体结扎大鼠左冠状动脉前降支30 min,再灌注60 min的方法制备心肌缺血再灌注模型。观察干姜附子汤对心电图ST段、心肌梗死百分率、血清丙二醛（MDA）含量、超氧化物歧化酶（S0D）活力等指标的影响。[结果]干姜附子汤能有效对抗大鼠心肌缺血再灌注损伤导致的心电图 ST段抬高,缩小心肌梗死百分率、降低血清中 MDA的含量、升高血清SOD的活性。[结论]干姜附子汤对大鼠心肌缺血-再灌注引起的氧化应激损伤有保护作用,其机制可能与减少心肌自由基的生成及增强心肌抗氧化能力有关。     

Cardiac Biomarkers in Hyperthyroid Cats

Background

Hyperthyroidism has substantial effects on the circulatory system. The cardiac biomarkers NT‐proBNP and troponin I (cTNI) have proven useful in identifying cats with myocardial disease but have not been extensively investigated in hyperthyroidism.

Hypothesis

Plasma NT‐proBNP and cTNI concentrations are higher in cats with primary myocardial disease than in cats with hyperthyroidism and higher in cats with hyperthyroidism than in healthy control cats.

Animals

Twenty‐three hyperthyroid cats, 17 cats with subclinical hypertrophic cardiomyopathy (HCM), and 19 euthyroid, normotensive healthy cats ≥8 years of age. Fourteen of the hyperthyroid cats were re‐evaluated 3 months after administration of radioiodine (¹³¹I).

Methods

Complete history, physical examination, complete blood count, serum biochemistries, urinalysis, blood pressure measurement, serum T4 concentration, plasma concentrations of NT‐proBNP and cTNI, and echocardiogram were obtained prospectively from each cat.

Results

Hyperthyroid cats and cats with HCM had plasma NT‐proBNP and cTNI concentrations that were significantly higher than those of healthy cats, but there was no significant difference between hyperthyroid cats and cats with HCM with respect to the concentration of either biomarker. In hyperthyroid cats that were re‐evaluated 3 months after ¹³¹I treatment, plasma NT‐proBNP and cTNI concentrations as well as ventricular wall thickness had decreased significantly.

Conclusions and Clinical Importance

Although there may be a role for NT‐proBNP in monitoring the cardiac response to treatment of hyperthyroidism, neither NT‐proBNP nor cTNI distinguish hypertrophy associated with hyperthyroidism from primary HCM. Therefore, the thyroid status of older cats should be ascertained before interpreting NT‐proBNP and cTNI concentrations.     

Prediction of Long‐Term Outcome by Measurement of Serum Concentration of Cardiac Troponins in Critically Ill Dogs with Systemic Inflammation

Background

Myocardial injury, detected by cardiac troponin I and T (cTnI and cTnT), has been associated with long‐term death in the noncardiac human intensive care unit (ICU).

Hypothesis

Presence of myocardial injury predicts 1‐year case fatality in critically ill dogs with systemic inflammation.

Animals

Thirty‐eight dogs with evidence of systemic inflammation and no primary cardiac disease.

Methods

Prospective cohort study. In dogs admitted to the ICU with evidence of systemic inflammation, blood samples were obtained at ICU admission for measurement of cTnI and cTnT, and cTnI was measured once daily during ICU hospitalization. Receiver operating characteristic (ROC) curves were used to examine prognostic capacity of admission cTnI, admission cTnT, and peak cTnI concentrations.

Results

One‐year case fatality rate was 47% (18/38 dogs). Admission cTnI concentrations were (median [range]) 0.48 [0.004–141.50] ng/mL, and peak cTnI concentrations were 1.21 [0.021–141.50] ng/mL. Admission cTnT concentrations were 15 [<13–3744] ng/L. For each marker, non‐survivors had significantly higher concentrations than survivors (P = .0082–.038). ROC analyses revealed areas under curves [95% CI] of 0.707 [0.537–0.843] for peak cTnI and 0.739 [0.571–0.867] for admission cTnT, respectively. At the optimal cut‐off, concentrations were 1.17 ng/mL (peak cTnI) and 23 ng/L (admission cTnT), sensitivities were 72% and 72%, and specificities were 70% and 80%, respectively.

Conclusions and Clinical Importance

While peak cTnI and admission cTnT are significantly related to 1‐year case fatality in critically ill dogs with systemic inflammation, low sensitivities and specificities prevent their prediction of long‐term outcome in individual patients. Troponins might play a role in identification of dogs at long‐term risk of death.     

Cardiac Troponin I and T as Prognostic Markers in Cats with Hypertrophic Cardiomyopathy

Background

Myocardial injury detected by cardiac troponin I and T (cTnI and cTnT) in cardiac disease is associated with increased risk of death in humans and dogs.

Hypothesis

Presence of myocardial injury predicts long‐term death in cats with hypertrophic cardiomyopathy (HCM), and ongoing myocardial injury reflects change in left ventricular wall thickness over time.

Animals

Thirty‐six cats with primary HCM.

Methods

Prospective cohort study. Cats with HCM were included consecutively and examined every 6 months. Echocardiography, ECG, blood pressure, and serum cTnI and cTnT were evaluated at each visit. Cox proportional hazards regression analysis was performed to evaluate prognostic potential of serum troponin concentrations at admission and subsequent examinations. Correlations were used to examine associations between troponin concentrations and cardiac hypertrophy.

Results

Troponin concentrations at admission were median [range] 0.14 [0.004–1.02] ng/mL for cTnI, and 13 [13–79.5] ng/L for cTnT. Both were prognostic for death (P = .032 and .026) as were the last available concentrations of each (P = .016 and .003). The final cTnT concentration was a significant predictor of death even when adjusting for the admission concentration (P = .043). In a model containing both markers, only cTnT remained significant (P = .043). Left ventricular free wall thickness at end‐diastole (LVFWd) at admission was correlated with cTnI at admission (r = 0.35, P = .035), however no significant correlations (r = 0.2–0.31, P = .074–.26) were found between changes in troponin concentrations and left ventricular thickness over time.

Conclusions and Clinical Importance

Myocardial injury is part of the pathophysiology leading to disease progression and death. Low sensitivities and specificities prevent outcome prediction in individual cats.     

豫西地区苹果花果害虫发生种类与为害情况

1 999～ 2 0 0 1年对豫西地区 1 4个县 (市、区 )为害苹果花、果的害虫进行了调查 ,共发现 6目 2 1科 32种害虫 ,其中蛀果害虫 8种 ,噬花害虫 8种 ,啃果害虫 1 1种 ,刺吸害虫 8种。新发现为害苹果果实的害虫 8种 ,分别为亚洲玉米螟、棉铃虫、梨实蜂、日本黄脊蝗、变棘螽、乌苏里呜螽、大青叶蝉和黑尾叶蝉。随着气候以及果园环境的变化和新技术的推广应用 ,蝽类、叶蝉类、蚧类害虫种类、数量呈递增趋势 ,预计会逐渐成为常发性害虫 ;蝗虫类、螽斯类、蟋蟀类害虫有可能为苹果果实的重要害虫。     

Beneficial effect of Cyclovirobuxine D on heart failure rats following myocardial infarction

The effect of Cyclovirobuxine D, an active ingredient from Buxus microphylla, was investigated in the potential prevention of cardiac dysfunction in rats with congestive heart failure. Heart failure was induced by left coronary artery occlusion and verified using echocardiography. Cyclovirobuxine D was administered for 30 days (0.5, 1.0 and 2.0 mg/kg, ig) and mortality, cardiac function, hemodynamics, microcirculation, histology and ultrastructure assessments were observed. Results from the present study suggest that Cyclovirobuxine D is beneficial for heart failure induced by myocardial infarction and supports the potential for Cyclovirobuxine D as a new therapy for heart failure.     

The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study

Background: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long‐term prognosis, and in monitoring the response to therapy in humans. Hypothesis: Circulating concentrations of the biomarkers N‐terminal pro‐B type natriuretic peptide (NT‐proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure. Animals: Six Maine Coon or Maine Coon cross cats with severe HCM. Methods: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT‐proBNP and cTnI were assayed before and on the last day of drug administration. Results: There was no statistically significant change in NT‐proBNP (median before, 394 pmol/L; range, 71–1,500 pmol/L; median after, 439 pmol/L; range, 24–1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10–0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09–1.0 ng/mL; P = .69) after administration of atenolol. Conclusions: Atenolol administration did not decrease NT‐proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings.     

Role of cAMP signaling in cardioprotective mechanism of ischemic postconditioning

AIM: To assess the role of the cAMP signaling in cardioprotection by brief intermittent ischemia at the time of onset of reperfusion (i.e. postconditioning). METHODS: The model of rat myocardial ischemia/reperfusion (I/R) was used. The left ventricular functions were assessed by measuring the left ventricular developed pressure (LVDP) and the coronary flow (CF). The injury of myocardium was further confirmed by detecting the releases of lactate dehydrogenase(LDH) and creatine kinase(CK) in coronary effluent. The mRNA expression of caspase-3, bcl-2 and bax in myocardium was determined by real-time PCR. RESULTS: I/R treatment led to the decrease in LVDP and CF, and the increase in the releases of CK and LDH in coronary artery effluent. The mRNA expression of caspase-3 and bax/bcl-2 ratio was up-regulated simultaneously. Postconditioning treatment relieved the injury induced by I/R, which was enhanced by the specific phosphodiesterase 4(PDE4) inhibitor rolipram. On the other hand, the specific adenylyl cyclase inhibitor SQ22536 attenuated those protective effects of postconditioning. CONCLUSION: The cAMP signaling participates in the protective effect of postconditioning on heart from I/R injury, and the effect may be associated with the regulation of apoptosis.     

心脏直视手术围手术期CK及CK-MB的动态变化

目的观察血清肌酸磷酸激酶(CK)及其同工酶(MB)在CPB心脏直视手术围手术期的动态变化,以了解其在围术期的变化规律,为临床诊断治疗提供依据。方法20例患者分别在术前1d,术后1h、1d(约15~18h)、2、3、4、5、6d晨分别取静脉血,留肝素化血浆测心肌酶,并同时作标准12导联EKG,20例患者分为冠状动脉搭桥术和先天型心脏病修复术2组。结果2组患者术前心肌酶均在正常范围,术后1h同时升高到术前的2~43倍,与术前相比有显著性差异(P<0.05),2组间心肌酶的释放量没有显著性差异(P>0.05),术后CHD组的5种心肌酶较CABG组的要稍微高一些,而CHD组较CABG组恢复的快一些。结论2组术前心肌酶均在正常范围,CK-MB释放术后1h达高峰,恢复最快,CK次之,术后心肌酶释放的高峰时间和恢复次序基本一致,心脏术后心肌酶升高的倍数如大于5倍尚不能诊断PMI,CK及CK-MB对CPB心脏直视手术后围术期心肌损伤的程度有较高的特异性和敏感度。