Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The changes of platelet functions including platelet membrane microviscosity (PMMV), plasma 5-HT, plasma TXB2 and 6-K-PGF1a were studied in 30 cases of AMI and 13 cases of unstable angina (UA), 20 normal subjects as control. After onset of AMI, PMMV, plasma 5-HT, 6-k-PGF1a all increased quickly, especially on the 1st day (P less than 0.001-0.01). During 3 weeks observation, only 6-K-PGF1a decreased to the normal level on 14th day. There were no obvious decrease of plasma TXB2, 5-HT and PMMV. It showed that in acute phase of AMI without intervention of any antiplatelet drugs the platelets were activated continuously. Plasma 5-HT was the most sensitive predictor for the severity of AMI as observed by the comparison between the cases with complications and serum peak CK greater than 1000 U/L, and those without complications and peak CK less than 1000 U/L (P less than 0.001-0.05). The great change of PMMV was a bad prognosis. In patients with UA, during acute myocardial ischemia, the platelets were also activated significantly, but the extent was not as high as that in AMI.
Zhonghua Xin Xue Guan Bing Za Zhi 1989 Oct
PMID:[Platelet functions in patients with acute myocardial infarction]. 263 23

In recent few years, many authors had discussed the possibilities of using bipolar precordial leads to replace lead V5 in diagnosing anterior wall myocardial ischemia. But there still remains some problems to be solved: (1) Are there any difference between bipolar precordial leads and lead V5 in wave forms? (2) What kind of factors influence the ST deviation? 36 patients were studied by comparing unipolar lead V5 with respect to three different bipolar chest leads CM5, CC5, CL5 both in lying and sitting positions. We found that: (1) The differences is least significant between bipolar CC5 and lead V5 while it is most significant between bipolar lead CM5 and lead V5. (2) The deviation of ST segment in bipolar leads is affected both by potential at negative electrode as well as potential at positive electrode. Statistical analysis revealed that ST segment is positively related to the potential on positive electrode and negatively related to the potential on negative electrode. For this reason, therefore, in the view point of most comparable ST deviation with lead V5 for monitoring of myocardial ischemia, it is advisable to locate the negative electrode at the site on chest with least potential. Usually we place the negative electrode on V6R to compose a bipolar lead CC5.
Zhonghua Xin Xue Guan Bing Za Zhi 1989 Apr
PMID:[Evaluation of 3 chest leads CM5, CC5, and CL5 and factors which influence the results]. 279 75

Isolated perfused rat heart model was used to observe the protective effects of berbamine on myocardial ischemia/reperfusion injury. The hearts were remarkably injured by 40 min global ischemia followed by 20 min reperfusion. Berbamine could significantly improve heart function, prevent ventricular fibrillation, reduce CK release, preserve Na, K-ATPase activity, and reduce Na+ gain and K+ loss during ischemia and Ca2+ overload during reperfusion. With the use of low temperature ESR technique, we found that, in hearts subjected to 40 min ischemia and 15 sec reperfusion, oxygen-centered free radical signals became much more intense. In the presence of berbamine, these signals decreased. The results showed that berbamine could alleviate myocardial ischemia/reperfusion injury. This effect might be due to (1) preserved myocardial Na, K-ATPase activity and inhibition of sodium overload at the end of ischemia, which might further lead to attenuation of reperfusion-induced calcium overload, and (2) reduction of oxygen free radical generation during reperfusion.
Zhonghua Xin Xue Guan Bing Za Zhi 1993 Oct
PMID:[Mechanism of the protective effects of berbamine on ischemia-reperfusion injury in isolated rat heart]. 820 Mar 15

A Langendorff isolated rat heart preparation was used to determine the effect of the metallic chelators, deferoxamine and penicillamine on the extent of myocardial ischemia reperfusion injury. Each heart was subjected to 15-60 minutes of total ischemia at 37 degrees C followed by 15-60 minutes of reperfusion with either saline, deferoxamine (0.61 mmol/L), or penicillamine (30 mmol/L) treated perfusate. Reperfusion injury was assessed by the production of free radicals with electronic spin resonance spectroscopy and spin trap PBN, by the amount of creatine phospholipase released into the perfusate, by the changes in the myocardial vascular resistance, and by pathologic examination of myocardium. The results showed that the drug treated groups released significantly less radical adducts of PBN (P < 0.01) and creatine phosphokinase into the perfusate than the saline treated group (P < 0.01). The mean vascular resistance significantly increased in the saline treated group than in the drug treated groups (P < 0.01). Ultrastructural examination showed prominent attenuation of mitochondrial swelling in drug treated groups in comparison with the saline one. These findings indicated that both deferoxamine and penicillamine can protect the isolated rat heart from ischemia reperfusion injury. The possible mechanism of which is that metallic chelators block the transitional metal-catalyzed fenton reaction, and subsequently decrease the production of hydroxyl radical.
Zhonghua Xin Xue Guan Bing Za Zhi 1993 Oct
PMID:[A study on the protective effect of metallic chelators on ischemia-reperfusion injury of isolated rat heart]. 820 Mar 16

36 cases of coronary heart disease with silent myocardial ischemia (SMI) were treated sequentially with Tong Xin Luo (TXL) capsule and isosorbide dinitrate in random order. The results showed that both drugs were effective in decreasing episodes of SMI and shortening the duration of asymptomatic myocardial ischemia. TXL, however, was found with a better action and was superior to isosorbide dinitrate. It was also found that TXL could improve diastolic function of the left ventricle as well.
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PMID:A clinical investigation on tong xin luo capsule in treatment of coronary heart disease with silent myocardial ischemia. 1103 93

In order to inquire into the therapeutic effects of Xin Mai Tong Capsule ([symbol: see text]) on coronary heart disease with myocardial ischemia, 40 patients were randomly divided into two groups (Xin Mai Tong group and the control group). The plasma endothelin (ET) levels in the two groups of patients were markedly higher than that of the healthy people (P < 0.001), and the calcitonin gene related peptide (CGRP) was similar to that of the healthy people (P > 0.05). After treatment, ET and symptomatic scores in the two groups decreased markedly (P < 0.01), and their S-T segments were elevated obviously (P < 0.01). But the decrease of ET and symptomatic scores and elevation of S-T segment in Xin Mai Tong group were superior to those of the control group (P < 0.05-0.01). The CGRP level in the control group did not vary obviously post-treatment, but it increased markedly (P < 0.01) with the addition of Xin Mai Tong Capsule in Xin Mai Tong group.
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PMID:Effects of xin mai tong capsule on vasoregulatory peptides in the patients of coronary heart disease. 1126 74

Ischemic heart disease (IHD) is the main cause of death and a major public health problem in the world. The traditional herbal medicinal formula Guan-Xin-Er-Hao (GXEH) has been used in China and East Asia for the treatment of coronary heart disease, however, the underlying cardioprotection mechanisms remain unclear. To make clear the antiischemic mechanism involved, GXEH was orally administered to 15 healthy volunteers. Heart rates (HR), blood pressure and coronary flow (CF) velocity before and 1 h after a single oral dose of GXEH were observed and compared. It was demonstrated that the oral administration of GXEH increased CF acutely in a dose-dependent manner without modification of systemic hemodynamic parameters. Moreover, the myocardial protection function of GXEH was also experimentally examined in ischemia-reperfusion (I/R) rat models. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling (TUNEL) method and confirmed by caspase-3 activity. The infarct size and TUNEL-positive cells of GXEH-treated group (20 g/kg) were reduced significantly, which was consistent with the decreased caspase-3 activity. These suggest that GXEH protects hearts from ischemia injury by increasing CF and reduces infarct size by inhibiting myocardial apoptosis.
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PMID:Effect of oriental herbal prescription Guan-Xin-Er-Hao on coronary flow in healthy volunteers and antiapoptosis on myocardial ischemia-reperfusion in rat models. 1758 91

Guan-Xin-Er-Hao (GXEH) is a Chinese medicine formula for treating ischemic heart diseases (IHD) and has a favorable effect. Our aim was to examine whether or not acute oral GXEH could protect the heart against myocardial infarction and apoptosis in acute myocardial ischemic rats. If so, we would explain the antioxidative mechanism involved. The left anterior descending coronary artery was occluded to induce myocardial ischemia in hearts of Sprague-Dawley rats. At the end of the 3h ischemic period (or 24h for infarct size), we measured the myocardial infarct size, myocardial apoptosis and the activities of antioxidative enzymes. GXEH reduced infarct size, myocardial apoptosis and the serum level of malondialdehyde (MDA), increased the activities of total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and GSH-peroxidase (GPX) activities and the serum level of glutathione (GSH). GXEH exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, likely through its antioxidation and antilipid peroxidative properties, and thus may be used as a promising agent for both prophylaxis and treatment of IHD.
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PMID:Chinese medicinal formula Guan-Xin-Er-Hao protects the heart against oxidative stress induced by acute ischemic myocardial injury in rats. 1895 Oct 1

Considerable evidence indicates that apoptosis plays a critical role in acute myocardial infarction. We have previously shown that Guan-Xin-Er-Hao (GXEH), a Chinese medicine formula, attenuates postischemia myocardial apoptosis. The present study was designed to determine the mechanisms by which GXEH exerts its antiapoptotic effect. Adult male Sprague-Dawley rats were randomized to receive vehicle or GXEH (5 or 15 g/kg) orally 30 min before ischemia and subjected to myocardial ischemia of 3 h (apoptosis peak) or 24 h (necrosis peak) for determination of infarct size. Compared with rats receiving vehicle, those rats treated with GXEH (15 g/kg) showed significantly reduced infarct size, the reduced myocardial apoptosis, as judged by the decreases in TUNEL-positive staining (22.40 +/- 5.68% vs. 40.31 +/- 10.58%, p < 0.01), and the decrease in the degree of caspase-3 activation (82.97 +/- 10.54 vs. 159.95 +/- 9.16 mumol cleaved acetyl-Asp-Glu-Val-Asp-p-nitroanilide/mg protein, p < 0.01). Treatment with GXEH (15 g/kg) significantly reduced the release of mitochondrial cytochrome c, a primary mediator of apoptosis, the degree of caspase-9 activation, and the Bax/Bcl-2 ratio. Caspase-9 cleaves and activates caspase-3. Bax promotes apoptosis, while Bcl-2 inhibits apoptosis. Thus, the antiapoptotic mechanisms of GXEH may involve the mitochondrial cytochrome c-mediated caspase-3 activation in cardiomyocytes after acute myocardial infarction. Taken together, GXEH tilted the balance between Bax and Bcl-2 toward an antiapoptotic state, decreased mitochondrial cytochrome c release, reduced caspase-9 activation, and attenuated subsequent caspase-3 activation and postischemic myocardial apoptosis in rats. GXEH may be used as a promising agent for future treatment of cardiovascular diseases.
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PMID:Antiapoptotic mechanisms of Chinese medicine formula, Guan-Xin-Er-Hao, in the rat ischemic heart. 1906 Apr 45

Hypertrophic cardiomyopathy (HCM) is characterized by extreme clinical heterogeneity, ranging from sudden cardiac death to long-term disease progression and heart failure-related complications. Myocardial ischemia, occurring at the microvascular level, is a major determinant of clinical expression and outcome. Accordingly, the severity of this microvascular dysfunction has been shown to represent an early and powerful predictor of unfavorable outcome in HCM. The assessment of microvascular function in vivo is technically challenging, although critical to a truly comprehensive evaluation and risk stratification of HCM patients. Available technologies include positron emission tomography and cardiac magnetic resonance (CMR). Studies of regional myocardial blood flow using positron emission tomography have demonstrated that the vasodilator response to dipyridamole is impaired in most HCM patients, not only in the hypertrophied ventricular septum but also in the less hypertrophied or non-thickened left ventricular free wall. CMR also allows measurement of myocardial flow, although the technique is currently time-consuming and largely limited to research situations. CMR provides further insight into the effects of ischemia in HCM patients, by visualizing the distribution and extent of fibrosis at the intramyocardial level. Late gadolinium enhancement (LGE) is a potential predictor of risk in HCM patients, and is believed to largely reflect replacement fibrosis resulting from recurrent microvascular ischemia. LGE is associated with increased prevalence of ventricular arrhythmias, and associated with microvascular dysfunction. The present review is to provide a concise overview for the available evidence of microvascular ischemia and its consequences in HCM.
Zhonghua Xin Xue Guan Bing Za Zhi 2009 Dec
PMID:[Myocardial hypoperfusion due to microvascular dysfunction in hypertrophic cardiomyopathy: role of positron emission tomography]. 2019 74


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