• The Journal of Korean Medicine
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• v.43 no.3
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• pp.164-180
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• 2022

Objectives: The purpose of this study was to evaluate the effects of shenfu injection on myocardial protective effects after mitral valve replacement surgery. Methods: We searched four international databases (PUBMED, Embase, Web of Science and CNKI) and three domestic electronic databases (OASIS, RISS and NDSL) for relevant studies. We used following keywords 'shenfu', 'valve replacement', 'mitral valve' at PUBMED, Embase and Web of Science; '二尖瓣', '参附注射液', '瓣膜' at CNKI and '이첨판', '판막', '삼부' at domestic databases. The search range included randomized controlled trials. When appropriate, meta-analyses were performed. Results: Seven randomized controlled trials were selected. All studies used Shenfu injection after mitral valve replacement surgery. We analyzed myocardial damage, cardiac function, patients' recovery rate, with various evaluation indicators. We also used meta-analysis for CK-MB, cTnI, MDA and voluntary recovery of heartbeat. CK-MB was analyzed in two subgroups: 8 hours and 24 hours after surgery. Std was -2.34(95% CI -4.10, -0.58) for 8 hours and -1.95(95% CI -4.79 to 0.88) for 24 hours. 8 hours showed statistically significant difference. cTnI appeared significant decrease with Std of -2.13(95% CI -2.60, -1.66). MDA showed significant decrease with Std of -0.95(95% CI -1.43 to -0.47). Voluntary recovery of heartbeat significantly increased with the odd ratio of 4.34(95% CI 1.76, 10.70). Conclusions: We suggest that Shenfu injection after Mitral valve replacement surgery may have significant myocardial protective effects in terms of reducing myocardial damages, reactive oxygen species, increasing cardiac function and patients' recovery after surgery. However, the evidence is limited, further research is required.

• The Korean Journal of Emergency Medical Services
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• v.20 no.2
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• pp.7-19
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• 2016

Purpose: To investigate the effect of early hypothermia on post-resuscitation myocardial recovery and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction(MI). Methods: Thoracotomies were performed in 10 male Sprague Dawley rats weighing 450-455g. Myocardial infarction was induced by ligation of the left anterior descending coronary artery. Ninety minutes after arterial ligation, ventricular fibrillation was induced, cardiopulmonary resuscitation was subsequently performed before defibrillation was attempted. Animals were randomized to control group and experimental group(acute MI-normothermia)($32^{\circ}C$ for 4 hours). Duration of survival was recorded. Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured using echocardiography. Results: Myocardial function was significantly better in hypothermia group than the control group during the first 4 hours post-resuscitation. The survival time of the experimental group was greater than that of the control group(p<.050). Conclusion: This study suggests that early hypothermia can attenuate post-resuscitation myocardial dysfunction after acute myocardial function, and may be a useful strategy in post-resuscitation care.

• Journal of Chest Surgery
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• v.23 no.6
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• pp.1067-1073
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• 1990

To clarify the changes of left ventricular function under normothermia, the time interval between the onset of ischemia and the beginning of contracture of left ventricle[TIC] were recorded in newborn piglet. Myocardial performance was assessed using intraventricular balloon to determine compliance and systolic function after 5 to 10 minutes interval per-fusing normothermic substrate free Krebs solution as a perfusate. The time to onset TIC was 29.5\ulcorner1.7 minutes and peak ischemic contracture was 46.7\ulcorner4.0 minutes[p<0.01]. In myocardial performance, systolic function of left ventricle[defined as cardiac contractility] was kept until 25 minutes of perfusion, but was decreased abruptly after 30 minutes of perfusion[p<0.0018] and diastolic function of left ventricle[defined as diastolic compliance] was kept until 15 minutes of perfusion, but was decreased after 20 minutes of perfusion [p=0.00\ulcorner9]. This study demonstrated maximal time of the tolerance to normothermic global ischemia and functional changes of left ventricle using Krebs perfusate under the same condition.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.2
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• pp.143-155
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• 2023

Percutaneous coronary intervention and acute coronary syndrome are both closely tied to the frequently occurring complication of coronary microembolization (CME). Resveratrol (RES) has been shown to have a substantial cardioprotective influence in a variety of cardiac diseases, though its function and potential mechanistic involvement in CME are still unclear. The forty Sprague-Dawley rats were divided into four groups randomly: CME, CME + RES (25 mg/kg), CME + RES (50 mg/kg), and sham (10 rats per group). The CME model was developed. Echocardiography, levels of myocardial injury markers in the serum, and histopathology of the myocardium were used to assess the function of the cardiac muscle. For the detection of the signaling of TLR4/MyD88/NF-κB along with the expression of pyroptosis-related molecules, ELISA, qRT-PCR, immunofluorescence, and Western blotting were used, among other techniques. The findings revealed that myocardial injury and pyroptosis occurred in the myocardium following CME, with a decreased function of cardiac, increased levels of serum myocardial injury markers, increased area of microinfarct, as well as a rise in the expression levels of pyroptosis-related molecules. In addition to this, pretreatment with resveratrol reduced the severity of myocardial injury after CME by improving cardiac dysfunction, decreasing serum myocardial injury markers, decreasing microinfarct area, and decreasing cardiomyocyte pyroptosis, primarily by blocking the signaling of TLR4/MyD88/NF-κB and also reducing the NLRP3 inflammasome activation. Resveratrol may be able to alleviate CME-induced myocardial pyroptosis and cardiac dysfunction by impeding the activation of NLRP3 inflammasome and the signaling pathway of TLR4/MyD88/NF-κB.

• YAKHAK HOEJI
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• v.32 no.1
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• pp.70-79
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• 1988

The effect of Ginseng on global myocardial ischemia and reperfusion was examined in isolated perfused rat hearts. The Ginseng ethanol extract (100mg/kg/day) was administered orally for 10 days. The rat hearts were removed and perfused at 75cm $H_{2}O$ by the Langendorff method. After 25 min. of global ischemia, the hearts were reperfused. The myocardial contents of adenosine 5'-triphosphate, creatine phosphate, and calcium were assayed. There no differences in ATP levels in all group of normal and Ginseng-treated hearts. Both in non-ischemic and ischemic heart, Ginseng increased significantly tissue creatine phosphate levels compared with control. Whereas, in ischemic-reperfused heart, there was no significant difference. In the control groups, myocardial calcium contents in the ischemic hearts were decreased compared with the non-ischemic hearts. But, in the Ginseng-treated groups, the calcium contents in the ischemic herts were not changed with the nonischemic hearts. Therefore, Ginseng appears to exert its protective effect against ischemic heart condition, not against ischemic-reperfused heart condition, by regulating energy metabolism and maintaing cellular function.

• Proceedings of the KAIS Fall Conference
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• 2011.12a
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• pp.170-173
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• 2011

Therapeutic hypothermia(TH) improves neurological outcomes and reduces mortality among survivors of out-of-hospital cardiac arrest. Animal and human studies have shown that TH results in improved salvage of the myocardium, reduced infarct size, reduced left ventricular remodeling and better long-term left ventricular function in settings of regional myocardial ischemia. This study is to investigate the effect of TH on post-resuscitation myocardial dysfunction and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction (MI). Thoracotomies were performed in 10 Male Sprague-Dawley rats weighing 450-550 g. MI was induced by ligation of the left anterior descending coronary artery (LAD). Ninety min after LAD ligation, ventricular fibrillation induction and subsequent cardiopulmonary resuscitation was performed before defibrillation attempts. Animals were randomized to two groups: a) Acute MI-Normothermia b) Acute MI-Hypothermia ($32^{\circ}C$ for 4 h). Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured echocardiographically together with duration of survival. Ejection fraction, cardiac output and myocardial performance index were $54.74{\pm}9.16$, $89.00{\pm}8.89$, $1.30{\pm}0.09$ respectively and significantly better in the TH group than those of the normothermic group at the first 4 h after resuscitation($32.20{\pm}1.85$,$41.60{\pm}8.62$,$1.77{\pm}0.19$)(p=0.00). The survival time of the hypothermic group ($31.8{\pm}14.8$ h) was greater than that of the normothermic group($12.3{\pm}6.5$ h, p<0.05). This study suggested that TH attenuated post resuscitation myocardial dysfunction in acute MI and would be a potential strategy in post resuscitation care.

• Advances in biomechanics and applications
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• v.1 no.1
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• pp.41-55
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• 2014

Acellular intra-myocardial biomaterial injections have been shown to be therapeutically beneficial in inhibiting ventricular remodelling of myocardial infarction (MI). Based on a biventricular canine cardiac geometry, various finite element models were developed that comprised an ischemic (II) or scarred infarct (SDI) in left ventricular (LV) antero-apical region, without and with intra-myocardial biomaterial injectate in layered (L) and bulk (B) distribution. Changes in myocardial properties and LV geometry were implemented corresponding to infarct stage (tissue softening vs. stiffening, infarct thinning, and cavity dilation) and injectate (infarct thickening). The layered and bulk injectate increased ejection fraction of the infarcted LV by 77% (II+L) and 25% (II+B) at the ischemic stage and by 61% (SDI+L) and 63% (SDI+B) at the remodelling stage. The injectates decreased the mean end-systolic myofibre stress in the infarct by 99% (II+L), 97% (II+B), 70% (SDI+L) and 36% (SDI+B). The bulk injectate was slightly more effective in improving LV function at the remodelling stage whereas the layered injectate was superior in functional improvement at ischemic stage and in reduction of wall stress at ischemic and remodelling stage. These findings may stimulate and guide further research towards tailoring acellular biomaterial injectate therapies for MI.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.6
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• pp.533-543
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• 2021

Myocardial fibrosis (MF) is the result of persistent and repeated aggravation of myocardial ischemia and hypoxia, leading to the gradual development of heart failure of chronic ischemic heart disease. Triptolide (TPL) is identified to be involved in the treatment for MF. This study aims to explore the mechanism of TPL in the treatment of MF. The MF rat model was established, subcutaneously injected with isoproterenol and treated by subcutaneous injection of TPL. The cardiac function of each group was evaluated, including LVEF, LVFS, LVES, and LVED. The expressions of ANP, BNP, inflammatory related factors (IL-1β, IL-18, TNF-α, MCP-1, VCAM1), NLRP3 inflammasome factors (NLRP3, ASC) and fibrosis related factors (TGF-β1, COL1, and COL3) in rats were dete cted. H&E staining and Masson staining were used to observe myocardial cell inflammation and fibrosis of rats. Western blot was used to detect the p-P65 and t-P65 levels in nucleoprotein of rat myocardial tissues. LVED and LVES of MF group were significantly upregulated, LVEF and LVFS were significantly downregulated, while TPL treatment reversed these trends; TPL treatment downregulated the tissue injury and improved the pathological damage of MF rats. TPL treatment downregulated the levels of inflammatory factors and fibrosis factors, and inhibited the activation of NLRP3 inflammasome. Activation of NLRP3 inflammasome or NF-κB pathway reversed the effect of TPL on MF. Collectively, TPL inhibited the activation of NLRP3 inflammasome by inhibiting NF-κB pathway, and improved MF in MF rats.

• The Korean Journal of Nuclear Medicine
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• v.39 no.2
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• pp.94-99
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• 2005

Electrocardiogram-gated single photon omission computed tomography (SPECT) provides valuable information in the assessment of both myocardial perfusion and ventricular function. Tl-201 is a suboptimal isotope for gating. Tl-201 images are more blurred compared with Tc-99m tracers due to the increased amount of scattered photons and use of a smooth filter. The average myocardial count densities are approximately one-half those of conventional technetium tracers. However, Tl-201 is still widely used because of its well-established utility for assessing myocardial perfusion, viability and risk stratification. Gated SPECT with Tl-201 enables us to assess both post-stress and rest left ventricular volume and function. Previous studies with gated Tl-201 SPECT measurements of ejection fraction (EF), end-diastolic volume (EDV), end-systolic volume (ESV) have shown high correlation with first-pass radionuclide angiography, gated blood pool scan, Tc-99m-MIBI gated SPECT, contrast ventriculography, echocardiography, and 3-dimensional magnetic resonance imaging. However, problems related to these studies include few agreement data of EDV and ESV, use of a reference method that is likely to have the same systemic errors (gated Tc-99m-MIBI SPECT), and other technical factors related to the count density of gated SPECT. With optimization of gated imaging protocols and more validation studies, gated Tl-201 SPECT would be an accurate method to provide perfusion and function information in patients with coronary artery disease.

• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.108-111
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• 2018

Extra-corporeal membrane oxygenation (ECMO) has the potential to rescue patients in cardiac arrest or respiratory failure. ECMO has two systems such as veno-arterial and veno-venous circulation. In cardiac arrest resulting from acute myocardial infarction, veno-arterial ECMO is mandatory for systemic circulation and oxygenation. A 75-year old female patient underwent primary coronary intervention for acute myocardial infarction. Despite successful revascularization, recurrent ventricular tachycardia and heart failure were progressing. We performed a veno-arterial ECMO through the femoral artery and vein, then the patient seemed to be stable clinically. However, laboratory studies, echocardiography, and vital signs indicated multi-organ failure and decreasing cardiac function. We found out an error that we performed veno-venous ECMO instead of veno-arterial ECMO. We added a femoral artery cannula and exchange the circuit system to veno-arterial ECMO. While the systemic circulation seemed to be recovered, the left ventricular function was decreased persistently. A hypovolemia resulting from pulmonary hemorrhage was occurred, which lead to ECMO failure. The patient died of cardiac arrest and multi-organ failure 23 hours after ECMO. Because the color of arterial and venous circuits represent the position and efficacy of ECMO, if unexpected or abnormal circuit colors are detected, prompt and aggressive evaluation for ECMO function is mandatory.