Aged ; Electrocardiography ; Female ; Humans ; Hyperkalemia ; complications ; physiopathology ; Myocardial Ischemia ; etiology

Animals ; Humans ; Ischemic Preconditioning, Myocardial ; methods ; Myocardial Ischemia ; complications ; therapy ; Myocardial Reperfusion ; methods ; Myocardial Reperfusion Injury ; etiology ; prevention & control

The aim of this study was to determine if the potassium aspartate and magnesium (PAM) prevent reperfusion-induced ventricular arrhythmias (RIVA) in ischemia-reperfusion (IR) rabbit heart. Thirty rabbits were randomly divided into control, ischemia and PAM groups. Arterially-perfused rabbit left ventricular preparations were made, and transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded in the whole process of all experiments. In control group rabbit ventricular wedge preparations were continuously perfused with Tyrode's solution, and in ischemia group and PAM groups the perfusion of Tyrode's solution was stopped for 30 min. Then the ischemia group was reperfused with Tyrode's solution and the PAM group with Tyrode's solution containing 2.42 mg/L PAM, respectively. ECG, QT interval, transmural repolarization dispersion (TDR) and action potentials from epicardium and endocardium were simultaneously recorded, and the RIVA of the wedge preparation was observed. Compared with control group, TDR and incidence of RIVA were significantly increased in ischemia group (P<0.05). The incidence of RIVA in control, ischemia and PAM group was 0/10, 9/10 and 1/10, respectively. Compared with ischemia group, TDR and incidence of RIVA were significantly reduced in PAM group (P<0.05). Potassium aspartate and magnesium significantly reduce TDR and prevent ventricular arrhythmia in ischemic rabbit heart.
Arrhythmias, Cardiac/etiology ; Arrhythmias, Cardiac/*prevention & control ; Myocardial Ischemia/*complications ; Myocardial Ischemia/physiopathology ; Myocardial Reperfusion Injury/*complications ; Potassium Magnesium Aspartate/*therapeutic use ; Random Allocation

Myocardial ischemia (MI) causes somatic referred pain and sympathetic hyperactivity, and the role of sensory inputs from referred areas in cardiac function and sympathetic hyperactivity remain unclear. Here, in a rat model, we showed that MI not only led to referred mechanical hypersensitivity on the forelimbs and upper back, but also elicited sympathetic sprouting in the skin of the referred area and C8-T6 dorsal root ganglia, and increased cardiac sympathetic tone, indicating sympathetic-sensory coupling. Moreover, intensifying referred hyperalgesic inputs with noxious mechanical, thermal, and electro-stimulation (ES) of the forearm augmented sympathetic hyperactivity and regulated cardiac function, whereas deafferentation of the left brachial plexus diminished sympathoexcitation. Intradermal injection of the α₂ adrenoceptor (α₂AR) antagonist yohimbine and agonist dexmedetomidine in the forearm attenuated the cardiac adjustment by ES. Overall, these findings suggest that sensory inputs from the referred pain area contribute to cardiac functional adjustment via peripheral α₂AR-mediated sympathetic-sensory coupling.
Animals ; Ganglia, Spinal ; Hyperalgesia/etiology* ; Myocardial Ischemia/complications* ; Pain, Referred/complications* ; Rats ; Sympathetic Nervous System

To compare the effects on hemodynamics of univentricular support with that of biventricular support on experimental ischemic biventricular dysfunction so as to provide experimental basis for clinical usage of the Luo-Ye pump. Eight canines were placed with a left ventricular assist device (LVAD; left atrial-aorta bypass) and a right ventricular assist device (RVAD; right atrial-pulmonary artery bypass). Left anterior descending coronary artery(LAD) was ligated, three minutes later, the proximal of right coronary artery (RCA) was ligated to establish animal madel of acute ischemic biventricular dysfunction. First start the LVAD, and then RVAD was started five minutes later. The hemodynamic data were recorded including central venous pressure(CVP), cardiac output (CO), mean artery pressure(MAP), and pulmonary artery pressure(PAP) and pulmonary capillary wedge pressure (PCWP). During biventricular assist devices (BVAD) the hemodynamics were improved remarkably, MAP increased from 37.4 +/- 8.8 mmHg to 84.2 +/- 9.7 mmHg (P < 0.01) (the normal level), CO increased from 0.82 +/- 0.1 L/min to 1.33 +/- 0.12 L/min (P < 0.01), CVP decreased from 14.6 +/- 2.3 cmH2O to 4.2 +/- 1.5 cmH2O (P < 0.01), PCWP decreased significantly from 14 +/- 3.9 mmHg to 1.6 +/- 0.9 mmHg. These data suggest that LVAD during biventricular dysfunction could not improve the hemodynamics to normal level. Howere BVAD could increase CO and MAP to normal level and decrease heart work and myocardial oxygen consumption, which could help to improve myocardial metabolism and myocardial function. Therefore, BVAD is the first choice in treating severe biventricular dysfunction which was not respond to drug therapy and intra-aortic balloon pump (IABP).
Animals ; Dogs ; Heart-Assist Devices ; Hemodynamics ; Myocardial Ischemia ; complications ; Ventricular Dysfunction ; etiology ; physiopathology ; surgery

Burns ; complications ; pathology ; physiopathology ; Humans ; Mitochondria, Heart ; pathology ; Myocardial Ischemia ; etiology ; prevention & control

Humans ; Myocardial Ischemia ; complications ; Tumor Necrosis Factor-alpha ; physiology ; Ventricular Fibrillation ; physiopathology

Coronary Artery Disease/complications* ; Death, Sudden, Cardiac/etiology* ; Humans ; Myocardial Ischemia/diagnosis*

OBJECTIVEThe clinical diagnosis and treatment of ischemia mitral regurgitation (IMR) remained difficult because of its unclear mechanisms. This paper reviews studies on the mechanisms of IMR during the last 20 years, and discusses the relevance of the various mechanisms.

DATA SOURCESData used in this review were mainly from CNKI and Pubmed in English. The search terms were "ischemia mitral regurgitation mechanism", "myocardial infarction" AND "mitral regurgitation".

STUDY SELECTIONArticles were selected if they involved mechanisms of IMR.

RESULTSIMR is one of the common complications of coronary artery disease. But currently, the clinical diagnosis and treatment of IMR remained difficult because of its unclear mechanisms.

CONCLUSIONSFor now, dominating theory of ischemic mitral regurgitation mechanisms are left ventricular remodeling, imbalance of leaflet tethering and the closing force, left ventricular dysfunction, changes in spatial structure of the annulus and the dyssynchrony of the left ventricular electromechanical activity.

Animals ; Humans ; Mitral Valve Insufficiency ; etiology ; Myocardial Ischemia ; complications ; Papillary Muscles ; physiology ; Systole ; Ventricular Dysfunction, Left ; complications ; Ventricular Remodeling

To explore the protective effects of right coronary artery ischemic preconditioning and post-conditioning on myocardial ischemia reperfusion injury in rabbit heart.
 Methods: A total of 30 rabbits were randomly divided into 4 groups: a control group (n=7), an ischemia reperfusion group (IR group, n=8), an ischemic preconditioning group (IPC group, n=8) and an ischemic post-conditioning group (IPO group, n=7). Venous blood samples were taken at pre-operation, 1 and 6 h post-operation, and the concentration of serum creatine kinase isoenzyme (CK-MB) and cardiac troponin-T (cTn-T) were measured. The infarct area of cardiac muscle was calculated.
 Results: Compared with the IR group, the levels of CK-MB and cTn-T at 1 and 6 h post-operation in the IPC group and the IPO group were reduced (all P<0.05). Compared with the IR group, the infarct size in the IPC group and the IPO group was significantly decreased, with significant difference (both P<0.05) .
 Conclusion: Right coronary artery ischemic preconditioning and post-conditioning exert significant protective effects on the myocardial ischemia reperfusion injury in New Zealand rabbits.
Animals ; Coronary Vessels ; Creatine Kinase, MB Form ; blood ; Heart ; Ischemia ; Ischemic Postconditioning ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial ; Myocardial Infarction ; etiology ; pathology ; physiopathology ; prevention & control ; Myocardial Ischemia ; complications ; therapy ; Myocardial Reperfusion Injury ; prevention & control ; Myocardium ; Rabbits ; Troponin T ; blood