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We will follow your request and designs. After reaching an agreement, we will finish your study in a timely manner.
Echocardiography, electrocardiogram, high precision pressure assessments (Mikro-tip pressure catheters), immunohistochemistry, molecular biological studies.
Myocardial infarction, ischemia-reperfusion injury (heart, lung, kidney, and liver), heart failure (post-MI remodeling), gene therapy, cell therapy, transverse aortic constriction (TAC), acute ischemic stroke, renal ischemia, and limb ischemia.
Ready-To-Go MI mouse model*
Mice were modified surgically. Seven day later, mice were anesthetized and monitored by echocardiogram (ECG) (A). After the surgical suture outside the chest was tightened and tied, ST segment was elevated, indicating ischemia (B). After another 7 days, mice were euthanized, hearts were collected. Infarcted area was present in MI mice, but not in controls (Sham mice) (C). Infarcted hearts were sectioned. Left ventricular infarction and dilation was confirmed (D).
*Everything has been done except the ligation of the left coronary artery. Specific measurements have been taken to prevent potential myocardial injury before the occlusion.
Myocardial infarction is caused by occlusion of the coronary artery, leading to deprivation of oxygen and nutrients from cardiac cells. The occlusion can result from atherosclerosis, thrombosis, and arterial spasm in patients. Prolonged ischemia causes death of myocardium.
In vivo models
Ex vivo Langendorff perfusion model (mouse, rat) in which hearts are isolated and mounted to a buffer-perfusion system. This model excludes the effects of blood cells and humoral factors on the heart.
Mouse hearts were exposed (A and B). ECG and left ventricular pressure (LVP) were monitored (C-F). When body temperature reached 37 0C, myocardial ischemia was induced (B), leading to ST elevation and LVP decline (D and F). After 30-min ischemia and 120-min reperfusion, hearts were collected for TTC staining (G and H). Ischemia-reperfusion resulted in myocardial infarction (G: infarct area stained white, and ischemic but viable area stained red). Remote ischemic preconditioning reduced infarct size (H).
Heart failure is characterized by insufficiency in blood supply relative to body's demand. There are many causes of heart failure, such as post-MI remodeling, diabetic cardiomyopathy, tokotsubo cardiomyopathy, and doxorubicin cardiomyopathy. In its pathology, loss of cardiomyocytes and fibrosis are common. Echocardiogram shows left ventricular dilation and dysfunction.
In vivo models
A normal echocardiographic image (A). Myocardial infarction induced by occlusion of the left coronary artery caused left ventricular dilation at 28 days post-MI (B and C). LV infarction was confirmed in isolated hearts (D and E). TTC staining showed enlarged LV lumen and infarct size (F and G). Treatments attenuated LV remodeling after MI (C, E, G).
Thoracic aorta was exposed (left panel). A 27G needle was tied over the vessel and then removed. Sham animals were used as control (CON). Four weeks later, cardiac hypertrophy was developed (middle panel), and left ventricular wall was thickened in TAC mice (right panel).
Drug treatment reduced arterial blood pressure in spontaneously hypertensive rats (SHR). A Mikro-tip pressure transducer (catheter) was inserted into the carotid artery. Arterial blood pressure was constantly measured and recorded (A). Drug treatment caused instant decrease in blood pressure (B, 1:1K compressed). SHR and normal control (CON) rats with the same treatment were recovered and assessed while conscious and fully ambulatory in their home cages. Blood pressure was monitored for 8 hrs (C). This is a novel and reliable method in measuring drug effect on blood pressure in active and awake animals.
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