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Introduction In recent years, intravascular ultrasound (IVUS) has evolved as a valuable adjunct to angiography. IVUS allows precise tomographic measurement of lumen area and plaque size, distribution and, to some extent, composition. It is essential in clinic decision making. Myocardial fractional flow reserve (FFR myo ) is a special index of the functional severity of coronary stenosis. Although the application of FFR myo to assess intermediate coronary lesion is widely performed in some centers in developed countries, its use in China was lagged. Because it is relatively expensive to measure FFR myo , it will be beneficial to save the expenses and to short operation time if CAG and IVUS criteria could be clinically used as tools to discriminate functional significant of intermediate stenosis. Materials and Methods In 46 lesions of intermediate severity (eg, 40%–60% diameter stenosis) we assessed 1. by pressure wire: myocardial fractional flow reserve (FFR myo , index of functional significance), and 2. by IVUS: minimal lumen cross-sectional area (MLA) and percent area stenosis at the lesion site. Receiver operating characteristic (ROC) curve analysis was performed to establish the best cut-off values of IVUS indexes (ie, MLA and percent area stenosis) that were most predictive of FFR myo Results FFRmyo in 46 lesions of angiographic intermediate stenosis (49±11%) was significantly lower than it was in angiographic normal artery (0.83±0.15 vs 0.97±0.02, p myo myo (r=−0.68, p myo (r=0.63, p 2 (sensitivity 93%, specificity 77%) to be the best cut-off values to fit with FFR myo Conclusion IVUS area stenosis ≥65% and minimal lumen cross-sectional area ≤4 mm 2 reliably identified functionally critical intermediate coronary stenosis.

Objectives To investigate the effect of ligustrazine (tetramethylpyrazine, TMP) in attenuating myocardial apoptosis on rats with myocardial ischaemia reperfusion (IR) injury and to explore its mechanism. Methods The animal model was built by ligation of the left anterior descending artery of rats (35 min of regional ischaemia followed by 120 min of reperfusion). Male Sprague-Dawley rats were randomly divided into sham, IR, TMP pretreated (TMP 10 mg/kg intravenous injection, 5 min before ligation), and TMP+L-NAME group (TMP 10 mg/kg intravenous injection, 5 min before ligation and L-NAME 30 mg/kg intravenous injection, 15 min before reperfusion). Caspase-3 activity and TUNEL staining were used to detect myocardial apoptosis. Nitric oxide production (NO x ) of myocardial tissue was examined using nitric oxide detection kit and expression of eNOS were observed by RT-PCR and western blot. Results There were some TUNEL-positive staining myocardial cells in experimental groups except the sham group. Compared with IR group, TMP reduced apoptosis index (15.0±2.9% vs 25.2±3.3% in the IR group, p x (0.40±0.04 µmol/g vs 0.30±0.03 µmol/g in IR group, p Conclusions Ligustrazine offers antiapoptotic and cardioprotection effects against myocardial IR injury possibly through increasing the expression of eNOS and the level of NO.

Objective To observe the diverse apoptosis of the myocardiac mitochondria on insulin therapy in diabetic rats and to investigate the anti-apoptotic mechanism of insulin interacting with the mitochondria. Methods Male wistar rats were administered with intraperitoneal injection of streptozotocin (STZ, 25 mg/kg) and high fat diet to induce type 2 diabetic mellitus. Twenty-two were randomly divided into two treatment groups, namely, the early treatment group and the late treatment group (each n=7), and one diabetic (DM)group (n=8). Another eight were chosen for control. Novolin 30R was administrated hypodermically to the early treatment group (IE group) at the first week and to the late treatment group (IL group) at the fourth week. DM group were injected subcutaneously with physiological saline. All groups were treated for 8 weeks. At the end of the experiment we compared SOD, MDA, GSH in different groups, as well as apoptotic index, mitochondrial membrane potential (ΔΨm), active oxygen and myocardial ultrastructure. Results Compared to the control group, DM rats had higher blood glucose (30.53±2.39 vs 7.48±1.03, p Conclusion Insulin has an anti-apoptotic effect on cardiocytes of diabetic rats, and earlier intervention is better than later.

Introduction The percentage of angina and cardiac dysfunction and cardiovascular events increased significantly in hypertensive diabetes mellitus compared with essential hypertension and type 2 diabetes mellitus alone. Hypertension and diabetes are often associated with cardiac microvascular abnormalities. The major cardiac microcirculation alterations are the capillary rarefaction and endothelial cell functional impairment, which may be in the development of coronary insufficiency. We presume that the more serious injury in cardiac microvascular structure and function followed by hypertensive diabetes mellitus. Aims The purpose of the present study is to investigate ultrastructural changes and expression of eNOS in rat myocardial capillary endothelial cells as a response to hypertension with diabetes mellitus. Methods The rat model of hypertension with diabetes mellitus (SHDM) and the rat model of diabetes mellitus (DM) alone were induced by an intraperitoneal injection of streptozotocin combined with high fat diet in spontaneously hypertensive rats (SHR) and SD rats, respectively. The groups were as follows: SD, DM, SHR, and SHDM. After 16 weeks, ultrastructure of the myocardial capillaries was examined by transmission electron microscopy and the expression of endothelial nitric oxide synthase (eNOS) was detected by immunohistochemistry. Results Ultrastructural alterations of myocardial capillaries in SHR, DM and SHDM were oedematous endothelial cell, endothelial protrusions into lumen and narrowed /or irregular lumen respectively. These alterations indicate that cell injury was more significant in the myocardium of DM and SHDM. Thickening of basal lamina in myocardial capillaries with SHR was less considerable compared with SD (31.3±4.2 nm vs 28.6±3.6 nm, p>0.05), while thickening was a prominent feature of DM (46.6±5.3) nm and SHDM (51.5±4.6) nm (compared with SD or SHR, p Conclusions These results suggest that a combination of hypertension and diabetes mellitus enhanced the damage of myocardial capillaries endothelial cell ultrastructure and function more than either hypertension or diabetes mellitus alone.

Introduction Pericytes are perivascular cells with multifunctional activities which are now being elucidated. Pericyte alteration or degeneration is linked directly with microangiopathy in diabetes, scleroderma and hypertension. Aims The purpose of the present study is to investigate the pathologic changes of the myocardial capillary pericytes in hypertension with diabetes rats. Methods The rat model of hypertensive with diabetes mellitus (SHDM) and the rat model of diabetes mellitus (DM) were induced by an intraperitoneal injection of streptozotocin combined with high fat diet in spontaneously hypertensive rats (SHR) and SD rats, respectively. The four groups were as follows: SD, DM, SHR and SHDM. The ultrastructure changes were examined by transmission electron microscope and the number of precity was assessed by immunohistochemistry of ventricular sections at 16 weeks. Results Ultramicroscopic analysis of capillaries showed the pericytes on myocardial capillaries of SHR, DM, and SHDM were conspicuously abnormal in shape and were with cytoplasm containing abundant myofilament and organelle. In addition, pericytes seemed to be loosely associated with the endothelium. The number of pericytes in SHR, DM and SHDM were significantly increased than that in SD. The number of pericytes in SHDM were much higher than that in SHR (11.8±3.6 vs 3.9±1.1, p 0.05). Conclusion These results suggest the phenotype changes and increase of myocardial capillary pericytes in response to hypertension with diabetes. These changes may contribute to arterialisations of myocardial capillary and pericapillary fibrosis.