Pathological observation of acute myocardial infarction in Chinese miniswine.

The acute myocardial infarction (AMI) model in Chinese miniswine was built by percutaneous coronary artery occlusion. Pathological observation of AMI was performed, and the expression of tumor necrosis factor alpha (TNF-α) in the infarct sites was detected at different days after modeling in Chinese miniswine. The experimental findings may be used as the basis for blood flow reconstruction and intervention after AMI. Seven experimental Chinese miniswine were subjected to general anesthesia and Seldinger right femoral artery puncture. After coronary angiography, the gelfoam was injected via the microtube to occlude the obtuse marginal branch (OM branch). At 1 d, 3 d, 5 d, 7 d, 10 d, 14 d and 17 d after modeling, hetatoxylin-eosin (HE) staining was performed to observe the pathological changes and to detect the expression of TNF-α in the myocardial tissues. Cytoplasmic acidophilia of the necrotic myocardial tissues at 1 d after modeling was enhanced, and cytoplasmic granules were formed; at 3 d, the margins of the necrotic myocardial tissues were infiltrated by a large number of inflammatory cells; at 5 d, the nuclei of the necrotic myocardial cells were fragmented; at 7 d, extensive granulation tissues were formed at the margin of the necrotic myocardial tissues; at 10 d, part of the granulation tissues were replaced by fibrous scar tissues; at 14-17 d, all granulation tissues were replaced by fibrous scar tissues. Immunohistochemical detection indicated that no TNF-α expression in normal myocardial tissues. The TNF-α expression was first detected at 3 d in the necrotic myocardial tissues and then increased at 5 d and 7 d. After reaching the peak at 10 d, the expression began to decrease at 14 d and the decrease continued at 17 d. Coronary angiography showed the disappearance of blood flow at the distal end of OM branch occluded by gelfoam, indicating that AMI model was constructed successfully. The repair of the infarcted myocardium began at 10-17 d after modeling with safe blood flow reconstruction. TNF-α expression in the infarcted myocardium was the highest at 10 d, which can be explained by inflammation and repair of the infarcted myocardium.

[Effects of docosahexaenoic acid on ion channels of rat coronary artery smooth muscle cells].

OBJECTIVE: To investigate the effects of docosahexaenoic acid (DHA) on large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels and voltage-dependent K(+) (K(V)) channels in rat coronary artery smooth muscle cells (CASMCs), and evaluate the vasorelaxation mechanisms of DHA. METHODS: BK(Ca) and K(V) currents in individual CASMC were recorded by patch-clamp technique in whole-cell configuration. Effects of DHA at various concentrations (0, 10, 20, 40, 60 and 80 µmol/L) on BK(Ca) and K(V) channels were observed. RESULTS: (1) DHA enhanced IBK(Ca) and BK(Ca) tail currents in a concentration-dependent manner while did not affect the stably activated curves of IBK(Ca). IBK(Ca) current densities were (68.2 ± 22.8), (72.4 ± 24.5), (120.4 ± 37.9), (237.5 ± 53.2), (323.6 ± 74.8) and (370.6 ± 88.2)pA/pF respectively (P < 0.05, n = 30) with the addition of 0, 10, 20, 40, 60 and 80 µmol/L DHA concentration, and half-effect concentration (EC(50)) of DHA was (36.22 ± 2.17)µmol/L. (2) IK(V) and K(V) tail currents were gradually reduced, stably activated curves of IK(V) were shift to the right, and stably inactivated curves were shifted to the left in the presence of DHA. IK(V) current densities were (43.9 ± 2.3), (43.8 ± 2.3), (42.9 ± 2.0), (32.3 ± 1.9), (11.7 ± 1.5) and (9.6 ± 1.2)pA/pF respectively(P < 0.05, n = 30)post treatment with 0, 10, 20, 40, 60 and 80 µmol/L DHA under manding potential equal to +50 mV, and EC(50) of DHA was (44.19 ± 0.63)µmol/L. CONCLUSION: DHA can activate BK(Ca) channels and block K(V) channels in rat CASMCs, the combined effects on BK(Ca) and K(V) channels lead to the vasodilation effects of DHA on vascular smooth muscle cells.

[Effects of docosahexaenoic acid on sodium channel current and transient outward potassium channel current in rat ventricular myocytes].

OBJECTIVE: To investigate the effects of docosahexaenoic acid (DHA) on sodium channel current (I(Na)) and transient outward potassium channel current (I(to)) in rat ventricular myocytes and to evaluate potential anti-arrhythmic mechanisms of DHA. METHODS: I(Na) and I(to) of individual ventricular myocytes were recorded by patch-clamp technique in whole-cell configuration at room temperature. Effects of DHA at various concentrations (0, 20, 40, 60, 80, 100 and 120 micromol/L) on I(Na) and I(to) were observed. RESULTS: (1) I(Na) was blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged while stably activated curves were not affected by DHA. At -30 mV, I(Na) was blocked to (1.51 ± 1.32)%, (21.13 ± 4.62)%, (51.61 ± 5.73)%, (67.62 ± 6.52)%, (73.49 ± 7.59)% and (79.95 ± 7.62)% in the presence of above DHA concentrations (all P < 0.05, n = 20), and half-effect concentration (EC(50)) of DHA on I(Na) was (47.91 ± 1.57)micromol/L. (2) I(to) were also blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged with increasing concentrations of DHA, and stably activated curves were not affected by DHA. At +70 mV, I(to) was blocked to (2.61 ± 0.26)%, (21.79 ± 4.85)%, (63.11 ± 6.57)%, (75.52 ± 7.26)%, (81.82 ± 7.63)% and (84.33 ± 8.25)%, respectively, in the presence of above DHA concentrations (all P < 0.05, n = 20), and the EC(50) of DHA on I(to) was (49.11 ± 2.68)micromol/L. CONCLUSION: The blocking effects of DHA on APD and I(to) may serve as one of the anti-arrhythmia mechanisms of DHA.