Cod liver oil supplementation improves cardiovascular and metabolic abnormalities in streptozotocin diabetic rats.

Abnormalities in the metabolism of essential fatty acids and the results of increased oxidative stress have been implicated in cardiovascular disorders observed in diabetes mellitus. This study, therefore, aimed to investigate the effects of cod liver oil (CLO, Lysi Ltd, Iceland), which comprises mainly an antioxidant vitamin A, n:3 polyunsaturated fatty acids (n:3 PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on cardiovascular abnormalities in streptozotocin (STZ)-diabetic rats. Two days after single STZ (55 mg kg(-1), i.p.) or vehicle injection, diabetes was verified by increased blood glucose, and non-diabetic and diabetic rats were left untreated or treated with CLO (0.5 mL kg(-1) daily, by intragastric probing) for 12 weeks. Plasma glucose, triacylglycerol and cholesterol concentrations were significantly elevated in 12-week untreated-diabetic rats; CLO provided better weight gain, entirely prevented the plasma lipid abnormalities, but partially controlled the glycaemia in diabetic rats. In isolated aorta rings, diabetes resulted in increased phenylephrine-induced vasoconstriction and isoprenaline-induced vasorelaxation, impaired endothelium-dependent vasodilatation and unchanged responsiveness to sodium nitroprusside. CLO treatment completely prevented endothelial deficiency, partly corrected the phenylephrine-induced vasoconstriction and did not affect the responses to isoprenaline and sodium nitroprusside in diabetic aorta. Diabetes also produced a marked decrease in the rate of spontaneously beating right atria and a significant increase in basal contractile force of left ventricular papillary muscle. The responsiveness of right atria to the positive chronotropic effect of isoprenaline was significantly decreased in diabetic rats, and was increased in CLO-treated diabetic rats. The positive chronotropic effect of noradrenaline was markedly increased in diabetic atria, but prevented by CLO treatment. Diabetes also resulted in an increased positive inotropic response of papillary muscle to both noradrenaline and isoprenaline, which were prevented by CLO treatment. CLO treatment also resulted in lower tissue sensitivity (pD(2)) to these agonists in diabetic papillary muscle. Ventricular hydroxyproline content was found to be unchanged among the experimental groups. The ultrastructure of diabetic myocardium displayed various degenerations (i.e. intracellular oedema, myofibrillar fragmentation, condensed pleomorphic mitochondria, thick capillary irregular basement membrane, swollen endothelial cells), which were partially prevented by CLO treatment. We conclude that the supplementation with CLO is effective in preventing cardiovascular disorders observed in experimental diabetes.

Effects of ischemic preconditioning in human heart.

BACKGROUND: The aim of this study is to investigate the effects of ischemic preconditioning (IP) on myocardium and the level of nitric oxide (NO) in patients undergoing aorta-coronary bypass surgery. METHODS: Twenty consecutive patients with coronary artery disease were subjected into two equal groups; the IP group and the control group. Following the onset of cardiopulmonary bypass in the study group, hearts were preconditioned with two 3-minute periods of cross-clamping separated by 2 minutes of reperfusion. In the control group, cardiopulmonary bypass was continued for 10 minutes without using cross-clamp. Arterial and coronary sinus blood samples were used to determine serum NO, malondialdehyde (MDA), creatine phosphokinase-MB (CKMB), and lactate dehydrogenase (LDH) levels. Need for defibrillation after cross-clamp removal, ECG changes, postoperative arrhythmias, ejection fraction, and fractional shortening rates were recorded as hemodynamic data. RESULTS: Serum NO level was higher in the study group 5 minutes after aortic clamp removal (199.3 +/- 92.7 vs. 112.2 +/- 35.8 micromol; p = 001). Serum MDA (2.55 +/- 0.4 vs. 4.06 +/- 0.5; etamol/ml; 5 minutes after the aortic clamp removal; p = 0.0002); CK-MB (22.8 +/- 2.5 vs. 37.4 +/- 4.1; U/L 12 hours after the operation, p < 0.0001), and LDH (501.8 +/- 46.7 vs. 611.4 +/- 128.3; IU/L 48 hours after the operation, p = 0.02) levels were significantly lower in the preconditioned group when compared with the control group. Also, need for electrical defibrillation was significantly lower in the study group; Ejection fraction (64.3 +/- 6.3 vs. 57.6 +/- 7.6; p = 0.04) and fractional shortening (31.7 +/- 3.9 vs. 26.2 +/- 4.0; p = 0.04) rates were better in the study group postoperatively. CONCLUSIONS: These data may suggest that cardioprotection by ischemic preconditioning offers higher NO production, a lower myocardial ischemia, and better functional recovery of the hearts in coronary artery surgery patients.

Effect of Calcium Entry Blocking Agents (Nifedipine and Verapamil) on Myocardial Recovery during Reperfusion.

A comparative study on isolated guinea pig hearts was carried out to determine the effect of calcium entry blocking agents: nifedipine- and verapamil-added reperfusion solutions on myocardial recovery after global ischemia. After 20 min of normothermic ischemia, three groups of solutions were used for reperfusion (10 animals each): (1) Nifedipine-added (10--8 mmol L(minus sign1)) Krebs--Henseleit solution; (2) verapamil-added (10--8 mmol L(minus sign)) Krebs-Henseleit solution; (3) Krebs--Henseleit solution. Postischemic myocardial functions (ventricular contractile force and heart work) and enzyme activities were compared with their preischemic values. The addition of calcium entry blocking agents does not have any significant advantage over control solutions in myocardial recovery.