[The protective effects of Haematococcus pluvialis on the exercise-induced myocardial injury in rat].

OBJECTIVE: To study the protective effects of Haematococcus pluvialis (H. pluvialis) on myocardial injury of rats induced by endurance and intensive exercise. METHODS: The model was based on intensive endurance training. Sixty-five male aged 42 days Wistar rats were randomly divided into 5 groups:control group (C group), general training group (M group), low dose H. pluvialis + training group (HM I group), middle dose H. Pluvialis + training group (HM Ⅱ group), high dose H. pluvialis + training group (HM Ⅲ group). Each group included 12 rats, and the rats were assigned to go on a 42-day swimming training regime. Professional gavage were taken daily. The rats in HM I, HM Ⅱ and HM Ⅲ group were treated with H. pluvialis at the doses of 0.067,0.133 and 0.4 g/kg by ig at 5 ml/kg and the normal saline were given to other groups. After a 42-day swimming training regime, myocardial injury markers such as serum alanine aminotransferase (ALT), myocardial superoxide dismutase(SOD) and malondialdehyde (MDA) were detected, the biochemical indexes such as serum and myocardial endothelin (ET) and calcitonin gene related peptide (CGRP)were detected. RESULTS: Serum ALT, lactate dehydrogenase(LDH), creatine kinase(CK), a-hydroxybutyrate dehydrogenase(a-HBDH), ET, myocardial MDA and ET in M group were significantly higher than those in C group (P<0.05 or P<0.01). The myocardial SOD activity and the myocardial and serum CGRP in M group were significantly lower than those in C group(P<0.05 or P<0.01). The contents of serum ALT, LDH and CK in HM groups were lower than those in the M group but there was no significant difference between the two groups. Compared with M group, H. pluvialis could decrease the levels of serum a-HBDH, ET and myocardial ET in a dose-dependent manner (P<0.05 or P<0.01). The above mentioned three parameters in HM Ⅲ group were lower than those in HM I group (P<0.05). H. pluvialis could decrease the levels of myocardial MDA and increase the levels of myocardial SOD activity and serum or myocardial CGRP in a dose-dependent manner (P<0.05 or P<0.01). CONCLUSIONS: The different doses of H.pluvialis can effectively reduce the free radicals caused by endurance and intensive training and enhance the immune function. Meanwhile H.pluvialis is able to guarantee the relative balance in ET an CGRP`s concentration. Therefore, the myocardial lipid peroxidation and myocardial injury are encumbered. Additionaly, high dose of H. pluvialis is proven to be the most effective.

Development and evaluation of a new canine myocardial infarction model using a closed-chest injection of thrombogenic material.

A new canine myocardial infarction model using thrombi induced by closed-chest injection of thrombin and autogenous blood with fibrinogen into coronary arteries was developed. Occlusive thrombi were formed in all treated animals. Occluded vessels did not spontaneously reperfuse 1 day after occlusion, but did so within 3 days. Infarction was confirmed by increased levels of creatine kinase-MB, glutamate-oxaloacetate transaminase and a-hydroxybutyrate dehydrogenase. Additionally, the left ventricular ejection fraction (LVEF) decreased within 0.5 h after occlusion and had not improved 4 weeks later. After 1 week, extensive transmural anteroinferior myocardial infarction was observed and heart mass had increased. By 4 weeks after occlusion, pulmonary capillary wedge pressure and central venous pressure were increased, and oxygen pressure was decreased. Dropout of nuclei in cardiomyocytes and increased amount of collagen fiber were observed in myocardial infarct regions of hearts excised 4 weeks after occlusion. This canine model may be useful and convenient in evaluating treatment efficacy and the long-term outcome of acute myocardial infarction.

Protection of branched-chain amino acids against ischemic myocardial injury in rats.

The protective effects of Branched-Chain Amino Acids (BCAA) on ischemic myocardium in rats were studied. Thirty Wistar rats (15 female and 15 male) were randomly divided into 3 groups of 10 animals each. Group A: control; group B: isoproternol (ISO); group C: ISO + BCAA. The rats in groups A and B received normal synthetic rat chow while those in group C received BCAA as supplement. After two weeks of dietary treatment, the rats in group A were injected with saline while those of groups B and C were injected with ISO which induced acute ischemic myocardial injury. After 4 days of injections with either saline or ISO, the rats were sacrificed. The activities of lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), creatine kinase (CK), pyruvate kinase (PK) in the serum and in the myocardium, and the concentrations of potassium (K+), magnesium (Mg2+), calcium (Ca2+) in the myocardium were measured. The results showed that the activities of LDH, GOT, alpha-HBDH, CK, PK in the serum and in the myocardium were significantly increased in group B. In addition, the concentrations of Ca2+ in the myocardium were significantly increased. However, the concentrations of Mg2+ in the myocardium were substantially decreased while those of K+ in group B were slightly lowered. In the group C animals both the activities of LDH, alpha-HBDH, PK, CK in the serum and the activities of LDH, GOT, alpha-HBDH, CK in the myocardium were significantly lower than those of the rats in group B, and were not significantly different from those of the control group. More significant was the concentrations of Ca2+ in the myocardium of the rats in group C were comparable to those of the control rats but were significantly lower than those of the rats in group B. It appeared that BCAA was effectively blocking the increase of Ca2+ in the myocardium without raising the level of Mg2+. It was concluded that dietary supplement with BCAA provided some protective effects against ischemic myocardium in rats.

The efficacy of selenium, WR-2721, and their combination in the prevention of adriamycin-induced cardiotoxicity in rats.

It is known that the antineoplastic drug adriamycin (ADR) can cause cardiotoxic effects. Some data imply that pretreatment with selenium (Se) and the radio- and chemoprotector, amifostine (WR-2721), may confer a protective effect. The aim of this study was to evaluate the efficacy of single doses of Se and WR-2721, alone or in combination, in the prevention of acute ADR-induced cardiotoxicity in male Wistar rats. Se, in the form of sodium selenite (1.6 mg/kg i.p.), and WR-2721 (300 mg/kg i.p.) were given 24 hours and 20 minutes, respectively, before ADR (6 mg/kg i.v.). The cardiotoxicity of ADR was recorded 48 hours after its administration because earlier studies revealed that structural damage of the myocardium occurs within this period. Evaluation of these toxic effects, as well as of the cardioprotective efficacy of the administered drugs, was performed using (1) ECG-records before and during the infusion of the proarrhythmogenic compound, aconitine (8 microg/kg/min i.v.) and (2) the serum activity of creatine kinase (CK), aspartate aminotransferase-(AST), lactate dehydrogenase (LDH), and its isoenzyme alpha-hydroxybutyrate dehydrogenase (alpha-HBDH). The results showed that the arrhythmogenic dose of aconitine was significantly reduced in ADR-treated rats (57.22 vs. 99.65 microg/kg in control; p < 0.05) and that this proarrhythmogenic compound caused a significant increase in heart rate in such animals compared to controls. Pretreatment with Se, WR-2721, and their combination partly reversed the arrhythmogenic dose of aconitine to control (72.09, 82.1, and 88.99 microg/kg, respectively). Se failed to prevent an aconitine-induced increase in heart rate, whereas WR-2721 and their combination successfully counteracted this effect. In addition, ADR produced a significant increase in the serum activity of all monitored enzymes. Pretreatment with Se failed to prevent this increase, whereas pretreatment with WR-2721 did. The best result was obtained with their combination. We conclude that the radio- and chemoprotector, WR-2721, particularly in combination with Se, may provide a significant protective effect against acute ADR-induced cardiotoxicity in rats.

Shed blood autotransfusion influences ischemia-sensitive laboratory parameters after coronary operations.

The diagnostic significance of ischemia-sensitive laboratory parameters in respect to possible interference with shed blood autotransfusion was assessed in a prospective study with 100 patients undergoing elective coronary artery bypass grafting. Serum levels of creatine kinase, creatine kinase MB activity, creatine kinase MB mass concentration, 2-hydroxybutyrate dehydrogenase, lactate dehydrogenase-1, troponin-T, myoglobin, and glutamicoxaloacetic transaminase were repeatedly assessed up to the sixth postoperative day. Thirty-seven patients were excluded from the study due to postoperative development of myocardial infarction (n = 4), transient ischemic events (n = 25), and left bundle-branch blocks (n = 8). In the remaining group of 63, 37 patients were retransfused with 580 +/- 370 mL shed blood up to the twelfth postoperative hour, and 26 patients did not receive autotransfusion due to minimal mediastinal blood loss. The results of our study show that the ischemia-sensitive laboratory parameters were significantly influenced by shed blood autotransfusion: 8 hours postoperatively, creatine kinase (272%), creatine kinase MB fraction (151%), 2-hydroxybutyrate dehydrogenase (130%), lactate dehydrogenase-1 (133%), troponin-T (200%), myoglobin (159%) and glutamic-oxaloacetic transaminase levels (153%) were significantly elevated (p < 0.05) in patients with postoperative autotransfusion, although there were no electrocardiographic signs of myocardial ischemia in this group of patients. Our study shows that postoperative autotransfusion of mediastinal shed blood may interfere with the diagnosis of perioperative myocardial ischemia by laboratory parameters in coronary bypass patients.

Pathophysiologic features of Q fever-infected guinea pigs.

Guinea pigs infected with 9-mile phase I strain of Coxiella burnetii had increased blood glucose concentrations; alkaline phosphatase (ALP), glutamic-oxalacetic transaminase (GOT), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), and creatine phosphokinase (CPK) activities; and bilirubin value. Hypocalcemia and hypophosphatemia were evident in the latter days of infection. At necropsy of the guinea pigs, necrotic foci were in liver, spleen, and heart. Seemingly, the major pathophysiologic changes in infected guinea pigs were the direct result of lesions in liver, spleen, and heart in which rickettsial bodies were readily observable with histologic staining procedures. The guinea pig may serve as an animal disease model for Q fever.