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PubMed1990

Heart protection and radical trapping by DMPO during reperfusion in isolated working rat hearts.

The purpose of this study was to use a direct method, that of electron spin resonance (ESR) spectroscopy, to demonstrate that reperfusion after a period of ischemia results in a sudden increase in the production of free radicals in the myocardium. Furthermore, the role of free radicals in the development of reperfusion arrhythmias and functional disturbances also was investigated using a 30-min period of global ischemia followed by 30 min of reperfusion in the isolated working rat heart. The spin trapping agent 5,5-dimethyl-1-pyrroline-1-oxide (DMPO) when it perfused the heart, 100 mumoles/liter, during the first 10 min of reperfusion attenuated the development of reperfusion arrhythmias and improved the functional recovery of the heart during reperfusion. Without treatment, 55% of hearts showed irreversible ventricular fibrillation, and this was completely prevented by DMPO. In DMPO-treated hearts, the recovery of heart function was improved; thus, coronary flow, aortic flow, left ventricular developed pressure, and first derivative of left ventricular developed pressure were significantly increased from their maximal control values of 16.2 +/- 1.9 ml/min, 12.7 +/- 0.9 ml/min, 11.1 +/- 0.5 kPa, and 426 +/- 31 kPa/s to 21.8 +/- 1.3 ml/min (p less than 0.05), 28.4 +/- 3.0 ml/min (p less than 0.001), 14.5 +/- 1.0 kPa (p less than 0.01), and 584 +/- 41 kPa/s (p less than 0.01), respectively. Left ventricular end-diastolic pressure was also significantly reduced from its control value of 2.8 +/- 0.2 kPa to 2.1 +/- 0.2 kPa (p less than 0.05), while the recovery of heart rate was not improved by DMPO treatment. Parallel ESR studies using DMPO as spin trap demonstrated the formation of .OH radicals in the effluent of the reperfused hearts. ESR signals of the formed DMPO-OH, alpha N = alpha beta H = 1.48 mT, were observed within the first seconds of reperfusion with peak concentrations after about 3 min. In the first series of ESR studies, DMPO (200 mmol/liter) was mixed up effluent and ESR signals were recorded, while in the second series of studies, DMPO was directly infused into the heart. Both methods were appropriate to demonstrate the radical formation that peaked at 3 min of reperfusion after 30 min of global ischemia. Cardiotoxic effects of DMPO can be excluded by using of the "mix-up" method (DMPO is added to effluent) because relatively high DMPO concentration (20-200 mmol/liter) is important for demonstration of free radical production.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1997

Controversies on the sensitivity of the diabetic heart to ischemic injury: the sensitivity of the diabetic heart to ischemic injury is decreased.

Controversy exists as to whether the diabetic heart is more or less sensitive to ischemic injury. Although a considerable number of experimental studies have directly determined the effects of ischemia on the diabetic heart, there is still no general agreement as to whether metabolic changes within the myocardium contribute to the severity of ischemic injury. This paper reviews the evidence suggesting that the diabetic heart can actually be less sensitive to an episode of severe ischemia. Possible reasons for this decreased sensitivity to injury are discussed, which include a decreased accumulation of glycolytic products during ischemia (lactate and protons), as well as alterations in the regulation of intracellular pH in the diabetic heart. Based on existing studies, we suggest that although impaired glucose metabolism in the diabetic heart contributes to injury in hypoxic hearts or in hearts subjected to low-flow ischemia, diabetes-induced decreases in glycolysis can actually be beneficial to the diabetic heart during and following a severe ischemic episode. A decreased clearance of protons via the Na+/H+ exchanger may also contribute to the decreased sensitivity to ischemic injury in the diabetic heart.

Animals↗
PubMed2002

Advanced training model for beating heart coronary artery surgery: the Zurich heart-trainer.

OBJECTIVE: Coronary artery surgery with beating heart technique is gaining increasing popularity. However, it is a challenging technique even for well-trained cardiac surgeons. Thus, a training model for beating heart surgery was developed to increase safety and accuracy of this procedure. METHODS: The model consists of differentially hardened polyurethane resembling mechanical properties of the human heart. The covering used in this model is a 1:1 replica of the human thoracic wall with optionally embedded skeletal structures. Sternotomy, lateral thoracotomy or trocar placement is possible to access the lungs, the pericardium and the heart with adjacent vessels. Disposable artificial coronaries variable in size, wall quality or wall thickness are embedded in the synthetic myocardium. Two-layer vessels, which can simulate dissection, are available. Bypass conduits utilize the same material. Coronaries/bypasses as well as part of the ascending aorta are water-tight and can be rinsed with saline. Lungs can be inflated. A purpose-built pump induces heart movement with adjustable or randomized stroke volume, heart rate and arrhythmia induction. RESULTS: The model was tested in a recent 'Wet-Lab' course attended by 30 surgeons. All conventional instruments and stabilizers with standard techniques can be used. Training with beating or non-beating heart was possible. Time needed for an anastomosis was similar to clinical experience. Each artificial tissue showed its individual nature-like qualities. Various degrees of difficulty can be selected, according to stroke volume, heart rate, arrhythmia, vessel size and vessel quality. The model can be quickly and easily set up and is fully reusable. CONCLUSIONS: The similarity to human tissue and the easy set-up make this completely artificial model an ideal teaching tool to increase the confidence of cardiac surgeons dealing with beating heart and minimally invasive surgery.

Cardiac Surgical Procedures↗
PubMed1987

Cloning and tissue distribution of rat heart fatty acid binding protein mRNA: identical forms in heart and skeletal muscle.

A fatty acid binding protein (FABP) has been identified and characterized in rat heart, but the function and regulation of this protein are unclear. In this study the cDNA for rat heart FABP was cloned from a lambda gt11 library. Sequencing of the cDNA showed an open reading frame coding for a protein with 133 amino acids and a calculated size of 14776 daltons. Several differences were found between the sequence determined from the cDNA and that reported previously by protein sequencing techniques. Northern blot analysis using rat heart FABP cDNA as a probe established the presence of an abundant mRNA in rat heart about 0.85 kilobases in length. This mRNA was detected, but was not abundant, in fetal heart tissue. Tissue distribution studies showed a similar mRNA species in red, but not white, skeletal muscle. In general, the mRNA tissue distribution was similar to that of the protein detected by Western immunoblot analysis, suggesting that heart FABP expression may be regulated at the transcriptional level. S1 nuclease mapping studies confirmed that the mRNA hybridized to rat heart FABP cDNA was identical in heart and red skeletal muscle throughout the entire open reading frame. The structural differences between heart FABP and other members of this multigene family may be related to the functional requirements of oxidative muscle for fatty acids as a fuel source.

Amino Acid Sequence↗
PubMed2005

Prenatal cocaine exposure increases apoptosis of neonatal rat heart and heart susceptibility to ischemia-reperfusion injury in 1-month-old rat.

Maternal cocaine administration during pregnancy increased apoptosis in near-term fetal rat heart. The present study tested the hypothesis that prenatal cocaine exposure increases the heart susceptibility to ischemia/reperfusion injury in the offspring. Pregnant Sprague-Dawley rats received cocaine (30 mg kg(-1) day(-1)) or saline from days 15 to 21 of gestational age. Maternal body weights were not significantly different at the end of cocaine treatment, but body weights of offspring were decreased slightly at ages of 1, 3, and 7 days. Although heart-to-body weight ratio was not affected at all ages examined, prenatal cocaine significantly increased left ventricular myocyte size at an age of 30 days. Additionally, prenatal cocaine increased DNA fragmentation measured in the hearts isolated from offspring of 1, 3, 7, and 21 days, but not of 30 days, with the peak at 3-day neonates. Antiapoptotic (Bcl-2 and Bcl-X(L)) and proapoptotic (Bax and Bad) proteins were expressed in neonatal rat hearts of both groups. Prenatal cocaine exposure decreased levels of Bcl-2 in 21-day and increased Bax in 21- and 30-day rat hearts. In addition, hearts of 30-day-old male progeny were studied using the Langendorff preparation, and were subjected to 25 min of ischemia and 60 min of reperfusion. Preischemic baseline values of left ventricular (LV) function were the same between the two groups. However, prenatal cocaine exposure significantly attenuated postischemic recovery of LV function, and significantly increased elevated LV end diastolic pressure during reperfusion. This was associated with a significant increase in ischemia/reperfusion-induced LV myocardial infarct size. The results suggest that prenatal cocaine exposure induces abnormal apoptosis and myocyte hypertrophy in postnatal heart, leading to an increased heart susceptibility to ischemic insults in postnatal life.

Animals↗
PubMed1998

Fibrinogen as a risk factor for coronary heart disease and mortality in middle-aged men and women. The Scottish Heart Health Study.

AIMS: Fibrinogen was measured in 5095 men and 4860 men aged 40-59 in a random population sample from 25 districts of Scotland recruited during 1984-87: the Scottish Heart Health Study. Fibrinogen was then related to the chance of fatal and non-fatal coronary events and death from any cause during a subsequent follow-up period of around 8 years. METHODS AND RESULTS: Fibrinogen was measured by the Clauss assay. The effect of fibrinogen on coronary heart disease and death was assessed through age-adjusted means and Cox proportional hazards regression models, accounting for age, cotinine (a measure of tobacco smoke inhalation) and 11 other major coronary risk factors. Fibrinogen was found to be an important risk factor for coronary heart disease in men and women, with and without pre-existing coronary heart disease. There appears to be a threshold effect, with those in the highest fifth of the distribution having a much increased risk. Estimated age-adjusted hazard ratios by sex and pre-existing coronary heart disease group for the highest to lowest fifth of fibrinogen range between 1.93 and 4.86. Fibrinogen is also important as a risk factor for coronary death and all-causes mortality, with a similar threshold effect. Comparing the two extreme fifths, the hazard ratios for coronary death are 3.01 and 3.42, and for all-cause mortality are 2.59 and 2.20, for men and women respectively. Adjustment for cotinine reduces the hazard ratios, but further adjustment for the other 11 risk factors has little effect for coronary heart disease events. After full adjustment there is a remaining significant (P < 0.05) hazard ratio for coronary death and death from any cause and for a coronary heart disease event for those free of coronary heart disease at baseline, amongst men, comparing the highest to the lowest fifth. CONCLUSION: Fibrinogen is a strong predictor of coronary heart disease, fatal or non-fatal, new or recurrent, and of death from an unspecified cause, for both men and women. Its effect is only partially attributable to other coronary risk factors, the most important of which is smoking.

Adult↗
PubMed1999

MRC/BHF Heart Protection Study of cholesterol-lowering therapy and of antioxidant vitamin supplementation in a wide range of patients at increased risk of coronary heart disease death: early safety and efficacy experience.

AIMS: In observational studies, prolonged lower blood total cholesterol levels - down at least to 3 mmol. l-1 - are associated with lower risks of coronary heart disease. Cholesterol-lowering therapy may, therefore, be worthwhile for individuals at high risk of coronary heart disease events irrespective of their presenting cholesterol levels. Observational studies also suggest that increased dietary intake of antioxidant vitamins may be associated with lower risks of coronary heart disease. The present randomized trial aims to assess reliably the effects on mortality and major morbidity of cholesterol-lowering therapy and of antioxidant vitamin supplementation in a wide range of different categories of high-risk patients. METHODS AND RESULTS: Men and women aged 40 to 80 years were eligible provided they were considered to be at elevated risk of coronary heart disease death because of past history of myocardial infarction or other coronary heart disease, occlusive disease of non-coronary arteries, diabetes mellitus or treated hypertension; had baseline blood total cholesterol of 3.5 mmol. l-1 or greater; and no clear indications for, or contraindications to, either of the study treatments. Eligible patients who completed a pre-randomization run-in phase on active treatment were randomly allocated to receive simvastatin (40 mg daily) or matching placebo tablets and, in a '2x2 factorial' design, antioxidant vitamins (600 mg vitamin E, 250 mg vitamin C and 20 mg beta-carotene daily) or matching placebo capsules. Follow-up visits after randomization are scheduled at 4, 8 and 12 months, and then 6-monthly, for at least 5 years. Between July 1994 and May 1997, 15 454 men and 5082 women were randomized, with 9515 aged over 65 years at entry. Diagnostic criteria overlapped, with 8510 (41%) having had myocardial infarction (most of whom were either female, or elderly or with low blood cholesterol), 4869 (24%) some other history of coronary heart disease, 3288 (16%) cerebrovascular disease, 6748 (33%) peripheral vascular disease, 5963 (29%) diabetes mellitus (of whom 3985 had no history of coronary heart disease) and 8455 (41%) treated hypertension. Baseline non-fasting total cholesterol levels were less than 5.5 mmol. l-1 in 7882 (38%) participants, and LDL (low density lipoprotein) cholesterol less than 3.0 mmol. l-1 in 6888 (34%). During a mean follow-up of 25 months (range: 13 to 47 months), no significant differences had been observed between the treatment groups in the numbers of patients with muscle symptoms, other possible side-effects leading to termination of study treatment, or elevated liver and muscle enzymes. After 30 months of follow-up, 81% of randomized patients remained compliant with taking their study simvastatin or placebo tablets, and allocation to simvastatin produced average reductions in non-fasting blood total and LDL cholesterol of about 1.5-1.6 mmol. l-1 and 1.1-1.2 mmol. l-1 respectively. Eighty-seven per cent of patients remained compliant with taking their vitamin or placebo capsules, and allocation to the vitamin supplement produced an average increase in plasma vitamin E levels of about 24 micromol. l-1. Based on this initial follow-up period, the estimated annual rate of non-fatal myocardial infarction or fatal coronary heart disease is 2.4%, annual stroke rate is 1.3%, and annual all-cause mortality rate is 2. 2%. CONCLUSION: The Heart Protection Study is large, it has included a wide range of patients at high risk of vascular events, and the treatment regimens being studied are well-tolerated and produce substantial effects on blood lipid and vitamin levels. The study should, therefore, provide reliable evidence about the effects of cholesterol-lowering therapy and of antioxidant vitamin supplements on all-cause or cause-specific mortality and major morbidity in a range of different categories of individuals for whom uncertainty remains about the balance of benefits and risks of these treatments. Copyrig

Adult↗