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Biomedical subjects

A Leaf

Publications and source records attributed to A Leaf.

At least 109 records · Page 6Linked to original sources

n-3 fatty acids increase postischemic blood flow but do not reduce myocardial necrosis.

The effects of a fish oil-supplemented diet on infarct size and regional myocardial blood flow were examined in a rat model of acute ischemia followed by reperfusion. Thirty-five rats were fed a diet containing 20% by weight: fish oil (FO), rich in n-3 polyunsaturated fatty acids; corn oil (CO), with predominantly n-6 polyunsaturated fatty acids; or beef tallow (BT), containing large amounts of saturated fatty acids. After 6-12 wk on the diet, animals underwent 40 min of left coronary artery occlusion followed by 2 h of reperfusion. Regional transmural myocardial blood flow was determined with radioactive microspheres at 30 min of occlusion and again 30 min after reperfusion. Infarct size was determined with triphenyltetrazolium chloride. Blood flow was virtually undetectable within the ischemic zone in all groups during occlusion. With reperfusion, however, ischemic zone absolute blood flow and relative flow (normalized to nonischemic zone flow) were significantly greater in the fish oil group [2.4 +/- 0.25 ml.min-1.g-1, 44 +/- 4% vs. 1.7 +/- 0.3, 29 +/- 5% for CO (P less than 0.05 vs. FO), and 1.4 +/- 0.3, 29 +/- 5% for BT (P less than 0.05 vs. FO)]. Despite differences in reperfusion blood flow, average percent transmural extent of infarction was nearly identical (68 +/- 4, 68 +/- 5, and 64 +/- 3%) and overall infarct size was similar (38 +/- 3, 36 +/- 4, and 29 +/- 3%) for FO, CO, and BT groups, respectively. In conclusion, dietary supplementation with fish oils increases postischemic blood flow but has no effect on extent of myocardial infarction in this ischemia-reperfusion model in rats.

Animals↗

Brain stem glioma presenting as gastro-oesophageal reflux.

Brain stem gliomas may present as gastro-oesophageal reflux. In such cases gastro-oesophageal reflux presents atypically late, and computed tomography may not detect the presence of the tumour until late in the course of the disease.

Brain Neoplasms↗

Screening for intrauterine growth retardation using ratio of mid-arm circumference to occipitofrontal circumference.

Uncritical application of standard weight percentile charts, derived from white infants, to infants from different ethnic groups may result in an overestimate of the incidence of intrauterine growth retardation in those groups. The ratio of mid-arm circumference to occipitofrontal circumference was studied in 194 babies (49 Asian, 58 black, and 87 white). In contrast with birth weight the ratio did not vary among the ethnic groups; it was also independent of sex. In a prospective study of 64 neonates whose weight was below the 10th percentile on standard charts the ratio of mid-arm circumference to occipitofrontal circumference was a more accurate predictor than weight of those infants who would develop symptoms associated with intrauterine growth retardation. The ratio of mid-arm circumference to occipitofrontal circumference therefore provides a simple, accurate, and cheap way of assessing intrauterine growth retardation in areas with a large multiethnic population, where birth weight varies greatly.

Anthropometry↗

Mitochondrial function and intracellular calcium in anoxic cardiac myocytes.

Mitochondrial dysfunction has been implicated as the cause of irreversible injury in the ischemic heart. To circumvent artifacts associated with organelle isolation, mitochondrial function was studied in intact isolated, Ca2+-tolerant rat ventricular myocytes. After 30 min of anaerobic incubation, myocyte viability decreased from 76 +/- 1 to 33 +/- 4%. Basal O2 consumption rates (nanoatoms . mg cell protein-1 . min-1) were 17.1 +/- 1.3 in aerobic cells and 51.0 +/- 9.8 in anoxic cells. Carbonylcyanide-p-trifluoromethoxyphenyl hydrazone (FCCP)-stimulated rates were 65.5 +/- 9.2 and 84.5 +/- 15.3 in aerobic and anoxic cells, respectively. Respiratory control ratio was lower in anoxic cells: 2.3 +/- 0.3 versus 4.2 +/- 0.4 in aerobic cells. These data suggest that early anoxic mitochondrial injury is due to increased permeability of the inner membrane. Addition of pyruvate, malate, and FCCP to cells made permeable by digitonin resulted in similar maximal O2 consumption rates: 276.5 +/- 31.8 in aerobic and 299.3 +/- 31.9 in anoxic cells, suggesting the electron transport chain is intact in anoxic cells. For purposes of investigating whether anoxic mitochondrial dysfunction is secondary to cellular or mitochondrial Ca2+ overload, total cell Ca2+, cytosolic free Ca2+ levels (measured by null-point titration), and mitochondrial Ca2+ contents (measured as FCCP-releasable Ca2+) were measured. There were no differences in these three parameters between aerobic and anoxic cells, suggesting that mitochondrial dysfunction and irreversible hypercontraction of isolated cardiac myocytes exposed to 30 min of anoxia are not related to Ca2+ overload.

Animals↗

Determination of isolated myocyte viability: staining methods and functional criteria.

Single ventricular cells tolerant to physiological levels of calcium have been successfully isolated from adult rat heart. These cells exhibit morphological as well as functional characteristics of the intact myocardium. Under anaerobic incubations either in the absence of extracellular calcium or in the presence of 6% PEG, myocytes excluded Trypan blue despite severe derangements in biochemical functions. We suggest that Trypan blue entry may be a rather insensitive criterion of cell injury. We recommend the combination of rod-shape morphology, ATP levels and the ability to contract under external pacing as alternative simple tests of cell viability.

Adenosine Triphosphate↗

Mechanism of protection by verapamil and nifedipine from anoxic injury in isolated cardiac myocytes.

This study was designed to determine whether slow Ca2+ channel blocking agents exert a direct protective effect on the anoxic myocardial cell and, if so, what the mechanism of protection is. Isolated Ca2+-tolerant rat cardiac myocytes were incubated under aerobic or anaerobic conditions, with or without verapamil or nifedipine, in the resting and contractile state. Protection against cell injury was assessed by preservation of rod-shaped morphology, cellular ATP levels, intracellular ionic composition, and lactate dehydrogenase release. Resting myocytes incubated anaerobically lost their rod-shaped appearance, accumulated Na+ and lost K+, and suffered a significant loss of cellular ATP. The release of lactate dehydrogenase into the medium was increased twofold, indicating significant membrane injury. Verapamil (1 microM) or nifedipine (1 microM) did not afford any protection against anoxic injury as measured by these parameters. Furthermore, on reoxygenation, anoxic verapamil- and nifedipine-treated myocytes had significantly higher cellular Ca2+ levels than control aerobic cells. When anoxic myocytes were paced at a rate of 300/min for 10 min, there were marked decreases in the number of rod-shaped cells and cellular ATP levels, whereas identically paced aerobic cells sustained no significant injury. Verapamil (1 microM) or nifedipine (1 microM) protected cells paced at 300/min from anoxic injury, but the cells were unable to sustain contraction rates at the frequency of the imposed pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Exercise and coronary heart disease.

The epidemiologic evidence examining the effect of physical activity on the development and course of coronary heart disease is reviewed. This evidence indicates that physically active individuals have a lower incidence of myocardial infarction and mortality from coronary disease. While there is no documentation that an exercise program following myocardial infarction will significantly increase patient survival, exercise does increase functional capacity, lessen angina pectoris, and improve self-image in patients with coronary heart disease. Possible mechanisms for the beneficial effects of exercise are considered.

Animals↗