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Biomedical subjects

N Bittar

Publications and source records attributed to N Bittar.

At least 37 records · Page 2Linked to original sources
PubMed1988

Ultrastructure, peroxisomes and lipid peroxidation in reperfused myocardium.

Reperfusion injury was studied in dog myocardium using a transmission electron microscope and 3,3'-diaminobenzidine (DAB) to locate areas of peroxidatic activity. Dark electron dense DAB reaction product was observed in peroxisomes and damaged mitochondria. These results suggest attack by reactive oxygen species on mitochondrial membranes, which might result in the formation of lipid peroxides and prostaglandin-like compounds. It is suggested that the release of lipid peroxide or prostaglandins from the injured cells may contribute to reactive hyperaemia, ventricular fibrillation and angina.

3,3'-Diaminobenzidine↗
PubMed1987

Efficacy of nifedipine gastrointestinal therapeutic system in combination with beta blockers in the management of exertional angina. A multicenter study of 54 patients.

This multicenter study assessed the efficacy of a new formulation of nifedipine in 54 patients with stable angina pectoris receiving beta-blocker therapy. This once-daily preparation of nifedipine was administered in double-blind fashion in doses of 30, 60, and 90 mg. All patients experienced pain-limited exercise at placebo baseline treadmill testing. Eight hours post-dose exercise testing resulted in a significant increase in time to onset of angina for all three dose levels of nifedipine but not for placebo. Exercise testing 24 hours after dosing showed significant improvement in time to angina and total exercise time for patients receiving 60-mg and 90-mg doses but not for the 30-mg or placebo categories. These preliminary results suggest that this new formulation of nifedipine is beneficial when added to stable doses of a beta blocker in patients in whom angina is still exhibited during exercise testing.

Adrenergic beta-Antagonists↗
PubMed1987

Visualization of endocytotic pits in capillary endothelia of dog heart by scanning electron microscopy.

Endocytotic transport may provide a mechanism for myocyte uptake of agents which ameliorate the effects of myocardial ischaemia. Examination of the inner capillary surface by transmission electron microscopy (TEM) is tedious and slow, while use of scanning electron microscopy permits the examination of greater areas in less time. Methods to obtain oblique exposures of capillaries and provide sufficient resolution to observe endocytotic pits were explored. Partial success was achieved using glutaraldehyde fixed tissue, treated with 30% glycerol, frozen-fractured under hexane at -85 degrees C, then dehydrated with acetone at -25 degrees C, critical-point dried and lightly coated with gold. Ultrastructural detail comparable with TEM images of heart tissue was obtained, but the resolution appeared limited by the coating process. It was not possible to verify stimulation of endocytosis by AMP in coronary capillary endothelia with scanning electron microscopy, due to this limitation.

Animals↗
PubMed1987

Contractility, ATP, and creatine phosphate during myocardial ischaemia and reperfusion: the effects of adenosine and inhibition of adenosine catabolism in the dog heart.

Provision of AMP or adenosine to heart cells during recovery from episodes of myocardial ischaemia accelerates physiological, biochemical, and structural recovery. Inhibition of adenosine loss from the tissue during ischaemia should have a similar effect. This hypothesis was tested in dog heart by infusion of adenosine and inhibitors of adenosine catabolism prior to, during, and following ischaemia. Post-ischaemic recovery of ATP and contractile function was accelerated significantly by adenosine and by inhibitors of adenosine catabolism both singly and in combination. Contractility and ATP levels during ischaemia were also increased by these inhibitors.

Adenosine↗
PubMed1987

Recovery of myocardial function after ischaemia: the effects of AMP and inhibition of endocytosis.

Recovery from ischaemia in heart tissue can be accelerated by addition of precursors of ATP such as AMP to the coronary circulation. Endocytosis in capillary endothelia is also stimulated by AMP; therefore endocytosis may be important in the transport of AMP from the circulation into myocytes. Alternatively, the increase in endocytotic transport itself could be responsible for accelerated recovery, irrespective of the stimulating agent. The effects of sham, AMP, cytochalasin-D (an inhibitor of endocytosis), and cytochalasin-D + AMP infusates given prior to, during, and following a 15 min ischaemic episode, were examined. AMP accelerated biochemical and functional recovery after episodes of ischaemia and stimulated endocytosis in coronary capillaries. Cytochalasin-D strongly inhibited contractility before, during, and after ischaemia, and similarly depressed ATP and creatine phosphate levels. Cytochalasin-D also strongly inhibited endocytosis and caused swelling of the capillary endothelium. When cytochalasin-D and AMP were provided together, the beneficial effects of AMP were only partially inhibited by cytochalasin-D. In fact, AMP was able to reverse most of the effects of cytochalasin-D including the inhibition of endocytosis. This suggests accelerated recovery of ischaemic myocytes requires precursors of ATP such as AMP, and the stimulation of endocytosis may abet transport of these precursors, or may be a spurious phenomenon.

Adenosine Monophosphate↗
PubMed1986

AMP stimulation of endocytotic transport from canine coronary circulation into myocytes.

Provision of ATP precursors before, during, and after an episode of myocardial ischaemia accelerates repletion of ATP levels and functional recovery of the tissue. To investigate ultrastructural effects of such provision, canine hearts were perfused in situ with sham and AMP solutions. Perfusion was begun 15 min before induction of ischaemia and continued during the 15 min ischaemic and 15 min reperfusion period. Some hearts were then treated with LaOH to label endocytotic vesicles, and the hearts were fixed for electron microscopy. A dramatic and significant increase was found in the number and size of capillary endothelial and subsarcolemmal vesicles in hearts treated with AMP, but not in hearts treated with sham additives. Endocytosis and exocytosis across capillary endothelia, and endocytosis into myocytes is suggested as a mechanism for rapid transport of ATP precursors from the coronary circulation into myocytes.

Adenosine Monophosphate↗
PubMed1985

Accelerated recovery of ischemic canine myocardium induced by AMP. Preliminary report.

Experiments were conducted on 18 dogs using an in situ blood-perfused canine heart model. Intracoronary infusion of AMP resulted in increased ATP and total adenine nucleotide levels. On reperfusion following a 15-min period of ischemia, ATP and total adenine nucleotide levels were significantly higher than control. Most important, contractile function recovered more rapidly in the AMP-treated dogs. It is therefore concluded that the delayed functional recovery noted after periods of ischemia is likely to be a direct result of delayed ATP resynthesis.

Adenosine Diphosphate↗
PubMed1985

Changes in morphology of endocytotic vesicles in cardiac capillary endothelial cells and myocytes of rats after treatment with adenine and AMP.

Isolated rat hearts were perfused with media containing no additions (sham), adenine, or AMP to determine if adenine or AMP would affect post-ischaemic myocyte ultrastructure. The most significant change induced by both adenine and AMP was a dramatic increase in the number and size of endocytotic vesicles apparent in capillary endothelia and myocytes. This observation suggests endocytosis as a possible transport mechanism for AMP or adenine, or other large polar molecules including purine nucleotide precursors, from the coronary circulation across capillary endothelia and into myocytes.

Adenine↗
PubMed1984

Double-blind, placebo-controlled trial of propranolol given once, twice and four times daily in stable angina pectoris: a multicenter study using serial exercise testing.

To determine if propranolol given twice daily (b.i.d.) or once daily (q.d.) was as effective as 4 times daily (q.i.d.) for treatment of stable angina pectoris, 78 patients with exercise-induced ST depression of 1.5 mm were randomized to q.i.d., b.i.d., q.d. and placebo groups. All patients received 5 tablets per day, and propranolol groups received 80, 160 and 320 mg/day on successive weeks. At weekly visits, patients underwent treadmill exercise testing before the 8:00 AM dose and at 2 and 9 hours afterward. Exercise duration (seconds) was significantly improved at the final visit compared with baseline by b.i.d. (120 +/- 36 [mean +/-] standard error of the mean p less than 0.001 n = 18) and q.i.d. (100 +/- 37, p less than 0.01; n = 17) regimens, but not by the q.d. (30 +/- 33; n = 18) and placebo regimens (27 +/- 37; n = 17). There was a significant decrease from baseline in the magnitude of ST depression at the final visit, measured at maximal common exercise duration in b.i.d. (-0.96 +/- 0.20 mm, p less than 0.001), q.i.d. (-0.84 +/- 0.20 mm, p less than 0.01) and q.d. (-0.58 +/- 0.18 mm, p less than 0.05) groups, but not in the placebo group (0.03 +/- 0.2 mm). Hourly heart rate by Holter was reduced in all 3 propranolol groups; however, the mean serum propranolol level was significantly lower just before the first dose with q.d. group (56 +/- 20 ng/ml) compared with b.i.d. and q.i.d. groups (146 +/- 22 and 119 +/- 28 ng/ml) with 320 mg/day (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Contractile activity and oxidative metabolism in single adult myocytes during normoxia and hypoxia.

Contractile activity and redox metabolism were measured by optical techniques in single myocytes isolated from adult rats. Observations were made during periods of perfusion with normoxic and hypoxic solutions. Contractile activity was determined by quantitation of light transmitted through myocytes, and the state of redox metabolism was determined by measurement of flavoprotein fluorescence. Contractile activity was found to decrease gradually and in proportion to the duration of hypoxia, and this decline followed a similar but more abrupt decline in flavoprotein fluorescence which indicated reduction of the electron transport system. This observation suggests the decline in contractile activity was due to a decrease in the oxidative formation of ATP, and also indicates the response of isolated myocytes to hypoxia is dissimilar to the response of in vivo myocytes to conditions of ischaemia.

Adenosine Triphosphate↗
PubMed1978

Functional role of collateral flow in the ischaemic dog heart.

Studies were carried out in four different canine preparations to determine the effect of collateral flow on early changes induced by acute segmental ischaemia. The results of these experiments indicated that collateral flow provided a limited and variable amount of protection. When collateral flow was eliminated, myocardial cell injury was more severe and less variable.

Animals↗
PubMed1976

Linear densities in mitochondria of human myocardial cells.

Ultrastructural study of myocardial biopsies from 5 patients who underwent myocardial revascularization procedures because of impending infarction showed mitochondria with linear densities. These densities, which occupied the intracristal space, appeared to have a high protein but low mineral content. It is suggested that linear densities may be an expression of severe, acute myocardial cell injury.

Adult↗
PubMed1976

Ultrastructural and physiological changes induced by atractylate in the canine myocardium.

The myocardial cellular response to the cardiac glycoside atractylate, a known inhibitor of mitochondrial adenine nucleotide translocation, was examined physiologically, morphologically, and morphometrically in eight dogs. An isolated in situ segment of left ventricular tissue was employed in these experiments to eliminate collateral flow and the potential for large sampling error. It was found that atractylate infusion rapidly induced physiological and morphological changes suggestive of a loss of membrane regulation of ion flux in the arteriole, capillary endothelium, and myocardial cell. Also mitochondrial changes suggestive of adenine nucleotide translocase inhibition were observed. As these responses are similar to those induced by acute myocardial ischaemia, it is suggested that ischaemia and atractylate induce cell injury by similar mechanisms.

Animals↗