Influence of alpha-adrenergic blockade on platelet-mediated thrombosis in stenosed canine coronary arteries.

The functional significance of platelet alpha-adrenergic receptors in vivo is uncertain. The aim of this study was to elucidate their role in experimental coronary thrombosis. In 46 open-chest dogs with a critical coronary stenosis produced by plicating the coronary artery wall with a suture, blood flow showed cyclical reductions followed by an abrupt return to control levels.

Molecular conversion between monomeric and dimeric states of the mitochondrial cytochrome b-c1 complex: isolation of active monomers.

Bovine heart cytochrome b-c1 complex dispersed in 0.1% dodecylmaltoside, 10 mM Tris-HCl (pH 7.4), was subjected to filtration on Ultrogel AcA 34 columns.

The interconversion between monomeric and dimeric bovine heart cytochrome c oxidase.

Monomers and dimers of bovine heart cytochrome c oxidase (EC 1.9.3.

Effect of alpha-adrenergic blockade on arrhythmias induced by acute myocardial ischemia and reperfusion in the dog.

Studies in cats suggest alpha-adrenergic contributions to arrhythmias during myocardial ischemia and reperfusion. The validity of this concept in other species, however, remains uncertain. Thus, 106 chloralose-anesthetized open-chest dogs undergoing a 25 min coronary artery occlusion followed by reperfusion received saline (n = 52), prazosin (1 mg/kg, n = 26), phentolamine (5 mg/kg, n = 18), or phentolamine (same dose) + propranolol (1 mg/kg, n = 10).

Gonococcal endocarditis: a case series demonstrating modern presentation of an old disease.

Gonococcal endocarditis appeared with striking frequency in the preantibiotic era compared with its surprising rarity today. We present a series of four episodes of gonococcal endocarditis, which presented to our institution in the last 2 years, after no cases in the previous decade. Three episodes involved the aortic valve and required emergency aortic valve replacement.

Influence of acute arterial hypertension on myocardial infarct size in dogs without left ventricular hypertrophy.

During acute myocardial infarction an increase in arterial pressure is common in patients who were previously normotensive and, therefore, do not have left ventricular hypertrophy. However, the effect of hypertension on infarct size in the absence of hypertrophy is uncertain. Thus, 32 open chest dogs underwent a 2 hour occlusion of the mid-left anterior descending coronary artery followed by 3 hours of reperfusion.

Platelet-mediated thrombosis in stenosed canine coronary arteries: inhibition by nicergoline, a platelet-active alpha-adrenergic antagonist.

The effects of nicergoline, a new agent that blocks alpha-adrenergic receptors and inhibits platelet phospholipase, were evaluated in a canine model of platelet-mediated coronary thrombosis. In 48 open chest dogs, the circumflex coronary artery was stenosed by plicating the artery wall with a suture. Thirty-four of the 48 dogs exhibited cyclic reductions in flow in the stenotic vessel, followed by a sudden return to control levels.

Intravascular microaggregation and in vitro platelet aggregation in coronary artery disease.

To investigate in vivo and in vitro microaggregation in coronary artery disease, we obtained blood samples from the coronary sinus (CS), pulmonary artery (PA), and aorta (AO) in patients undergoing cardiac catheterization. An electronic particle size analyzer was used to quantify microaggregates 13 to 81 mu in diameter in blood. In the first group of 58 patients, preformed circulating microaggregates and platelet responsiveness to ADP were assessed in AO and PA blood only.

Blood flow to infarct and surviving myocardium: implications regarding the action of verapamil on the acutely ischemic dog heart.

After coronary occlusion, myocardium originally supplied by the occluded vessel ultimately separates into infarct and surviving muscle. To clarify this process, evolution of collateral blood flow to infarct and to surviving myocardium was retrospectively analyzed after permanent left anterior descending occlusion in 24 closed chest dogs. Microspheres were injected before occlusion and 5 and 20 minutes and 4 hours after occlusion.

In-vitro translation of different mRNA-containing fractions of Chlamydomonas chloroplasts.

Starting from isolated chloroplasts of the Chlamydomonas reinhardii cw 15 mutant, several mRNA-containing chloroplast subfractions, i.e. thylakoid-bound polysomes, detached polysomes or isolated RNA, were prepared and incubated in homologous and heterologous translation systems.

Beneficial effects of the alpha-adrenergic antagonist nicergoline during acute myocardial ischemia and reperfusion in the dog.

Recent experimental and clinical data have stimulated interest in the use of alpha-adrenergic antagonists in acute myocardial infarction. We evaluated nicergoline, a new relatively selective alpha 1-antagonist which uniquely lowers heart rate. Open-chest dogs, randomized to control (n = 25) or intravenously treated group (n = 20; 0.

Role of cellular proteinases in acute myocardial infarction. I. Proteolysis in nonischemic and ischemic rat myocardium and the effects of antipain, leupeptin, pepstatin and chymostatin administered in vivo.

To test the hypothesis that cellular proteinases contribute to ischemic myocellular death, measurements were made of tyrosine release (an index of overall proteolysis) from incubated slices of nonischemic and ischemic myocardium obtained at various times after coronary artery occlusion in rats. Proteolysis failed to increase in ischemic myocardium throughout the first 24 hours of occlusion, when irreversible damage develops, indicating that cellular proteinases do not undergo generalized activation in this phase. These data represent the first assessment of myocardial proteolysis throughout the development of ischemic death, and suggest that cellular proteinases do not play a causal role in this process.

Early degradation of collagen after acute myocardial infarction in the rat.

After acute myocardial infarction (MI), proteolysis of necrotic myocardium is mediated by infiltrating inflammatory cells at the infarct margins. Collagen forms a structural fibroskeleton in healthy myocardium, and after MI this collagen may continue to provide significant tensile strength to the necrotic muscle wall. To determine whether collagen is also degraded (which might decrease infarct wall strength) and, if so, whether inflammatory cell proteases are implicated, hydroxyproline was measured from infarct zone and normal zone tissue from 24-hour infarcts produced in control rats and in rats made leukopenic (white blood cell count less than 300/mm3) by prior whole-body irradiation.

Preparation of monomeric cytochrome C oxidase: its kinetics differ from those of the dimeric enzyme.

Bovine cytochrome c oxidase in 0.1% dodecylmaltoside, 50 mM KCl and 10 mM Tris-HCl, pH 7.4 is monodisperse with an apparent Mr 360,000 (dimer) as estimated by filtration on Ultrogel AcA 34.

Concealed antidromic re-entrance during rapid atrial pacing in the Wolff-Parkinson-White syndrome.

In a patient with Wolff-Parkinson-White syndrome, rapid atrial pacing up to rates of 140/min resulted in A-H prolongation; increases in rate up to 200/min, however, failed to lengthen A-H further. The delta-H interval increased as rate rose to 120/min, but remained stable thereafter. These and other findings suggest retrograde activation of the His bundle via the accessory pathway at rates greater than 140/min.

The effects of nitroglycerin-methoxamine combination on infarct size in conscious dogs.

The effect of nitroglycerin combined with methoxamine in reducing infarct weight was studied in conscious dogs. Ten minutes after permanent left anterior descending (LAD) coronary artery occlusion, 10 dogs received nitroglycerin (450 micrograms bolus IV, then 300 micrograms/min for 4 hours) and methoxamine as needed to maintain blood pressure and heart rate. No dogs in heart failure.

Isolation and characterization of polysomes from thylakoid membranes of Chlamydomonas reinhardii.

Chloroplast polysomes that were originally bound to thylakoid membranes were isolated from the cell wall mutant CW-15 from Chlamydomonas reinhardii. Polysomes were isolated from synchronously grown cells harvested in the middle of the third light period, when the ratio of chloroplast to cytoplasmic polysomes was maximal. Thylakoid membranes were isolated from a chloroplast fraction and polysomes were released by Triton X-100.