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Biomedical subjects

P Gregor

Publications and source records attributed to P Gregor.

At least 145 records · Page 8Linked to original sources
PubMed1983

Possible role of increased brain methylation in methionine sulfoximine epileptogenesis: effects of administration of adenosine and homocysteine thiolactone.

An intraventricular pulse of [14COOH]L-methionine to mice pretreated with the convulsant L-methionine-dl-sulfoximine (MSO) resulted in significantly higher than control specific radioactivity values of cerebral [14COOH]L-methionine (Met), [14COOH]S-adenosyl-L-methionine (AdoMet) and [14COOH]S-adenosyl-L-homocysteine (AdoHcy). MSO administration (3 hr) also decreased brain steady-state levels of Met, AdoMet, and AdoHcy. Following an intraventricular pulse of [3H-methyl]L-methionine, the levels of [3H-methyl]phosphatidylmonomethylethanolamine and of membrane associated and soluble [3H-methyl]carboxylmethylated proteins were increased over corresponding saline-treated controls. The activity of cerebral histamine N-methyltransferase was also increased after MSO treatment. The administration of a combination of adenosine and homocysteine thiolactone to MSO-pretreated animals counteracted the MSO-induced decreases in brain Met, AdoMet, and AdoHcy as well as the increase in histamine N-methyltransferase activity. In addition, administration of adenosine together with homocysteine thiolactone decreased the incidence of, and increased the latency to MSO seizures, with the most effective anticonvulsant action occurring when cerebral AdoHcy levels were at their highest.

Adenosine↗
PubMed1983

Echocardiography during attack of angina pectoris.

Two patients with angina pectoris were echocardiographically examined during an attack of angina pain. In both patients, segmental asynergy of the left ventricle was present during chest pain. The echocardiographic finding before the attack and after its regression was normal. It appears that angina pectoris and an echocardiographically detectable asynergy of the left ventricle are two processes taking place almost simultaneously, their common cause being myocardial ischaemia. Wall motion abnormalities which develop during an attack of angina pectoris are fully reversible. These findings also indirectly support the assumption that two-dimensional echocardiography can practically immediately after the onset of chest pain in myocardial infarction prove asynergy of the left ventricle.

Angina Pectoris↗
PubMed1981

Hemodynamic effects of disopyramide at rest and during exercise in normal subjects.

The hemodynamic effects of disopyramide phosphate, 2.0 mg/kg body weight, given intravenously over a period of five minutes were studied at rest and during exercise in ten patients without clinical or angiographic evidence of heart disease. Following disopyramide, the resting cardiac index was lower (4.0 +/- 0.6 vs 4.3 +/- 0.6 liters/min/m2, mean +/- 1 SD,P less than 0.05), while left ventricular end-diastolic pressure (16 +/- 4 vs 11 +/- 4 mm Hg, P less than 0.001), pulmonary arterial (PA) mean pressure (20 +/- 5 vs 17 +/- 5 mm Hg, P less than 0.05), and brachial arterial (BA) mean pressure (105 +/- 8 vs 96 +/- 7 mm Hg, P less than 0.05), were higher than the pre-infusion resting values. During exercise, there was no change in left ventricular end-diastolic pressure while cardiac index rose from 4.0 +/- 0.6 to 6.5 +/- 0.6 liters/min/m2 (P less than 0.001) and left ventricular stroke work index increased from 62 +/- 19 to 84 +/- 22 gm/beat/m2 (P less than 0.001). The normal hemodynamic response during exercise after disopyramide despite the apparent depression of left ventricular function at rest probably reflects the positive inotropic effect of enhanced sympathoadrenergic activity.

Adult↗