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Biomedical subjects

R D Reynolds

Publications and source records attributed to R D Reynolds.

At least 127 records · Page 7Linked to original sources
PubMed1982

Ultra-short acting beta-blockers: a proposal for the treatment of the critically ill patient.

Beta-blockade is of proven value in the therapy of acute myocardial infarction but, unfortunately, may produce cardiac failure by removal of needed sympathetic support. The long duration of action of available blockers (hours) makes reversal of failure a complicated problem and precludes rapid modification of therapy to match changing autonomic conditions. To improve the safety and efficacy of beta-blockade in this setting we have developed the concept of ultra-short beta-blockade and have identified a novel beta-blocker (ASL-8052) which possesses a duration of action less than 15 minutes. This compound is cardioselective and possesses efficacy in an animal model of acute myocardial infarction. It, therefore, appears to be suitable for rapid attainment of controlled levels of beta-blockade via intravenous infusion and rapid recovery from beta-blockade if required by the clinical situation. The compound should, therefore, be useful for safe therapy in critically ill cardiac patients.

Adrenergic beta-Antagonists↗
PubMed1982

AMSA--a promising new agent in refractory acute leukemia.

Forty-five patients with various forms of acute leukemia refractory to usual methods of treatment were treated with AMSA at doses of 100-200 mg/m2 iv daily for 5-7 days, for total doses of 500-1000 mg/m2/course. Among 41 evaluable patients, six (15%) achieved complete remissions, including two of 19 patients with typical acute nonlymphocytic leukemia, none of four with atypical acute nonlymphocytic leukemia, two of nine with chronic granulocytic leukemia in blast crisis, two of eight with acute lymphoblastic leukemia, and none of one with acute undifferentiated leukemia. Durations of complete remissions were 6, 7, 8, 12, 13, and 14 weeks. Four of the patients who died with infection during marrow hypoplasia 2-5 weeks after receiving AMSA had no evidence of leukemia on premortem bone marrow aspirates or postmortem examination. The primary toxic effects of AMSA were severe myelosuppression, stomatitis, and alopecia. One incident of life-threatening liver failure occurred. AMSA appears to be a promising agent for use in heavily pretreated patients with acute leukemia and chronic granulocytic leukemia in blast crisis.

Acute Disease↗
PubMed1981

Limitation of myocardial infarct size by atenolol, nadolol and propranolol in dogs.

The importance of cardioselectivity and membrane depressant activity in the ability of beta-adrenergic antagonists to limit myocardial infarct size was assessed in the dog. Infarction was produced by a 60 min occlusion of the left circumflex coronary artery followed by reperfusion into a critical stenosis. Infarct size was significantly reduced by atenolol, nadolol and propranolol. Thus, limitations of infarct size by beta-adrenergic antagonists occur with agents which possess or lack cardiac selectivity or membrane depressant activity.

Adrenergic beta-Antagonists↗
PubMed1981

Effects of propranolol on myocardial infarct size with and without coronary artery reperfusion in the dog.

The ability of propranolol to limit myocardial infarct size (IS) following coronary artery occlusion with and without reperfusion into a critical stenosis was assessed in the dog. IS was determined by the nitrobluetetrazolium staining method and expressed as percent of the left ventricle (free wall plus septum). In Series 1 dogs the left circumflex coronary artery (LCX) was ligated at its origin. IS at 6 h was similar in groups pretreated with saline (36.0 +/- 1.3%) or propranolol (0.2 mg . kg-1, 34.7 +/- 1.7%; 1.0 mg . kg-1, 36.7 +/- 1.5%; 4.4 mg . kg-1, 34.8 +/- 0.3%). In Series 2 dogs a relatively small infarction was produced by ligating the largest branch of the LCX between the left anterior descending and posterior descending arteries. IS at 6 h was not significantly different in dogs pretreated with saline (8.1 +/- 1.7%) or propranolol (0.2 mg . kg-1, 7.1 +/- 2.5%; 1.0 mg . kg-1, 4.6 +/- 1.2%). In Series 3 dogs the LCX was ligated approximately 10 mm from its origin for 60 min followed by reperfusion into a critical stenosis. IS determined at 24 h was significantly less in dogs treated with propranolol (1.0 mg . kg-1) before LCX occlusion (4.6 +/- 0.6%) or 5 min after LCX reperfusion (9.5 +/- 1.8%) than in dogs treated with saline (22.6 +/- 2.8%). In Series 4 dogs treatment was exactly as in Series 3 except that reperfusion was not instituted. IS was similar in dogs pretreated with saline (29.0 +/- 1.5%) or propranolol (31.1 +/- 3.0%). Thus, in the present study, propranolol limited IS in the presence but not in the absence of reperfusion. In the reperfusion model propranolol was effective when administered before coronary occlusion or after initiation of reperfusion.

Animals↗
PubMed1981

Pyridoxal 5'-phosphate in whole blood, plasma and blood cells of postpartum nonlactating and lactating rats and their pups.

Pregnant rats were fed either a diet containing 20.2 mg pyridoxine/kg (control) or a diet containing 1,430 mg/kg (high vitamin B-6). At the time of delivery, pups were removed from half of the dams fed each diet. This resulted in four treatment groups: lactating and nonlactating dams fed the control diet and lactating and nonlactating dams fed the high vitamin B-6 diet. At delivery and at weeks 1, 2, and 3 postpartum, groups of dams and pups were killed and the content of pyridoxal 5'-phosphate (PLP) in whole blood, plasma and blood cells was measured. The PLP content in the whole blood of dams and pups was increased significantly by the high vitamin B-6 diet. Lactation had no effect on the PLP in whole blood of dams. Diet increased the PLP content in the plasma of dams and pups only slightly, whereas lactation greatly depressed PLP in the dams' plasma. In the blood cells, the PLP content was increased by diet and decreased by lactation.

Animals↗
PubMed1980

Antiarrhythmic effects of four different beta-adrenergic blockers in the mouse chloroform arrhythmia model.

The antiarrhythmic activity of four different beta-adrenergic blockers was assessed in the mouse chloroform arrhythmia model. ED50 values and 95% confidence intervals established by i.p. administration of drug were: propranolol (22.8, 10.9--67.0 mg/kg), sotalol (38.0, 15.9--58.5 mg/kg) and practolol (167, 111--235 mg/kg). Butoxamine provided some protection against the arrhythmia within a narrow dose range (53 to 79 mg/kg).

Adrenergic beta-Antagonists↗
PubMed1980

Comparison of the autonomic effects of procainamide and N-acetylprocainamide in the dog.

The autonomic effects of procainamide (PA) and N-acetylprocainamide (NAPA) were studied in anesthetized dogs. High plasma concentrations of PA (31 +/- 1.3--64 +/- 3.4 micrograms/ml) and NAPA (64 +/- 3.4--127 +/- 8.3 micrograms/ml)) reduced base-line mean arterial pressure and heart rate and attenuated the pressor and positive chronotropic responses to bilateral carotid occlusion and the negative chronotropic response to vagal stimulation. Neither drug reduced the pressor or positive chronotropic responses to catecholamines (epinephrine, phenylphrine, isoproterenol), however. In fact, at some doses PA and NAPA accentuated the pressor and positive chronotropic effects of epinephrine. Similarly, the depressor response to acetylcholine was not reduced by these drugs; it was significantly increased at some doses. In the isolated hindlimb (constant flow) PA and NAPA reduced the pressor response to preganglionic (sympathetic chain) stimulation but not to postganglionic (femoral and sciatic nerves) stimulation. We conclude that NAPA, like PA, at high plasma levels is vagolytic and attenuates baroreceptor-mediated reflexes associated with reduced arterial pressure. These effects appear to be due to ganglionic blockade.

Acecainide↗