Harvey R. Kaplan
University of Michigan
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Harvey R. Kaplan.
European Journal of Pharmacology | 1972
Harvey R. Kaplan; John W. Barker; Salvatore A. La Sala
Abstract 1-Dopa, 10 mg/kg, i.v., caused an initial increase and a secondary decrease in arterial blood pressure in MAO-inhibited chloralose-anesthetized dogs. When 1-dopa was restricted to the head circulation of vascularly isolated and neurally intact cross-circulated dogs, blood pressure was lowered in the recepients trunk. Administration of 1-dopa to the vascularly isolated trunk caused only a pressor response. The results direct evidence for central hypotensive and peripheral pressor actions of 1-dopa.
Journal of Cardiovascular Pharmacology | 1992
Sandra E. Burke; Clifford D. Wright; Ronald E. Potoczak; Denise M. Boucher; George D. Dodd; David G. Taylor; Harvey R. Kaplan
Summary: CI-959, a cell-activation inhibitor that prevents the formation of oxygen-derived free radicals by inflammatory cells, was studied to determine its effects on myocardial infarct size and subsequent scar formation in dogs. The left circumflex coronary artery was occluded for 90 min, followed by 6 h of reperfusion. Drug infusion was started 15 min before reperfusion at a loading dose of 8 mg/kg i.v., followed immediately by 2 mg/kg i.v. infused over 80 min. The infarct size, assessed by TTC staining techniques, was significantly reduced in 12 dogs treated with CI-959 (23.3 ± 3.6% of the area at risk) when compared to 11 vehicle-treated animals (35.5 ± 4% of the area at risk, p < 0.05). This reduction in infarct size was not attributed to changes in regional myocardial blood flow, as measured by radioactive microspheres, or to a reduction in myocardial oxygen demand, as estimated by changes in the rate-pressure product. The scar thickness, measured after a 6-week recovery period in 9 animals treated with CI-959, was not significantly reduced in comparison with 11 controls. In vitro, CI-959 effectively inhibited oxygen free radical formation by canine neutrophils. The results of this study show that CI-959 significantly reduces the myocardial infarct size without causing scar thinning, which might lead to ventricular aneurysm, and suggests the most likely mechanism for its beneficial action is the prevention of formation of toxic oxygen radicals.
European Journal of Pharmacology | 1969
Harvey R. Kaplan; Salvatore A. La Sala; Arthur Simon; Ronald D. Robson
Abstract ST 155 applied to the cardiac pacemaker region (intact dogs) or incorporated into the perfusion fluid of Langendorff hearts, did not influence heart rate. The cardiac slowing and changes in chronotropic response to noradrenaline, caused by ST 155 in guanethidine-pretreated dogs were prevented by interruption of cardiac parasympathetic transmission.
European Journal of Pharmacology | 1971
Harvey R. Kaplan; Salvatore A. Lasala; Ronald D. Robson
Abstract Equieffective oral doses of levo- and racemic bunolol, dl-5-[3-(tert.-butylamino)-2-hydroproproxyl]-3,4-dihydro-1-(2H)-naphthalone hydrochloride, differed in their duration of β-adrenergic blockade. Blockade of isoprenaline-induced tachycardias by levo-bunolol was less persistent than those caused by racemic bunolol or combinations of levo- and dextro-bunolol and dextro-propranolol or levo-bunolol, p.o., and dextro-bunolol, i.v. The results indicate that both stereoselective and non-stereoselective mechanisms have significance in the activity and biological disposition of bunolol and its optical isomers.
Expert Opinion on Drug Discovery | 2008
Icilio Cavero; Harvey R. Kaplan
Background: The American Society for Pharmacology and Experimental Therapeutics (ASPET) celebrated its centennial during the April 2008 Experimental Biology meeting held in San Diego, CA, USA. Objectives: This report summarizes a centennial symposium on past, present and future paradigms in drug discovery. The John Langley (1905) concept of ‘receptive substances’ initiated a cascade of cardinal discoveries for pharmacology. During the following 100 years, receptors achieved the status of well-defined multifunctional cellular proteins mediating all drug effects. The G-protein-coupled receptors (GPCRs) were discussed in relation to multiple targets they represent for clinically used or new medicines. The development of inbred and transgenic animal strains is a fundamental twentieth century achievement for biological research activities. Progress in treating CNS disorders still awaits breakthrough treatments. Drug development remains a risky and expensive venture; improvements are expected from emerging biomarker and translational medicine technologies. Future clinical research has to document the benefits that new medications provide to concerned stakeholders. Conclusions: We wish ASPET a new century of great achievements and acknowledge the dedication of several generations of colleagues, many of whom are our ‘unsung heroes’. They have left us a precious heritage to be pursued with passion in the quest for better medicines.
Angiology | 1989
Harvey R. Kaplan; David G. Taylor; Stephen C. Olson; Laura K. Andrews
Journal of Medicinal Chemistry | 1987
C. J. Blankley; James Stanley Kaltenbronn; D. E. Dejohn; A. Werner; Lawrence Ray Bennett; G. Bobowski; U. Krolls; Don Johnson; W. M. Pearlman; Milton Louis Hoefle; Arnold D. Essenburg; David Cohen; Harvey R. Kaplan
Journal of Pharmacology and Experimental Therapeutics | 1980
T J Steffe; T E Mertz; S G Hastings; R E Potoczak; Harvey R. Kaplan
Journal of Medicinal Chemistry | 1981
Robert F. Meyer; Ernest. Nicolaides; Francis G. Tinney; Elizabeth A. Lunney; Ann Holmes; Milton Louis Hoefle; Ronald D. Smith; Arnold D. Essenburg; Harvey R. Kaplan; Ronald G. Almquist
Journal of Medicinal Chemistry | 1982
Ronald G. Almquist; Jac Crase; Clive Jennings-White; Robert F. Meyer; Milton Louis Hoefle; Ronald D. Smith; Arnold D. Essenburg; Harvey R. Kaplan