By Robert Charlier
If the various healing acquisitions of the earlier few years have enriched very varied fields of human pathology, it does appear that coronary pathology has been given very precise awareness, as witness the big variety of antianginal medicinal drugs positioned on the disposal of the scientific career. there are numerous causes for this scenario, certainly one of them most likely being that the medica tions successively proposed don't absolutely fulfill the practitioner and one other that the entire variety of participants struggling with the clinicaI manifestations of heart illness deals, via its dimension, an unlimited revenue capability for the pharma ceuticaI undefined. This box of purposes opens up such customers that it has inspired a prolific quantity of festival among quite a few examine laborato ries, and it's no exaggeration to assert that each significant company has its individuaI anti anginaI drug in its healing cataIogue. an extra issue has aIso contributed significantly to this proliferation of medi cinal arrangements meant for the remedy of angina pectoris: this can be the speedy increase in our knowIedge of the physiopathoIogy of angina, which in flip has produced originaI strategies of pharmacological and biochemical examine. hence, there have emerged new components whose motion mechanisms have claimed to be most fitted to the cardiovascular issues chargeable for cardiac discomfort.
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Additional info for Antianginal Drugs: Pathophysiological, Haemodynamic, Methodological, Pharmacological, Biochemical and Clinical Basis for Their Use in Human Therapeutics
In 12 dogs, foree-veloeity relations were determined during the inseription of ventrleular funetion eurves and in every instance when depressed funetion was evident from the ventrieular funetion eurve, the simultaneously determined foree-veloeity eurve also demonstrated impaired performance. Cardiac Dynamics During the Anginal Attack 31 since this work does not inerease signifieantly in spite of a markedly inereased left ventrieular filling pressure. In a subsequent publleation  PARKER points out that stroke work of the left ventricle decreases, whieh would indieate, in the llght of the faet that the end-diastoHe pressure does not deerease in the same proportions, that the ischaemie ventriele of the angina subjeet works to a depressed funetional eurve as eompared with that of a normal ventricle.
Both adrenaline and noradrenaline inerease [1523, 225 e] 12, a faet whieh has all the more elinieal value in that it does not appear in the normal subjeet undergoing identieal museular exereise . It thus provides the proof that hyperaetivity of the sympathetie system would appear to be a elinieal feature of angina peetoris. These facts led RAAB to suggest that the triggering faetors in angina set up a eondition of hypersympathieotony leading to the release of eateehoIamines from the surrenaI gIands and the sympathetie nerve endings in the myoeardium.
ELLIOTT and GORLIN further point out that, during eertain attaeks, the eoronary vaseular system takes part in this eonstrietion, sinee the arterial supply of oxygen to the eardiae musele is redueed whereas its oxygen requirements are greater. Ineidentally, these phenomena are identieal to those observed during an intravenous perfusion of noradrenaline in man , beeause the resulting inerease in myoeardial oxygen eonsumption is not aeeompanied by a lowering of eoronary resistanee but by a rise in the oxygen extraetion eoeffieient, whieh indieates that the oxygen requirements are not covered by an adequate inerease in eoronary How.