Download Antianginal Drugs: Pathophysiological, Haemodynamic, by Robert Charlier PDF

By Robert Charlier

If the various healing acquisitions of the prior few years have enriched very diverse fields of human pathology, it does appear that coronary pathology has been given very particular cognizance, as witness the wide range of antianginal medicines positioned on the disposal of the clinical career. there are numerous causes for this scenario, one among them most likely being that the medica tions successively proposed don't absolutely fulfill the practitioner and one other that the entire variety of contributors struggling with the clinicaI manifestations of heart ailment bargains, by way of its dimension, an enormous revenue power for the pharma ceuticaI undefined. This box of purposes opens up such clients that it has inspired a prolific quantity of pageant among quite a few learn laborato ries, and it's no exaggeration to claim that each significant company has its individuaI anti anginaI drug in its healing cataIogue. yet another issue has aIso contributed tremendously to this proliferation of medi cinal arrangements meant for the remedy of angina pectoris: this can be the speedy develop in our knowIedge of the physiopathoIogy of angina, which in flip has produced originaI thoughts of pharmacological and biochemical learn. therefore, there have emerged new elements whose motion mechanisms have claimed to be most suitable to the cardiovascular issues answerable for cardiac discomfort.

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Extra resources for Antianginal Drugs: Pathophysiological, Haemodynamic, Methodological, Pharmacological, Biochemical and Clinical Basis for Their Use in Human Therapeutics

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Such a ehange would inerease myoeardial fiber length whieh, by the LAPLACE relation, would raise oxygen eonsumption. This rise would be in addition to the normal heightening in left ventrieular oxygen requirements during exereise related to the eateeholamine release, inerease in heart rate, systemie pressure and rate offiber shortening [1116, 1789]. There was also elear evidenee of depressed left ventrieular funetion during myoeardial isehaemia indueed by pacing. Sinee there was no ehange in eardiae index and only minor ehanges in systemie pressure, there was an associated deciine in stroke index and left ventrieular stroke work inversely related to the change in heart rate.

These cardiovascWar effects of adrenaline are virtually identical to the ehanges in coronary circulation occurring during exercise. It has also been shown that the intracoronary injection of nitroglycerin increases by 50% the eoronary flow of the angina patient where a coronarography has revealed the presence of advanced stenotic atherosclerosis [146]. 4% after 90 see (see p. 126). Finally, CONTI et al. [3d] published in 1970 an interesting report dealing with the behaviour of myoeardial blood flow during angina whieh was provoked in patients with eoronary artery disease by speeding up the heart rate by atrial pacing.

Sinee eonventional inert gas measurements of eoronary blood flow have shown no differenee between patients with and without eoronary artery disease, the possibility that a differenee exists but has been masked by methodologieal diffieulties was evaluated using multiple gas traeers, variable saturation periods and ehromatographie measurements of blood traeer eoneentrations. Arterial and eoronary sinus desaturation eurves were obtained after 2-20 minute exposures to various combinations of helium, neon, hydrogen, methane, argon, krypton and nitrous oxide.

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