Titlebook: Acute Coronary Care; Principles and Pract Robert M. Califf,Galen S. Wagner Book 1985 Martinus Nijhoff Publishing, Boston 1985 angina pector

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Getting Rid of Motion Sickness,on, (b) with coronary stenosis, and (c) in those having functional collateral vasculature. The control of coronary vasomotion during normal and pathologic states by both metabolic and neurogenic mechanisms is not discussed. In the past five years, there have been two excellent review articles [1,2]

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Telematics and Communication Fundamentals,hich ischemic cell injury becomes irreversible, and the ultimate infarct size remain incompletely understood. These interrelationships have been difficult to evaluate in patients and must be inferred in large part from animal studies. This chapter considers collateral coronary blood flow as a determ

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Telematics and Communication Fundamentals,d to ADP by energy-consuming reactions, and the ADP thus formed can either be rephosphorylated to ATP or can be metabolized to nucleosides and bases that can diffuse out of the myocyte. A constant supply of purine substrate is necessary to ensure that ADP is available for phosphorylation either by o

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Autonomous Vehicles and the Lawn 1809 [1] suspected coronary artery spasm as a cause of angina pectoris, until Sir William Osier in 1910 stated that he could not think of a better explanation of anginal pain [2], coronary artery spasm was believed to be the primary mechanism underlying acute myocardial ischemia. The pendulum bega

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