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Contextualizes 50 years of vascular biology progress for clinicians; leaves open translation into future research priorities.
It is an interesting endeavor to review progress in a field that did not exist 50 years ago in the present context of the term “vascular biology.” Certainly, in 1950, there was basic understanding of the role of arteries and veins in cardiovascular physiology and of capillaries in gas and nutrient transport. Furthermore, there was considerable clinical knowledge about the role of atherosclerosis in ischemia and infarction of the heart and other organs and that of hypertension in inducing microvascular damage and organ failure, particularly in the kidney. “Vascular biology,” which connotes the study of the biology of the constituent cells of the normal and diseased vascular wall, first gained some currency in the 1970s in defining this new field of study, which has enjoyed explosive growth in the past 25 years. Thus, the state of knowledge in 1950 must be placed in the modern context inferentially. The vascular smooth muscle cell was appreciated for its role in controlling vascular tone in the resistance arteries. Nitroglycerin had been known for decades to relieve angina pectoris, and Osler had speculated about the role of vasospasm in precipitating ischemia and infarction. It was presumed, although not generally specifically stated, that hypercontractility of a particular coronary artery segment was being invoked, inferentially indicting the vascular smooth muscle cells. The endothelium was known to be a nonthrombogenic surface, although little was understood of the underlying molecular mechanisms. Conversely, acute cardiovascular ischemic events, such as stroke and myocardial infarction, were known to be associated frequently with localized arterial thrombus formation. As alluded to above, investigators knew that hypertension damaged blood vessels but did not know the specific mechanisms involved. Finally, investigators knew that atherosclerosis itself involved inflammatory cell and lipid accumulation in the arterial wall, although their mechanisms of entry were not known. These facts …
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Alexander et al. (2000) studied this question.
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