The migratory and proliferative activities of SMCs are regulated by numerous factors. Among the most important pro–growth factors are platelet-derived growth factor (PDGF), endothelin, thrombin, fibroblast growth factors, and inflammatory mediators such as interferon-γ (IFN-γ) and interleukin-1 (IL-1). Factors that maintain SMCs in a quiescent state include heparan sulfate, NO, and transforming growth factor-α (TGF-α).
Allvesselsarelinedbyendothelium;althoughallECssharecertainhomeostaticproperties,ECsinspecificvascularbedshavespecialfeaturesthatallowfortissue-specificfunctions(e.g.,fenestratedECsinrenalglomeruli).
TherelativeSMCandECMcontentofvesselwalls(e.g.,inarteries,veins,andcapillaries)variesaccordingtohemodynamicdemands(e.g.,pressure,pulsatility)andfunctionalrequirements.
ECfunctionistightlyregulatedinboththebasalandactivatedstates.VariousphysiologicandpathophysiologicstimuliinduceendothelialactivationanddysfunctionthataltertheECphenotype(e.g.,procoagulativeversusanti-coagulative,proinflammatoryversusanti-inflammatory,nonadhesiveversusadhesive).
Although rarely symptomatic, unusual anatomic variants of blood vessels can cause complications during surgery, as may occur when a vessel in an unexpected location is injured. Cardiac surgeons and interventional cardiologists also must be familiar with coronary artery variants that can occur in up to 1% to 5% of patients. Among the other congenital vascular anomalies, three deserve further mention:
Berry aneurysms are thin-walled arterial outpouchings in cerebral vessels, classically at branch points around the circle of Willis; they occur where the arterial media is congenitally attenuated and can spontaneously rupture causing fatal intracerebral hemorrhage (Chapter 23).
Arteriovenous (AV) fistulas are abnormal connections between arteries and veins without an intervening capillary bed. They occur most commonly as developmental defects but can also result from rupture of arterial aneurysms into adjacent veins, from penetrating injuries that pierce arteries and veins, or from inflammatory necrosis of adjacent vessels. AV fistulas can be created surgically to provide vascular access for hemodialysis. Extensive AV fistulas can cause high-output cardiac failure by shunting large volumes of blood from the arterial to the venous circulation.
Fibromuscular dysplasia is a focal irregular thickening of the walls of mediumand large-sized muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture.
Systemic and local blood pressure must be maintained within a narrow range to maintain health. Low blood pressure (hypotension) results in inadequate organ perfusion, organ dysfunction, and sometimes tissue death. Conversely, high blood pressure (hypertension) causes vessel and end-organ damage and is one of the major risk factors for atherosclerosis (see later).
Blood pressure is a function of cardiac output and peripheral vascular resistance, both of which are influenced by multiple genetic and environmental factors (Fig. 10.3 ). The integration of the various inputs ensures adequate systemic perfusion, despite regional demand differences.