Arterial System

Due to the pivotal role of platelets in thrombus formation, especially in the arterial system, inhibition of platelet function has become a central pharmacological approach. Antiplatelet drugs are given in order to prevent and treat thromboembolic diseases such as coronary heart disease, peripheral and cerebrovascular disease. They have also revolutionized the procedures of invasive coronary interventions as they reduce the risk of restenosis and thrombosis. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Thrombosis is the development of a thrombus , consisting of platelets, fibrin, red and white blood cells in the arterial or venous circulation. Platelet-rich white thrombi are found in the arterial system and can be prevented by antiplatelet drugs. 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

Compare the functions of the arterial system and venous system... 

A marker substance is injected into a central vein. A peripheral arterial line is used to measure the amount of the substance in the arterial system. A graph of concentration versus time is produced and patented algorithms based on the Stewart-Hamilton equation (below) are used to calculate the cardiac output. 

Atherosclerosis is a condition of the organism characterized by elevated levels of atherogenic lipoproteins in blood plasma, lipid deposits (including cholesterol) in the form of esters inside walls of the arterial system, and it is expressed by a gradual difficulty of blood circulation. The most appropriate name for this disease is lipoproteinemia. Clinically, it is manifested in the form of ischemic heart disease, stroke, abnormal cerebral blood flow, and peripheral ischemia. 

It is by no means impossible that the overall effect of oral contraceptives on the arterial system is exercised through a complex of different mechanisms. In this respect it is worth recalling the insulin resistance syndrome or metabolic syndrome, which comprises a set... 

Fig. 17.2. a Superficial arteries of the spinal cord. X-ray film of an injected specimen in a.p. view. The anterior spinal artery system is visible on the ventral surface of the cord, b Intrinsic spinal cord arteries. X-ray microangiogram of a transverse section (lumbar enlargement). The sulcal or central artery within the anterior fissure (arrow) is dominant. Note the posterior and posterolateral spinal arteries at both sides of the posterior root entry zone (arrowheads). AST, anterior spinal artery... 

Fig. 17.3. Selective spinal DSA in a 59-year-old woman, p.a. projection. Injection of the 12th left thoracic segmental artery. Filling of the radiculomedullary arteries T12 and T10 on the left side (arrows) and the anterior spinal artery system. Collateral filling of the right-sided segmental arteries via retrocorpo-ral anastomoses (arrowheads). These extradural anastomoses can compensate for focal vessel occlusions at the level of the radicular artery...

Selective spinal DSA has a better spatial resolution and plays a main role in the exclusion of spinal vascular malformations. In selected cases affection of the radicular artery and occlusion of the anterior spinal artery system can be demonstrated as well as collateral supply even in the later course of the ischemia (Mull et al. 2002). Thus, spinal DSA helps to identify pathologic vascular conditions in spinal cord ischemia. The main indication remains to exclude a spinal vascular malformation. Angiographic information about the acute phase of spinal cord ischemia is not yet available. 

We know from studies of hypertensive animals that blockage of fluid flow in the arterial system not only increases blood pressure but leads to vessel dilation and increases in wall thickness. There appears to be a direct relationship between external (increased blood pressure) mechanical stimulation and up-regulation of mechanochemical transduction processes by increasing the tensile loads that are placed on collagen fibers. This increase in external mechanical stimulation is then directly transferred to smooth muscle cells within the vessel wall. Increased tensile forces lead to increased activation of MAPK pathways as discussed in Chapter 9. We now have the beginning information that details how external mechanical loading influences tissue growth and development. 

In CHF, the impaired contractile function of the heart is exacerbated by compensatory increases in both preload and afterload. Preload is the volume of blood that fills the ventricle during diastole. Elevated preload causes overfilling of the heart, which increases the workload. Afterload is the pressure that must be overcome for the heart to pump blood into the arterial system. Elevated afterload causes the heart to work harder to pump blood into the arterial system. Vasodilators are useful in reducing excessive preload and afterload. Dilation of venous blood vessels leads to a decrease in cardiac preload by increasing venous capacitance arterial dilators reduce systemic arteriolar resistance and decrease afterload. 

Compared to the arterial system, it seems to be more difficult to develop a thrombosis model in venous... 

Afterload refers to the load on the contracting ventricle created by the resistance to the blood injected by the ventricle into the arterial system, i.e. the total peripheral resistance. Afterload is thus a pressure load and is excessive, e.g. in arterial h)rpertension. 

Takasakl, S., Hano, H. Three-dimensional observations of the human hepatic artery (Arterial system in the hver). J. Hepatol. 2001 34 455-466... 

Impressive images of portal arteries and hepatic veins can be produced by MR angiography. (131, 152) Nowadays, CM-supported MRA is the method of choice in monitoring the portal artery system (primarily before and after TIPS insertion). (152)... 

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