Liver vasculature

Fig. 7. (XiA-AR expression in mouse liver vasculature. The a1A-AR is expressed in the various blood vessels of the mouse liver. The a1A expression was not found in the hepatocyte. Original magnification x40.

Occlusion of portal branches of the liver parenchyma to be resected redistributes the totality of its portal blood flow, and consequently all its hepatotrophic contents, towards the FRL. This is the basic rationale of the method that triggers off regenerative activity of the nonembolized portion of the liver. Moreover, PVE dilates the portal branches in the FRL, exposing liver vasculature to stretch stress which act as a trigger for IL-6 release from endothelial cells and contribute to the activation of regenerative cascade in the FRL [26]. Induction of heat shock protein in the nonembolized lobe is supposed to have similar effects [40]. PVE also acts through two potentially complementary pathways specifically related to embolization ischemia and inflammation. With most of the embolic agents, PVE induces a mild ischemia apoptosis or necrosis of some hepatocytes, and intercellular disjunction. 

Choi B, Kim TK, Han JK, et al. Power versus conventional color Doppler sonography comparison in the depiction of vasculature in liver tumors. Radiology 1996 200 55-58. 

Mechanism of Action An alpha-adrenergic agonist that stimulates alphaj-adrenergic receptors. Inhibits sympatheticcardioaccelerat or and vasoconstrictor center to heart, kidneys, peripheral vasculature. Therapeutic Effect Decreases systolic, diastolic blood pressure (BP). Chronic use decreases peripheral vascular resistance. Pharmacohinetics Well absorbed from gastrointestinal (GI) tract. Widely distributed. Protein binding 90%. Metabolized in liver. Excreted in urine and feces. Not removed by hemodialysis. Half-life 6 hr. 

Figure 6.2 The vasculature supplying and draining the liver and its relationship to the systemic circulation. Source. From Ref. 3.

Occasionally toxic compounds can directly damage the hepatic sinusoids and capillaries. One such toxic compound is monocrotaline, a naturally occurring pyrrolozidine alkaloid, found in certain plants (Heliotropium, Senecio, and Crotolaria species). Monocrotaline (Fig. 7.7) is metabolized to a reactive metabolite, which is directly cytotoxic to the sinusoidal and endothelial cells, causing damage and occlusion of the lumen. The blood flow in the liver is therefore reduced and ischemic damage to the hepatocytes ensues. Centrilobular necrosis results, and the venous return to the liver is blocked. Hence, this is known as veno-occlusive disease and results in extensive alteration in hepatic vasculature and function. Chronic exposure causes cirrhosis. 

Both benign and malignant liver tumors may arise from exposure to hepatotoxins and can be derived from various cell types. Thus, adenomas have been associated with the use of contraceptive steroids and exposure to aflatoxin Bi, and dimethylnitrosamine can produce hepatocellular carcinomas, whereas vinyl chloride causes hemangiosarcomas derived from the vasculature (see chap. 7). 

Beta-2 Receptors. Beta-2 receptors are found primarily on the smooth muscle of certain vasculatures, the bronchioles, the gallbladder, and the uterus.9 Their presence in bronchiole smooth muscle is especially important in the pharmacologic management of respiratory conditions such as asthma (see Chapter 26). These receptors are also responsible for mediating changes in the metabolism of skeletal muscle and liver cells. Beta-2 receptors are also located on the heart, although the predominant effects on cardiac tissue seem to be mediated through the beta-1 subtype. 

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