The scarring of the liver acini (Cirrhosis)

Abstract

Cirrhosis is defined as the scarring of the liver acini in zone 3, zone 1 or in both; the resulting nodules are scarred and modified remnants of acini of various orders. The division of the nodules into "micronodules" and "macronodules" is difficult to justify as their two dimensional appearance changes at different planes of section. Early scar formation precedes changes in the microcirculatory dynamics. Sprouting of vascular branches, especially of arterioles, takes the leading role in the development of mature scars, i.e. of fibro-vascular membranes. The fibrous repair is at the same time the road builder for collateral flow. The pathophysiology of the collateral circulation is the basic determinant in the formation of the cirrhotic patterns. The three microcirculatory phases in the cirrhotic process are due to a changeover of the intrahepatic circulatory path from the normal trichotomy of the preterminal vascular branches to convoluted collateral channels. The three phases of the cirrhotic process are: The Triadal Nodule. It receives blood from the TPV and THA and from the perinodular plexus. The nodular parenchyma may already be segregated from the ThV, a situation that leads to portal hypertension. The Para-triadal Nodule. It is a conglomerate of nodules that often are not completely separated from each other; they are derived from neighbouring acini of various orders which receive blood from large triads contained in the perinodular scar. The blood arrives into the sinusoids primarily via the perinodular plexus. Some sinusoids may receive additional blood through sclerosing remnants of terminal afferent branches and through irregular vascular twigs which, along with septa, enter the nodules at various sites. The A-triadal Nodule. It is completely separated from neighbouring nodules by thick scars, its parenchyma totally segregated from afferent and efferent vascular branches. The nodules receive blood only from a dense perinodular plexus of wide capillaries.

Interaction of human liver connective tissue cells, skin fibroblasts and smooth muscle cells with collagen gels

“…Similar interfaces are observed between regenerative nodules and surrounding tissues in cirrhosis (24). The formation of active fibrous septa may thus represent the LCTC populations spreading and migrating along discontinuous interfaces of extracellular matrix.…”

The carvacrol ameliorates acute pancreatitis-induced liver injury via antioxidant response

“…Oxidative stress may stimulate both the accumulation of collagen and extracellular matrix deposition (Kroy et al 2014). Rappaport et al (1983) reported that liver injuries induced changes in microcirculation that were associated with collagen deposition and consequently fibrosis. Acute pancreatitis is considered as high risk factor for vascular disorders (Björk and Arfors 1982).…”

Decreased S100B expression in chronic liver diseases

“…The proliferated Schwann cells seemed to form a scaffold guiding regenerating nerve fibers [19]. Considering that the noradrenergic fibers run along blood vessels, changes in vascular patterns may also alter hepatic innervation patterns [19,20]. Moreover, scar formation, with changes in the microcirculatory dynamics could influence nerve regeneration [20], and changes in vascularity and inflammation can affect nerve expression [19,21].…”