Jaundice, the circulation and the kidney.
(Fig. 1) Cholemia per se (i.e. independent of parenchymal liver damage) causes a profound disturbance of systemic hemodynamics. This includes decrease in total peripheral vascular resistance, and possible impairment of left ventricular performance. These, in turn, lead to a decrease in effective blood volume, a tendency to hemorrhagic shock and prerenal failure. Early in the course of cholemia , the natriuretic effects of bile salts in the circulation may aggravate the hypovolemia. In marked contrast to the decrease in total peripheral vascular resistance, the regional vascular beds of the kidney and the brain constrict during cholemia . The combined effect of cholemia may thus lead to redistribution of cardiac output away from the kidney and the brain. When parenchymal liver damage complicates obstructive jaundice, the tendency to arterial hypotension is aggravated. The overall interrelationship between jaundice and circulatory homeostasis is depicted in figure 1.
D000818:Animals; D001646:Bile / Q000502:physiology; D001647:Bile Acids and Salts / Q000502:physiology; D001775:Blood Circulation; D002319:Cardiovascular System / Q000503:physiopathology; D002779:Cholestasis / Q000503:physiopathology*; D004195:Disease Models, Animal; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D007668:Kidney / Q000503:physiopathology*; D010215:Papio; D011817:Rabbits; D051381:Rats
D001647:Bile Acids and Salts