Conservation of sodium and water during hemorrhage is mediated by an increase in the levels of aldosterone and antidiuretic hormone. Stretch receptors in the afferent arterial walls of the juxtaglomerular apparatus (JGA) respond to a drop in blood pressure by stimulating an increase in renin secretion. Renin converts angiotensinogen to angiotensin I, which is then converted in the lung and liver to angiotensin II. The effects of angiotensin II include intense vasoconstriction of arteriolar smooth muscle and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is also secreted in response to elevation of potassium and adrenocorticotropic hormone (ACTH) levels, both of which occur during acute hemorrhage. Aldosterone increases the reabsorption of sodium and the excretion of potassium in the distal convoluted tubule. Water passively follows sodium and is therefore reabsorbed and conserved. Aldosterone also stimulates the secretion of hydrogen ions, thus decreasing acidosis.
Osmo- and baroreceptors also regulate the release of arginine vasopressin or antidiuretic hormone (ADH), which is synthesized in the hypothalamus and stored in the posterior pituitary. Release of ADH occurs in response to both a fall in blood pressure and a decrease in sodium concentration. ADH increases the permeability of the renal distal tubule collecting ducts, and loop of Henle to NaCl and water, with the net result being fluid and salt retention. In higher concentrations, ADH also acts as a vasoconstrictor.
Acute hemorrhage causes local activation of the coagulation system. In response to injury, affected blood vessels contract, and activated platelets rapidly adhere to the edges of the damaged vessels. Platelets release thromboxane A2, which is a potent local vasoconstrictor and further platelet activator. Platelets form an unstable jelly-like plug during the first 20 min after injury. Control of hemorrhage during this period depends upon a regional reduction in flow caused by systemic hypotension and local vasoconstriction. Vessel injury exposes collagen and releases tissue thromboplastin, causing fibrin deposition in the platelet plug and gradual formation of a stable clot. The entire process for complete fibrinous transformation takes approximately 24 h.
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