Blood flow in the splanchnic circulation is often compromised in individuals experiencing severe blood loss due to trauma. A clinical problem that can result from the prolonged ischemic perfusion of the gut is pulmonary edema or adult respiratory distress syndrome. This condition, which is often fatal, results from the massive release of inflammatory mediators, bacterial toxins, and other noxious agents into the systemic circulation after gut blood flow is restored by volume resuscitation. These mediators and toxins promote the activation and sequestration of circulating leukocytes in the lung, which results in microvascular injury and excess accumulation of edema fluid in the air spaces. These fluid-filled lungs have a diminished capacity to oxygenate blood.
receptors because they are responsive to pressures several times lower than those in the systemic arteries. These atrial receptors are also often referred to as volume receptors because venous pressure is primarily dependent on total blood volume and because their primary role is to help control blood volume rather than arterial pressure. But, as you will recall, blood volume is a primary determinant of cardiac output and, thus, arterial pressure. A fall in atrial pressure initiates a reflex release of antidiuretic hormone (also known as vasopressin) from the hypothalamus. Antidiuretic hormone causes the kidney to reabsorb filtered fluid at the level of the collecting ducts. Stimulation of the low-pressure receptors also causes constriction of the afferent renal arterioles, and consequently reduces the glomerular filtration rate, by a neural reflex. Both effects reduce fluid loss at the kidneys, which in turn increases blood volume. Vasopressin also constricts arteriolar and
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