Endocrine control of plasma protein and volume

Abstract

The loss of blood volume initiates a sequence of events that begin with detection of the volume loss by cardiovascular receptors and the transmission of the signals of that loss to the central nervous system. Central neural processing leads to the release of multiple hormones that act together to induce an increase in extracellular osmolality. In response to the increase in extracellular osmolality, fluid shifts from cells to the interstitium, increasing intersititial volume and pressure. The increase in interstitial pressure leads to increased capillary and lymphatic return of fluid and to increased lymphatic return of preformed albumon. These events combine to form the second definitive phase of the restitution of blood volume, which is crucial both for the support of critical cardiovascular function and for the inhibition of the initial neuroendocrine response. If left unabated, this response may lead to the detrimental features of the metabolic response to injury. The degree of hyperosmolality following volume loss in injury may serve as an index of severity of that injury. The presence of the mechanism outlined provides a further rationale arguing in favor of prompt and adequate fluid therapy of the injuried and volume-depleted patient.