The posterior pituitary gland secretes vasopressin (antidiuretic hormone), a strong vasoconstrictor, in response to hemorrhage (see 41). As arterial blood pressure decreases, the plasma concentration of vasopressin progressively rises (Fig. 19.23). The release of vasopressin is stimulated by the aortic arch and carotid sinus baroreceptors (high pressure) as well as the stretch receptors in the left atrium (low pressure).

Hemorrhagic hypotension leads to diminished renal perfusion, which triggers the secretion of renin from the juxtaglomerular apparatus (see Chapter 35). Renin acts on angiotensinogen, a plasma protein, to produce the decapeptide angiotensin I. Angiotensin I is further cleaved by angiotensin-converting enzyme to form the active octapeptide angiotensin II, a powerful vasoconstrictor.

During hemorrhage, the kidneys conserve fluid and electrolytes in response to various stimuli. These stimuli include increased vasopressin secretion (as mentioned earlier, see Fig. 19.23) and increased renal sympathetic nerve activity, which enhances NaCl reabsorption by the nephron, leading to decreased excretion. The reduced arterial pressure decreases the glomerular filtration rate, further reducing the excretion of water and electrolytes. Additionally, elevated levels of angiotensin II stimulate the release of aldosterone from the adrenal cortex. Aldosterone promotes NaCl reabsorption by the nephrons, contributing to decreased NaCl and water excretion (see also Chapter 35).

In contrast to negative feedback mechanisms, hemorrhage also triggers latent positive feedback mechanisms that amplify the primary change caused by blood loss. These positive feedback mechanisms exacerbate hypotension and can initiate vicious cycles, potentially leading to death.

The occurrence of a vicious cycle depends on the gain of the positive feedback mechanism. Gain refers to the ratio of the secondary change caused by the mechanism to the initial change itself. A gain greater than 1 initiates a vicious cycle, while a gain less than 1 does not. Consider a positive feedback mechanism with a gain of 2. If arterial pressure decreases by 10 mm Hg, the positive feedback mechanism with a gain of 2 would induce a secondary pressure reduction of 20 mm Hg. This further decrease would lead to an additional reduction of 40 mm Hg. Each subsequent change would be twice as significant as the previous one, resulting in a continuous and accelerating decline in arterial pressure until death occurs. This process is illustrated in curve B in Fig. 19.20.

Conversely, a positive feedback mechanism with a gain of 0.5 also amplifies any change in arterial pressure, but it may not necessarily lead to death. If arterial pressure suddenly decreases by 10 mm Hg, the positive feedback mechanism would initiate a secondary fall of an additional 5 mm Hg. This decrease would then provoke a further decrease of 2.5 mm Hg, and the process would continue in diminishing steps until arterial pressure approaches an equilibrium value.
Vasopressin (antidiuretic hormone), a potent vasoconstrictor, is secreted by the posterior pituitary gland in response to hemorrhage (see 41).
The plasma concentration of vasopressin rises progressively as arterial blood pressure diminishes (
Fig. 19.23 ). The receptors responsible for the augmented release of vasopressin are the aortic arch and carotid sinus baroreceptors (high pressure) and stretch receptors in the left atrium (low pressure).
The diminished renal perfusion during hemorrhagic hypotension leads to the secretion of renin from the juxtaglomerular apparatus (see
Chapter 35).
This enzyme acts on a plasma protein, angiotensinogen, to form the decapeptide angiotensin I, which in turn is cleaved to the active octapeptide angiotensin II by angiotensin-converting enzyme; angiotensin II is a very powerful vasoconstrictor.
Renal Conservation of Salt and Water
Fluid and electrolytes are conserved by the kidneys during hemorrhage in response to various stimuli, including increased secretion of vasopressin, as noted previously (see
Fig. 19.23 ), and increased renal sympathetic nerve activity, which enhances NaCl reabsorption by the nephron (decreased excretion). The lower arterial pressure decreases •Fig. 19.22 Changesinarterialbloodpressureandplasmacolloid osmoticpressureinresponsetowithdrawalof45%oftheestimated•Fig. 19.23 Meanpercentagechangesinarterialbloodpressureandbloodvolumeovera30-minuteperiod,beginningattime0.(Redrawnplasmavasopressinconcentrationinresponsetobloodloss.(RedrawnfromZweifachBW.Anesthesiology. 1974;41:157.)fromShenYT,etal.Circ Res. 1991;68:1422.) the glomerular filtration rate, which also curtails the excretion of water and electrolytes. In addition, the elevated levels of angiotensin II, as described earlier, stimulate the release of aldosterone from the adrenal cortex. Aldosterone, in turn, stimulates reabsorption of NaCl by the nephrons. Thus NaCl and water excretion is decreased (see also
Chapter 35).
In contrast to negative feedback mechanisms, hemorrhage also evokes latent positive feedback mechanisms. These mechanisms exaggerate any primary change initiated by the blood loss. Specifically, positive feedback mechanisms aggravate the hypotension induced by blood loss and tend to initiate vicious cycles, which may lead to death.
Whether a positive feedback mechanism will lead to a vicious cycle depends on the gain of that mechanism. Gain is the ratio of the secondary change evoked by a given mechanism to the initiating change itself. A gain greater than 1 induces a vicious cycle; a gain of less than 1 does not. Consider a positive feedback mechanism with a gain of 2. If Pa were to decrease by 10 mm Hg, a positive feedback mechanism with a gain of 2 would then evoke a secondary reduction in pressure of 20 mm Hg, which in turn would cause a further decrease of 40 mm Hg. Thus each change would induce a subsequent one that is twice as great. Hence, Pa would decline at an ever-increasing rate until death occurred. This process is depicted in curve B in
Fig. 19.20
Conversely, a positive feedback mechanism with a gain of 0.5 also exaggerates any change in Pa, but the change would not necessarily lead to death. If arterial pressure suddenly decreased by 10 mm Hg, a positive feedback mechanism would initiate a secondary, additional fall of 5 mm Hg. This decrease, in turn, would provoke a further decrease of 2.5 mm Hg. The process would continue in ever-diminishing steps until arterial pressure approached an equilibrium value.