During hemorrhage, the stimulation of the carotid baroreceptors is decreased due to reductions in Pa and pulse pressure. This leads to various cardiovascular responses that aim to restore arterial pressure to normal levels. These responses include a decrease in vagal tone and an increase in sympathetic tone, resulting in an increased heart rate and enhanced myocardial contractility.

The increased sympathetic tone also causes generalized venoconstriction, which has similar hemodynamic effects as blood transfusion. This vasoconstriction acts as an autotransfusion, moving blood back into circulation. In humans, the major blood reservoirs include the cutaneous, pulmonary, and hepatic branches of the vasculature.

A significant response to reduced baroreceptor stimulation during hemorrhage is generalized arteriolar constriction. This reflexive increase in peripheral resistance helps minimize the decrease in arterial pressure caused by reduced cardiac output.

Figure 19.21 illustrates the impact of an 8% blood loss on mean aortic pressure under different conditions. When only the carotid sinus baroreceptors were operative (with the influence of aortic arch baroreceptors eliminated), the hemorrhage resulted in a 14% decrease in mean aortic pressure (Figure 19.21A). This reduction was not significantly different from the decline observed before vagotomy (12% decrease, not shown). When the carotid sinuses were denervated while the aortic baroreceptor reflexes remained intact, the 8% blood loss led to a 38% decrease in mean aortic pressure (Figure 19.21B).

Therefore, the carotid sinus baroreceptors proved to be more effective than the aortic baroreceptors in attenuating the fall in pressure. However, when both sets of afferent baroreceptor pathways were interrupted (Figure 19.21C), an 8% blood loss resulted in a 48% reduction in arterial pressure.

Although arteriolar constriction is widespread during hemorrhage, it is not uniform. Vasoconstriction is most pronounced in the cutaneous, skeletal muscle, and splanchnic vascular beds, while it is minimal or absent in the cerebral and coronary circulations. In fact, in response to hemorrhage, cerebral and coronary vascular resistance may decrease. The reduced cardiac output is redirected to prioritize blood flow to the brain and heart.

In the early stages of mild to moderate hemorrhage, renal resistance undergoes only slight changes. The tendency for increased sympathetic activity to constrict the renal vessels is counteracted by autoregulatory mechanisms. However, with more prolonged and severe hemorrhage, renal vasoconstriction becomes intense.
The reductions in Pa and pulse pressure during hemorrhage decrease stimulation of the baroreceptors in the carotid •Fig. 19.21 Changes in Mean Aortic Pressure in Response to an 8% Blood Loss in Three Conditions. A, Thecarotidsinusbaroreceptorswereintactandtheaorticreflexeswereinterrupted.B, Theaorticreflexeswereintactandthecarotidsinusreflexeswereinterrupted.C, Allsinoaorticreflexeswereabrogated.(DatafromShepherdJT.Circulation. 1974;50:418.DerivedfromthedataofEdisAJ.Am J Physiol. 1971;221:1352.) ). Several cardiovascular responses are thus evoked, all of which tend to restore arterial pressure to the normal level. Such responses include reduction of vagal tone and enhancement of sympathetic tone, increased heart rate, and enhanced myocardial contractility.
The increased sympathetic tone also produces generalized venoconstriction, which has the same hemodynamic consequences as transfusion of blood (see
Fig. 19.9). Sym pathetic activation constricts certain blood reservoirs. This vasoconstriction acts as an autotransfusion of blood into the circulation. In humans, the cutaneous, pulmonary, and hepatic branches of the vasculature constitute the principal blood reservoirs.
Generalized arteriolar constriction is a prominent response to the reduced baroreceptor stimulation during hemorrhage. The reflex increase in peripheral resistance minimizes the fall in arterial pressure caused by the reduction in cardiac output.
Fig. 19.21 shows the effect of an 8% blood loss on mean aortic pressure. When both vagus nerves were cut to eliminate the influence of the aortic arch baroreceptors and only the carotid sinus baroreceptors were operative (see
Fig. 19.21A), this hemorrhage decreased mean aortic pressure by 14%. This pressure change did not differ significantly from the decline in pressure (12%) evoked by the same hemorrhage before vagotomy (not shown). When the carotid sinuses were denervated and the aortic baroreceptor reflexes were intact, the 8% blood loss decreased mean aortic pressure by 38% (see
Fig. 19.21B).
Hence, the carotid sinus baroreceptors were more effective than the aortic baroreceptors in attenuating the fall in pressure. However, when both sets of afferent baroreceptor pathways were interrupted (see
Fig. 19.21C), an 8% blood loss reduced arterial pressure by 48%.
Arteriolar constriction is widespread during hemorrhage but it is by no means uniform. Vasoconstriction is most pronounced in the cutaneous, skeletal muscle, and splanchnic vascular beds, and it is slight or absent in the cerebral and coronary circulations in response to hemorrhage. In many instances, cerebral and coronary vascular resistance is diminished. The reduced cardiac output is redistributed to favor flow through the brain and the heart.
In the early stages of mild to moderate hemorrhage, renal resistance changes only slightly. The tendency for increased sympathetic activity to constrict the renal vessels is counteracted by autoregulatory mechanisms (see ). With more prolonged and severe hemorrhage, however, renal vasoconstriction becomes intense.