The medullary vasomotor region is minimally affected by PaO2 levels. The primary impact of hypoxia is mediated by reflexes involving the carotid and aortic chemoreceptors. A moderate decrease in PaO2 stimulates the vasomotor region, while a severe decrease depresses vasomotor activity, similar to the depression seen in other brain regions under very low O2 tension.

Regulation of peripheral blood flow involves a balance between intrinsic and extrinsic factors. This dual control allows the body to redirect blood flow to areas with higher demands and away from areas with lower requirements. Some tissues have fixed effects from intrinsic and extrinsic mechanisms, while others have changeable ratios depending on tissue activity.

Cerebral ischemia, which can occur due to excessive pressure from an expanding intracranial tumor, leads to a significant increase in peripheral vasoconstriction. This stimulation is likely caused by the accumulation of CO2, reduction in O2, and possibly excitation of intracranial baroreceptors. Prolonged and severe ischemia eventually results in central depression and a decrease in blood pressure.

In vital structures like the brain and heart, which have limited tolerance for reduced blood supply, intrinsic flow-regulating mechanisms are dominant. For example, a massive discharge of the vasoconstrictor region through sympathetic nerves has minimal effects on cerebral and cardiac resistance vessels, while cutaneous, renal, and splanchnic blood vessels constrict significantly.

Extrinsic vascular control is dominant in the skin. Cutaneous vessels not only strongly participate in general vasoconstriction but also respond selectively via hypothalamic pathways to regulate heat loss and conservation for body temperature regulation. However, local temperature changes can elicit intrinsic control that modifies or overrides central influence on resistance and capacitance vessels.

In skeletal muscle, both extrinsic and intrinsic mechanisms interact. Neural control (vasoconstrictor tone) is dominant in resting skeletal muscle, as evidenced by the large increase in blood flow after sympathetic nerve section. During exercise, intrinsic flow-regulating mechanisms take control, resulting in vasodilation in active muscles due to local metabolite increase. Inactive tissues experience vasoconstriction as a result of general sympathetic discharge. However, the local metabolic effect overrides constrictor impulses in active muscles, increasing blood flow where needed and diverting it from relatively inactive areas.

Similar effects can be observed in response to increased PCO2 levels. Normally, exercise-induced hyperventilation maintains normal PCO2 levels. However, elevated PCO2 would lead to generalized vasoconstriction due to CO2 stimulation of the medullary vasoconstrictor region. In active muscles, where CO2 levels would be highest, arteriolar smooth muscle would relax in response to local PCO2. Factors that impact and are impacted by the vasomotor region are summarized as well.
PaO2 has little direct effect on the medullary vasomotor region. The primary effect of hypoxia is mediated by reflexes via the carotid and aortic chemoreceptors. A moderate reduction in PaO2 stimulates the vasomotor region, but a severe reduction depresses vasomotor activity in the same manner by which other areas of the brain are depressed by very low O2 tension.
Balance Between Extrinsic and Intrinsic Factors in Regulation of Peripheral Blood Flow
Dual control of peripheral vessels by intrinsic and extrinsic mechanisms evokes a number of important vascular adjustments. Such regulatory mechanisms enable the body to direct blood flow to areas where it is most needed and away from areas that have fewer requirements. In some tissues, the effects of the extrinsic and intrinsic mechanisms are fixed; in other tissues, the ratio is changeable and depends on the state of activity of that tissue.
Cerebralischemia,whichmayoccurbecauseofexcessivepressureexertedbyanexpandingintracranialtumor,resultsinamarkedincreaseinperipheralvasoconstriction.ThestimulationisprobablycausedbylocalaccumulationofCO2andareductioninO2andpossiblybyexcitationofintracranialbaroreceptors.Withprolonged,severeischemia,centraldepressioneventuallysupervenes,andbloodpressurefalls.
CHAPTER 18 Regulation of the Heart and Vasculature
In the brain and heart, which are vital structures with limited tolerance for a reduced blood supply, intrinsic flow-regulating mechanisms are dominant. For instance, massive discharge of the vasoconstrictor region via the sympathetic nerves, which might occur in severe, acute hemorrhage, has negligible effects on the cerebral and cardiac resistance vessels, whereas the cutaneous, renal, and splanchnic blood vessels become greatly constricted.
In the skin, extrinsic vascular control is dominant. The cutaneous vessels not only participate strongly in a general vasoconstrictor discharge but also respond selectively via hypothalamic pathways to subserve the functions of heat loss and heat conservation required for regulation of body temperature. However, intrinsic control can be elicited by local temperature changes that modify or override the central influence on resistance and capacitance vessels (see also
In skeletal muscle, the extrinsic and intrinsic mechanisms interact. In resting skeletal muscle, neural control (vasoconstrictor tone) is dominant, as can be demonstrated by the large increase in blood flow that occurs immediately after section of the sympathetic nerves to the tissue. After the onset of exercise, the intrinsic flow-regulating mechanism assumes control, and vasodilation occurs in the active muscles because of the local increase in metabolites. Vasoconstriction occurs in the inactive tissues as a manifestation of the general sympathetic discharge. However, constrictor impulses that reach the resistance vessels of the active muscles are overridden by the local metabolic effect. Operation of this dual control mechanism thus increases blood flow where it is required and shunts it away from relatively inactive areas (see also
Chapter 17).
Similar effects may be achieved in response to an increase in PCO2. Normally, the hyperventilation associated with exercise keeps PCO2 at normal levels. However, if PCO2 is increased, generalized vasoconstriction would occur because CO2 stimulates the medullary vasoconstrictor region. In active muscles, where [CO2] would be highest, the smooth muscle of the arterioles would relax in response to the local PCO2. Factors that affect and are affected by the vasomotor region are summarized in