Suggested Answers

Suggested answers:

1. In the normal person, resistance to blood flow is greatest in the arterioles (resistance vessels). However, in this patient the large arteries are severely blocked by disease, whereas the arterioles are probably maximally dilated because of the release of vasodilator metabolites from the muscle as a result of inadequate blood supply.

2. The vascular smooth muscle of the arteries is damaged by the disease process, but the smooth muscle of the arterioles is functional but relaxed because of the presence of vasodilator metabolites.

3. The arterioles of this patient would constrict in response to simulation of the sympathetic nerve fibers to the legs, and they would also constrict in response to norepineprhine, which is the neurohumor released by the sympathetic nerve endings in the blood vessels.

4. Calcium is the ion of greatest importance in contraction of vascular smooth muscle, just as it is for other smooth muscle and for skeletal and cardiac muscle.

5. When stimulated by such agents as acetylcholine or ATP or by shear stress, the endothelium can synthesize and release nitric oxide, which is a potent vasodilator. In this patient, this could occur in the undamaged sections of the large arteries and in the arterioles and capillaries.

6. With moderate walking, the leg muscles' need for oxygen is increased, but the blood supply, and hence the oxygen supply, is limited by the arterial obstruction. Thus, ischemia of the muscle occurs and elicits pain. The substance responsible for the pain is not known, but some evidence suggests it is bradykinin and/or adenosine.

7. Metabolic regulation of blood flow is the adjustment of blood flow to the metabolic requirements of the tissue. Such regulation is mediated by release of endogenous vasodilator metabolites. In this patient, the mechanism is operating continuously; that is, the inadequate blood flow causes vasodilator release and maximally dilated arterioles.

8. Basal tone in arterioles is partial contraction, independent of the nerves. Active hyperemia is vasodilation in response to increased metabolic activity. In this patient, basal tone would be abolished by the metabolites, and because the arterioles are already maximally dilated (even at rest), increased muscle activity or arterial occlusion could not dilate them further.

9. Normally, the sympathetic nerves exert a tonic effect on the resistance vessels and can constrict these vessels when the nerves are reflexively activated. In this patient, there would be little if any tonic action and a limited reflex constriction because of the overriding metabolic effects.

10. Sympathetic denervation would not be of much help because sympathetic tone has been overridden by the action of the vasodilator metabolites.

11. A peripheral vasodilator would decrease arterial blood pressure and increase venous pressure (shift of blood from arterial to venous side of the circulation). Heart rate would reflexively increase via the baroreceptor reflex. The reduced blood pressure would make the leg symptoms worse by reducing an already inadequate blood flow.

12. A peripheral constrictor would exaggerate the symptoms by constricting the arterioles of the leg. This would in part be compensated by the elevated arterial blood pressure caused by constriction of resistance vessels in other parts of the body. Heart rate would decrease reflexively in response to the increased blood pressure.

13. In the normal person at rest, neural regulation of muscle blood flow predominates, but with exercise, the local factors supervene. In this patient, the local factors predominate at rest and during exercise.