Abstract
In light of well-established cardiovascular- and pain-regulatory dysfunction in type I diabetes mellitus, relationships among pain regulatory mechanisms and cardiovascular regulation are of particular interest. The present study examined differences for individuals with type 1 diabetes mellitus in terms of perceived pain, and cardiovascular measures (blood pressure, heart rate, stroke volume, cardiac output, and total peripheral resistance) at rest and during responses to two stressful behavioral (cold pressor test and mental arithmetic) tasks, as well the relationship between pain and cardiovascular regulation. It has been hypothesized that baroreceptor reflex function plays a role in the relationship between pain and cardiovascular regulation. Therefore, the contribution of baroreceptor sensitivity (derived during infusions of phenylephrine and nitroprusside) to the relationships between pain perception and cardiovascular reactivity was investigated in 32 subjects with long term type 1 diabetes mellitus, ( ≥ 8 years duration) and 22 non diabetic controls with no first degree relatives with diabetes (mean +/- SD age 35 +/- 8 years). The type 1 diabetes subjects were asymptomatic or displayed minimal evidence of sensory neuropathy, and glycemia was well controlled (mean +/- SD HbA1c = 7.2 +/- 2.2).Blood pressure reactivity to the cold pressor test was predictive of perceived pain in control subjects, but not subjects with type 1 diabetes mellitus. Heart rate reactivity to the cold pressor was also predictive of pain. During mental arithmetic, heart rate and cardiac output reactivity were predictive of pain among control subjects, but not subjects with type 1 diabetes. Baroreceptor sensitivity derived during phenylephrine (pressor response) was predictive of pain in controls only, but baroreceptor sensitivity derived during nitroprusside was predictive of pain in both groups. Baroreceptor sensitivity (phenylephrine) was predictive of blood pressure reactivity among controls only. Furthermore, controlling for the effects of baroreceptor sensitivity negated the relationship between cold pressor blood pressure reactivity and pain in controls and between cold pressor heart rate reactivity and pain. Controlling for baroreceptor sensitivity did not influence the relationships between pain and mental arithmetic heart rate and cardiac output reactivity. It is concluded that baroreceptor feedback is a critical factor in cardiovascular and sensory regulation, and that these relationships are disrupted in type 1 diabetes mellitus. It is determined that duration of diabetes and psychological regulation are factors that influence baroreceptor relationships to cardiovascular- and pain-regulation.