THYROTROPIN-RELEASING-HORMONE PRODUCES DIFFERENT HEMODYNAMIC-EFFECTS IN VEGETATIVE AND BRAIN-DEAD PATIENTS

To define a mechanism for the pressor effects of thyrotropin-releasing hormone (TRH), we evaluated changes in mean blood pressure (MBP) when a synthetic form of TRH (0.1 mg/kg, i.v.) was injected into two types of comatose patients: vegetative and brain dead. The patients in the vegetative group (n = 7, age 58 +/- 6) retained spontaneous respiratio n and brainstem function, whereas the brain-dead (BD) patients (n = 7, age 68 +/- 4) lacked these functions. In the vegetative group, TRH ca used significant increases in MBP (from 91 +/- 8 mm Hg to 110 +/- 10 m m Hg) at 2 min after the injection [p < 0.05, analysis of variance (AN OVA) with a Scheffe F-test]. In contrast, five of the seven BD patient showed no alterations in the measured parameter in response to the TR H injection. However, the remaining two BD patients, who had spinal re flexes, exhibited an elevation in MBP. In such BD patients, barorecept or reflex function was virtually absent, suggesting that the blood pre ssure regulation mediating through the baroreceptor reflex system migh t be abolished. These results indicate that in comatose patients, the hemodynamic effects of TRH may differ depending on impairments in the central nervous system; the results support previous reports indicatin g a mediation of the central sympathetic nervous system in the develop ment of pressor effects of TRH. Furthermore, because brain-dead patien ts with spinal reflexes showed hypertensive responses to TRH, there is a possibility that these responses may have resulted from an activati on of TRH receptors in the spinal cord.