Abstract
Two sets of experiments were performed to characterize the role of the Pre-Optic Area of the Anterior Hypothalamus (POAH) in the decrease in set point and hypothermia that follows severe hemorrhage. In the first set, lidocaine or artificial cerebrospinal fluid (ACSF) was microinjected into the POAH of rats at the time of hemorrhage. Lidocaine microinjection attenuated the hemorrhagic hypothermia by approximately 50%. The mean drop in core temperature (Tc) following hemorrhage was 1.5 °C with ACSF microinjection ( N = 6), 0.70 °C ( N = 6) with lidocaine, and 1.77 °C ( N = 6) after sham microinjection. This partial attenuation of the hemorrhagic hypothermic response indicates that an intact POAH is necessary for at least some of the hypothermia following hemorrhage. In the second experimental set, hypothalamic tissue temperature (Thyp) was modulated in an attempt to alter the hemorrhagic hypothermic response. Bilateral closed-ended cannulas were inserted into the POAH. One cannula consisted of a water-perfused thermode to change local tissue temperature. The other housed a thermocouple to measure local temperature. The effectiveness of the thermode was first confirmed in conscious rats, evidenced by an inverse deflection in Tc upon Thyp modulation. Then, the POAH region was either heated, cooled, or sham perfused following hemorrhage. The mean drop in Tc following hemorrhage was 2.16 °C ( N = 5) with hypothalamic heating, 1.35 °C ( N = 5) with cooling, and 1.44 °C ( N = 5) following the sham perfusion control. Heating of the POAH significantly exacerbated the hemorrhagic hypothermic response. These data further suggest that the POAH is at least partially responsible for mediating hemorrhagic hypothermia.
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