Abstract
We chronically implanted microtubules into the rostral pons of 6 goats to assess the response to hypoxia following irreversible damage to RPN. All goats recovered uneventfully after implantation. After breathing room air for 30 minutes (min), goats were subjected to 10.6% O2 for 30 min. PaO2 at min 6 and 26 of hypoxia was 28.41±0.57 and 26.87±0.58mmHg respectively. The normal response to hypoxia (Table) was a 1° (∼3 min) spike in pulmonary ventilation (VI) followed by a “roll‐off” in VI (∼6 min), and lastly a 2° increase in VI (within 20 min) associated with an increase in body temperature, shivering, VO2, and VCO2. Following irreversible damage to RPN, the 1° spike and “roll‐off” in VI were unchanged from pre‐damage conditions, but the 2° increase was attenuated (P<0.05). We conclude that damage to RPN does not alter the presumed peripheral chemoreceptor 1° response to hypoxia nor the VI “roll‐off”, but attenuates the 2° physiologic response. Comparison of physiologic variables in response to hypoxia, before and after RPN damage. VE(%) PaCO2(Δ mmHg) Temp(Δ °C) VO2 (l/min) VCO2 (l/min) 1° increase Roll‐off 2° increase 6 min hypoxia 26 min hypoxia Final 26 min hypoxia 26 min hypoxia Pre‐damage 174 130 251 −5.47 −8.18 0.96 158.1 197.1 Post‐damage 176 128 195* −5.31 −6.82 0.59* 8.9* 85.1* Significant difference between pre‐ and post‐damage by one‐way ANOVA (P<0.05). Supported s.
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