Role of Microglia in Ventilatory and Blood Pressure Responses to Acute Hypoxia

Microglia induces neuroinflammation in response to intermittent and chronic hypoxia, and enhances ventilatory augmentation and blood pressure elevation during hypoxic exposure. However, the role of microglia in ventilatory and blood pressure responses to acute hypoxia, especially to brief period of hypoxic exposure, has not been well investigated. In the present study we aimed to clarify the role of microglia in ventilatory and blood pressure responses to short duration acute hypoxia. To investigate this issue we conducted experiments using adult rats. A blood pressure telemeter was implanted intraperitoneally with a pressure transducer tip in the abdominal aorta. After at least one week recovery period, ventilatory and blood pressure responses to hypoxia were measured in an unanesthetized freely moving condition by whole body plethysmography and blood pressure telemetry, respectively. Measurement was first conducted without pretreatment with minocycline which is an inhibitor of microglial activation. Then, in more than one week after this control measurement, the animal was pretreated with minocycline for three consecutive days, and ventilatory and blood pressure responses to hypoxia were measured under the suppression of microglial activation. To test hypoxic responses, mild (13% O2, 4 min) and severe (7% O2, 5 min) hypoxia was loaded with a sufficient interval. In results we did not find differences ether in ventilatory or blood pressure response to either level of hypoxia between the conditions before and after pretreatment with minocycline. These results indicate that microglial activation does not affect ventilatory or blood pressure response to short duration acute hypoxia, which is not in agreement with previous reports, and this disagreement may be attributed to the different period of hypoxic loading between the previous reports and our present study, which could you too short to induce neuroinflammatory action by activated microglia. Support or Funding Information This work was supported by JSPS KAKENHI Grant Numbers 17K08559, 17H05540, 18K17783, 19K17386 and 19K17620 and a Grant‐in‐aid of the Cardiovascular Research Fund, Tokyo, Japan.