Corticotropin-releasing factor (CRF) is released in response to various types of stressors and mediates endocrine, autonomic, immune, and behavioral responses to stress through interaction with CRF1 and CRF2 receptors. To investigate the role of CRF1 receptors in physiological responses to surgical stress, we analyzed the effects of two different non-peptide selective CRF1 receptor antagonists (JTC-017 and CP-154,526) and a peptide non-selective CRF receptor antagonist (astressin) on laparotomy-induced sympathetic nervous responses in isoflurane-anesthetized rats. JTC-017, CP-154,526, and astressin similarly suppressed plasma ACTH elevation induced by laparotomy. JTC-017 and CP-154,526 significantly augmented plasma noradrenaline and adrenaline responses to laparotomy, while astressin showed no effect on these responses. Laparotomy-induced maximum increases in mean blood pressure and heart rate were augmented by JTC-017, but were not affected by astressin. The results suggested for the first time that there was a pathway to attenuate sympathetic nervous response to surgical stress through CRF1 receptors in the central nervous system.

A 71-year-old woman with a history of persistent atrial fibrillation underwent clipping of a ruptured cerebral artery aneurysm. During the surgery her cardiac rhythm was atrial fibrillation and the ventricular rate increased to 130 beats.min(-1). Administration of landiolol was started with 1-min loading infusion at 0.125 mg.kg(-1).min(-1) and continuous infusion at 0.04 mg.kg(-1).min(-1), which was effective in controlling the ventricular rate without causing hypotension. Approximately 120 min after the landiolol infusion was started, the atrial fibrillation was converted to sinus rhythm. Her sinus rhythm was maintained until she left the operating room, even after discontinuation of landiolol.

Coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a pandemic and caused a huge burden to healthcare systems worldwide. One of the characteristic symptoms of COVID-19 is asymptomatic hypoxemia, also called happy hypoxia, silent hypoxemia, or asymptomatic hypoxemia. Patients with asymptomatic hypoxemia often have no subjective symptoms, such as dyspnea, even though hypoxemia is judged by objective tests, such as blood gas analysis and pulse oximetry. Asymptomatic hypoxemia can lead to acute respiratory distress syndrome, and the delay in making a diagnosis and providing initial treatment can have fatal outcomes, especially during the COVID-19 pandemic. Thus far, not many studies have covered asymptomatic hypoxemia. We present a review on the human response to hypoxemia, focusing on the respiratory response to hypoxemia rather than the pathophysiology of lung injury arising from SARS-CoV-2 infection. We have also discussed whether asymptomatic hypoxemia is specific to SARS-CoV-2 infection or a common phenomenon in lung-targeted viral infections.

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