Permissive hypercapnia: Is there any upper limit?

Nayak, Snehamayee; Jindal, Atul

doi:10.4103/0972-5229.148655

Cited by 4 publications

(5 citation statements)

References 6 publications

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“…These are consistent with the change of hypoxemia and permissive hypercapnia in ARDS [27][28][29][30].…”

Section: Discussionsupporting

confidence: 88%

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy: implication in neuroinflammation in hypoxemic adult rats

Ding

Liu

et al. 2019

Preprint

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Background: Hypoxemia is a typical symptom of acute respiratory distress syndrome (ARDS). Ventilations are always needed for correcting hypoxemia. To avoid pulmonary morbidity, low tidal volume ventilation is often applied. The ventilation strategy will certainly result in hypercapnia. Our previous study found that hypercapnia could induce IL-1β overproduction in hypoxia-activated microglia. However, the underlying mechanism has remained unclear. This study aimed to explore whether hypercapnia would promote microglial pyroptosis via inhibiting mitophagy in adult rats with hypoxemia. Methods: Cerebral oxygen extraction ratio (CERO2), partial pressure of brain tissue oxygen (PbtO2), and reactive oxygen species (ROS) production in brain tissue in a rat model of hypercapnia/hypoxemia were evaluated. Along with this, the oxygen consumption rate (OCR) and ROS production of BV-2 microglial cells were evaluated after 15% CO2/0.2% O2 treatment. Mitophagy was observed using transmission electron microscopy (TEM). The protein expression level of LC3-II/I, p62, caspase-1, gasdermin D-N domains (GSDMD-N), IL-1β and IL-18 in microglial cells were detected before and after application of a ROS scavenger in vivo and in vitro. Results: PbtO2 level was elevated by hypercapnia in the hypoxemic rats in the first 1.5 h, but it was significantly decreased 2 h after ventilation. This was further evident by the increased levels of CERO2 at 3 h after ventilation. Besides, a high concentration of CO2 treatment could increase the levels of OCR in hypoxic BV-2 microglial cells in vitro. Expression levels of LC3-II were reduced, while those of p62 were increased by hypercapnia in the hypoxic hippocampus and BV-2 microglia. Autophagosomes could be seen in hypoxia treated microglial cells under TEM, while those were rarely observed in hypercapnia + hypoxia treated microglia. Hypercapnia markedly increased the production of ROS and the expression of caspase-1, GSDMD-N, IL-1β, and IL-18 in hypoxia-activated microglia both in vivo and in vitro. Pharmacological scavenging ROS inhibited microglial pyroptosis and expression of IL-1β and IL-18.Conclusion: Hypercapnia-induced mitophagy inhibition may promote pyroptosis and enhance IL-1β and IL-18 release in hypoxia-activated microglia.

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“…These are consistent with the change of hypoxemia and permissive hypercapnia in ARDS [27][28][29][30].…”

Section: Discussionsupporting

confidence: 88%

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy: implication in neuroinflammation in hypoxemic adult rats

Ding

Liu

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…In the hypercapnia/hypoxemia models, PO 2 levels of the arterial blood and culture supernatant were maintained at 55‐60 mmHg and pH levels of the arterial blood and culture supernatant at 7.20‐7.25. These are consistent with the change of hypoxemia and permissive hypercapnia in ARDS 27‐30 …”

Section: Discussionsupporting

confidence: 86%

“…9 In Sham group, the rats were exposed to air when the ventilator settings were fixed. [27][28][29][30] We reported in our previous study that hypercapnia could induce IL-1β overproduction in hypoxia-activated microglia. However, the underlying mechanism has remained unclear.…”

Section: % Co 2 Increased Il-18 Expression Via Inducing Ros Overpmentioning

confidence: 89%

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy in hypoxemic adult rats

Ding

et al. 2020

CNS Neurosci Ther

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Acute respiratory distress syndrome (ARDS) is a common critical disease in intensive care units (ICUs). 1,2 Persistent hypoxemia is a typical symptom of ARDS. Ventilations are always needed to correct hypoxemia. 3,4 To avoid or reduce pulmonary morbidity, low tidal volume ventilation is often applied. 5,6 The ventilation strategy will certainly result in hypercapnia, which is called "permissive hypercapnia". 7,8 Our previous study found that hypercapnia could induce IL-1β overproduction in hypoxia-activated microglia. 9 However, the underlying mechanism has remained unclear. The NLRP3 inflammasome is widely expressed in microglia, which plays an important role in initiating the central immune and

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“…Here, Group H had a significantly higher rSO 2 (P<0.05), indicating that PHC is conducive to improving the autoregulation of the cerebral blood flow and the cerebral oxygen supply/consumption balance, which is consistent with a previous study (7). The reason may be that since CO 2 is the most effective regulator of cerebral blood flow, the PHC ventilation strategy in the patients undergoing CVR increases PaCO 2 , catalyzes the activity of neuronal nitric oxide synthase, increases nitric oxide production, causes the expansion of cerebral blood vessels, and increases cerebral blood flow and cerebral oxygen supply, thereby reducing the risk of cerebral ischemia and hypoxia and effectively protecting brain function (14).…”

Section: Comparison Of Mmse Scores At Each Time Point Between the Two Groupssupporting

confidence: 91%

Impact of permissive hypercapnia on regional cerebral oxygen saturation and postoperative cognitive function in patients undergoing cardiac valve replacement

Zhu¹,

Shi²,

Zhu³

et al. 2020

Ann Palliat Med

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Background: Cardiac valve replacement (CVR) is currently the main surgical treatment for patients with valvular heart diseases (VHD). Postoperative cognitive dysfunction (POCD) is one of the most serious complications of cardiac surgery.. Permissive hypercapnia (PHC), an important lung-protective ventilation strategy, has protective effects on vital organs, including the heart, lungs, and central nervous system (CNS). The main objective of this study is to assess the effect of the PHC ventilation strategy on rSO 2 and postoperative cognitive function in patients undergoing CVR.Methods: A total of 66 patients undergoing CVR were included and randomly divided into the PHC ventilation group (Group H, n=33) and conventional ventilation group (Group C, n=33). Patients of both groups were subjected to conventional ventilation before cardiopulmonary bypass (CPB). patients in Group H were subjected to the PHC ventilation strategy to keep the partial pressure of carbon dioxide (PaCO 2 ) at 46-60 mmHg.Results: (I) Group H had a lower HR at T0 and T1 (P<0.05) and higher CO at T3 and T4 (P<0.05) than Group C. (II) Group H had higher rSO 2 at T4 (P<0.05), lower pH and lactate (Lac) at T4 (P<0.05), higher PaCO 2 at T3 and T4 (P<0.05), and lower PaO 2 at T3 and T4 (P<0.05). (III) Compared to 1 d before surgery, the MMSE scores of both groups were lower 24 h after surgery (P<0.05).Conclusions: PHC can increase the rSO 2 of patients undergoing CVR, increase cerebral blood flow, improve the cerebral oxygen supply/consumption balance, and play a protective role in the brain. It has no significant impact on the incidence of POCD.

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Permissive hypercapnia: Is there any upper limit?

Cited by 4 publications

References 6 publications

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy: implication in neuroinflammation in hypoxemic adult rats

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy: implication in neuroinflammation in hypoxemic adult rats

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy in hypoxemic adult rats

Impact of permissive hypercapnia on regional cerebral oxygen saturation and postoperative cognitive function in patients undergoing cardiac valve replacement

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