# Limb remote ischemic preconditioning attenuates biomarkers of acute lung injury and inflammation during thoracoscopic lobectomy: a randomized controlled trial

## TL;DR

Limb RIPC reduces lung injury and inflammation biomarkers during surgery but does not improve short-term oxygenation.

## Contribution

Limb RIPC is shown to reduce lung injury and inflammation biomarkers during thoracoscopic lobectomy.

## Key findings

- Limb RIPC significantly lowers plasma CC16, IL-6, and MDA levels during surgery.
- Oxygenation indices and hospital stay were not significantly affected by RIPC.
- RIPC may offer molecular lung protection without immediate functional benefits.

## Abstract

•Limb RIPC decreases plasma CC16, a key biomarker of lung epithelial injury.•RIPC attenuates systemic Inflammation (IL-6) and oxidative stress (MDA).•A simple, non-invasive intervention for molecular lung protection.•No short-term improvement in oxygenation indices was observed postoperatively.

Limb RIPC decreases plasma CC16, a key biomarker of lung epithelial injury.

RIPC attenuates systemic Inflammation (IL-6) and oxidative stress (MDA).

A simple, non-invasive intervention for molecular lung protection.

No short-term improvement in oxygenation indices was observed postoperatively.

One-Lung Ventilation (OLV), though essential for thoracic surgery, triggers inflammation and oxidative stress that may lead to Acute Lung Injury (ALI). Remote Ischemic Preconditioning (RIPC) is a simple, non-invasive intervention that may activate protective pathways and reduce ischemia-reperfusion injury. This randomized controlled trial assessed whether limb RIPC attenuates OLV-induced lung injury during thoracoscopic lobectomy.

Fifty-four patients undergoing thoracoscopic lobectomy with OLV were randomized to the RIPC (n = 27) or Control (NC, n = 27) group. RIPC consisted of five cycles of 5-min ischemia and 5-min reperfusion using a lower limb tourniquet before OLV. Blood samples were collected at T0 (post-induction), T1 (30-min after OLV), T2 (90-min after OLV), and T3 (30-min after resumption two-lung ventilation). The primary endpoint was plasma CC16. Secondary endpoints included IL-6, MDA, arterial blood gases, Intraoperative Oxygenation Indices (OI, RI, A-aDO2, a/A), and hospital stay.

Plasma CC16, IL-6, and MDA levels were significantly lower in the RIPC group from T1 to T3 (all p < 0.001). In contrast, oxygenation indices, blood gas parameters, and hospital stay did not differ significantly between groups (all p > 0.05).

Limb RIPC effectively reduced systemic markers of lung injury (CC16), inflammation and oxidative stress during OLV but not in short-term improvements in oxygenation or clinical recovery. These findings suggest that RIPC confers molecular protection, with potential functional benefits requiring longer follow-up or evaluation in high-risk populations. Larger multicenter trials are warranted.