Dexmedetomidine attenuates pneumocyte apoptosis and inflammation induced by aortic ischemia-reperfusion injury

ABSTRACT

Objective

Despite significant improvements in interventional vascular aneurysm repair procedures and intensive care patient management, there has been no significant decrease in mortality due to ruptured abdominal aortic aneurysm. Oxidative stress is known to play a key role in secondary organ damage due to infrarenal aortic clamping. The aim of this study was to examine the potential protective effect of the alpha-2 adrenergic receptor agonist dexmedetomidine (DMT) on aortic occlusion-induced lung injury.

Methods

Thirty Sprague Dawley rats were allocated into control, ischemia-reperfusion (IR), and IR+DMT groups randomly. Vascular clamps were attached to the abdominal aorta in the IR and IR+DMT groups. Two-hour reperfusion was established 1 h after ischemia. The IR+DMT group received a single intraperitoneal 100 µg dose of DMT 30 min before infrarenal abdominal aortic clamping.

Results

IR due to aortic occlusion led to apoptosis, widespread inflammation, alveolar septal wall thickening due to bleeding and vascular congestion were observed in both types I and II pneumocytes. Malondialdehyde levels increased while glutathione decreased. However, DMT was found to lower apoptotic pneumocytes, alveolar-septal thickness, hemorrhage, vascular congestion, and malondialdehyde levels, while glutathione levels in lung tissue increased.

Conclusions

This study is the first to address the effects of DMT on the lung in a ruptured abdominal aortic aneurysm model. Our findings suggest that the alpha-2 adrenergic receptor agonist DMT reduces oxidative stress and apoptosis, thus protecting against aortic occlusion-induced pulmonary injury.

KEYWORDS:

• Abdominal aortic aneurysm
• dexmedetomidine
• lung
• oxidative stress
• reperfusion

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability statement

All data generated during this study are available in this published article.

Additional information

Funding

This work was supported by the Recep Tayyip Erdogan University Scientific Research Support Fund under Grant [TSA-2018-878].