Impact of spinal anesthesia on myocardial damage, ultrastructure and cellular mechanisms in rats undergoing thoracic incision surgery

Abstract

Aims

This study aimed to investigate the impact of surgery on cardiac injury and microscopic ultrastructural changes in the heart, as well as the potential protective cellular mechanisms of spinal anesthesia.

Methods

Male Sprague-Dawley rats were randomly assigned to four groups: Control (regular rats), Sham (received spinal saline injection), Surgery (received spinal saline followed by surgery) and Bupivacaine (received spinal bupivacaine 0.5 %, 50 μL followed by surgery), and Bupivacaine (received spinal bupivacaine 0.5 %, 50 μL followed by surgery). The serum and hearts of the rats were assessed for troponin I, NT-proBNP, electron microscopy, catecholamines, markers of oxidative stress and endoplasmic reticulum stress, as well as apoptosis and autophagy.

Results

After surgery, the hearts showed signs of injury, with decreased tissue troponin I and elevated NT-proBNP levels. Electron microscopy revealed mitochondrial swelling, disarrangement and cytosolic vacuoles. Serum epinephrine levels and expression of β1 and β2 adrenergic receptors were elevated. Serum nitrate and nitrite levels (markers of oxidative stress), along with the ER stress indicator GRP78 and autophagy indicators LC3 and LAMP-1, were heightened, and cardiomyocyte apoptosis increased. These effects can be mitigated with the use of spinal bupivacaine.

Conclusions

Surgery can cause ultrastructural and cellular damage, elevate sympathetic activity, oxidative stress, and endoplasmic reticulum stress, leading to autophagy and cardiomyocyte apoptosis. Spinal anesthesia can protect the heart from these injuries.