Hyperbaric Oxygen Therapy Dampens Inflammatory Cytokine Production and Does Not Worsen the Cardiac Function and Oxidative State of Diabetic Rats.

Hyperbaric oxygen therapy (HBOT) is frequently used after soft tissue injuries and in diabetic patients with ulcerated wounds; however, its ability to increase oxidative stress casts doubts. Diabetes (DM) in male Wistar rats ( = 20) weighing 300 g were induced by a single dose of streptozotocin. Ten diabetics (DMHBOT) and 10 controls (CHBOT) underwent a one-hour long hyperbaric oxygen treatment protocol (2.

Depressed calcium cycling contributes to lower ischemia tolerance in hearts of estrogen-deficient rats.

Objective: Estrogens enhance ischemia tolerance (IT) in the myocardium, the mechanism of which remains unclear. We investigated the effects of long-term estrogen deprivation on the intracellular calcium (Ca(2+)(i)) transient of the heart and its possible influence on IT.

Methods: Hearts of ovariectomized (OVX) and sham-operated (control) adult female rats (some receiving estrogen therapy) were studied 10 weeks after surgical operation: control (n = 8), OVX (n = 10), sham-operated estrogen-substituted (n = 7), and ovariectomized estrogen-substituted (n = 9).

Toll-like receptor 4-dependent microglial activation mediates spinal cord ischemia-reperfusion injury.

Background: Paraplegia continues to complicate thoracoabdominal aortic interventions. The elusive mechanism of spinal cord ischemia-reperfusion injury has delayed the development of pharmacological adjuncts. Microglia, the resident macrophages of the central nervous system, can have pathological responses after a variety of insults.

Interruption of spinal cord microglial signaling by alpha-2 agonist dexmedetomidine in a murine model of delayed paraplegia.

Background: Despite investigation into preventable pharmacologic adjuncts, paraplegia continues to complicate thoracoabdominal aortic interventions. The alpha 2a adrenergic receptor agonist, dexmedetomidine, has been shown to preserve neurologic function and neuronal viability in a murine model of spinal cord ischemia reperfusion, although the mechanism remains elusive. We hypothesize that dexmedetomidine will blunt postischemic inflammation in vivo following thoracic aortic occlusion with in vitro demonstration of microglial inhibition following lipopolysaccharide (LPS) stimulation.

Attenuation of spinal cord ischemia-reperfusion injury by specific α-2a receptor activation with dexmedetomidine.

Background: Despite surgical adjuncts, paralysis remains a devastating complication after thoracoabdominal aortic interventions. Dexmedetomidine, a selective α-2a agonist commonly used for sedation in the critical care setting, has been shown to have protective effects against ischemia-reperfusion injuries in multiple organ systems. We hypothesized that treatment with dexmedetomidine would attenuate spinal cord ischemia-reperfusion injury via α-2a receptor activation.