The impact of endogenous N/OFQ on DPN: Insights into lower limb blood flow regulation in rats.

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes, often accompanied by impaired vascular endothelial function in the lower limbs. This dysfunction is characterized by a reduced vasodilatory response, leading to decreased blood flow in the lower limbs and ultimately contributing to the development of diabetic peripheral neuropathy. To delve deeper into this pathological process, the study employed bioinformatics to identify and analyze genes highly active in DPN.

Perioperative changes of serum orphanin in diabetic patients and its relationship with sympathetic nervous system.

The occurrence of cardiovascular events in diabetic patients during the perioperative period is related to the activation of sympathetic nerves. Basic research shows that serum nociceptin/orphanin FQ (N/OFQ) levels in diabetic neuropathy rats increased, and N/OFQ reduces the release of norepinephrine (NE). We hypothesize that N/OFQ will affect the sympathetic nervous system during perioperative myocardium of diabetic patients.

Non-peptide orphanin receptor antagonist activity in rat myocardial ischemia-induced cardiac arrhythmias.

One of the causes of sudden cardiac death is arrhythmia after acute myocardial ischemia. After ischemia, endogenous orphanin (N/OFQ) plays a role in the development of arrhythmias. It is discussed in this paper how nonpeptide orphanin receptor (ORL1) antagonists such as J-113397, SB-612111 and compound-24 (C-24) affect arrhythmia in rats following acute myocardial ischemia and what the optimal concentrations for these antagonists are.

Antagonism of N/OFQ attenuates externalization of β1-adrenergic receptor and ventricular arrhythmias in acute myocardial ischemia rat model.

Nociceptin/orphanin FQ (N/OFQ) and adrenergic activations play roles in promoting cardiac arrhythmia in acute myocardial ischemia but whether N/OFQ and β1-adrenergic activities interact and how they interact in the arrhythmogenesis are still unknown. We designed this study to investigate the potential interaction of N/OFQ and β1-adrenergic activities and the underlying mechanism in arrhythmogenesis in acute myocardial ischemia. Ventricular arrhythmia was evaluated in anaesthetized rats following permanent coronary artery occlusion (CAO), in presence and absence of UFP-101 (a selective antagonist of N/OFQ receptor).

Tramadol reduces myocardial infarct size and expression and activation of nuclear factor kappa B in acute myocardial infarction in rats.

Background And Objective: Some anaesthetics show cardioprotective properties, but the underlying mechanism remains elusive. The aim of this study was to investigate the cardioprotective effect of tramadol and the association of the effect with the changes in expression and activation of nuclear factor kappa B (NF-kappaB) in acute myocardial infarction in a rodent model.

Methods: Male Sprague-Dawley rats were randomly divided into three groups: the sham group, exposure of anterior parts of the heart was carried out without ligation of the coronary artery; coronary artery occlusion (CAO) group, ligation of the left anterior descending branch of the coronary artery was performed; and the group in which the animals were pretreated with tramadol (12.

Time-dependent expression of skeletal muscle troponin I mRNA in the contused skeletal muscle of rats: a possible marker for wound age estimation.

To estimate the age of skeletal muscle contusion, the expression of troponin I mRNA in contused skeletal muscle of rats was detected using real-time polymerase chain reaction (PCR). A total of 51 Sprague-Dawley male rats were divided into control and contusion groups, and another nine rats received contusion injury after death. At 0.