Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V(1A) receptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,-O-Me-Tyr2,Arg8]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72% and 45% of the control (P < 0.05), extended the mean TE from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V(1A) receptor antagonist and by application of lidocaine or CoCl2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V(1A) receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V(1A) receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V(1A) receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.
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PMID:Vasopressin produces inhibition on phrenic nerve activity and apnea through V(1A) receptors in the area postrema in rats. 1735 38

Obese subjects often present a low-grade chronic inflammation in the white adipose tissue, which seems to play an important role in the initiation and development of obesity-related diseases. It has been reported that this inflammatory process may be due to a hypoxic state occuring within this tissue. Oxygen is used in current medicine as a treatment for several conditions. The aim of this study is to analyze the effects of 95 percent O2 on specific metabolic variables and on the expression of some genes on murine adipocytes. 3T3-L1 adipocytes were exposed during 48 h to different treatments: 95 percent O2 hyperoxia (HPx group), CoCl2 (CoCl2 group), hyperoxia with CoCl2 (HPx+CoCl2 group) and 1 percent O2 hypoxia (Hx group). Cell viability, intracellular ROS content, glucose utilization, lactate and glycerol concentrations were measured. Also, mRNA expression of HIF-1alpha, GLUT-1, ANGPTL4, PPAR-gamma, adiponectin, IL-6 and MCP-1 genes was analyzed. Importantly, 95 percent O2 decreased cell viability and increased intracellular ROS production. Also, glycerol and lactate release were significantly increased and decreased, respectively, in HPx treated cells. This treatment also provoked a down-regulation of GLUT-1 and ANGPTL-4, while IL-6 and MCP-1 were up-regulated. Exposure to a hyperoxia of 95 percent O2 provoked an inflammatory response in adipocytes. The two hypoxia-inducing conditions (CoCl2 and 1 percent O2) produced different outcomes in metabolic measurements as well as in the expression of some genes (GLUT-1, ANPGTL4, PPAR-gamma and adiponectin), while it remained similar in others (HIF-1alpha, IL-6 and MCP-1). Indeed, hyperoxia increased significantly the ROS levels and the lipolytic activity, while it reduced lactate production. In addition to the effects on inflammation, the changes in GLUT-1, ANGPTL4 and PPAR-gamma genes lead to suppose that hyperoxia may be beneficial for the hypertrophied adipose tissues of obese subjects and for improving insulin sensitivity.
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PMID:Influence of different oxygen supply on metabolic markers and gene response in murine adipocytes. 2303 57