Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.5 (cathepsin D)
 4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Decreased oxygen delivery and cellular hypoxia are important factors in the pathophysiology of hemorrhagic shock. We studied the effects of 100% oxygen at 1 and 3 ATA (atmosphere absolute) in a severe model of hemorrhagic shock induced by bleeding 50% of the total blood volume in rats. Post-treatment with 100% oxygen at 1 and 3 ATA maintained mean arterial blood pressure (MABP) in hemorrhaged rats at significantly higher values compared to untreated controls (P less than 0.01 at 1 and 3 ATA). Treatment with oxygen attenuated the increase in plasma activities of the lysosomal hydrolase cathepsin D (P less than 0.05 at 1 ATA; P less than 0.01 at 3 ATA). Oxygen at 3 ATA also attenuated the plasma accumulation of free amino-nitrogen compounds (P less than 0.05). Furthermore, hyperoxia prevented the final increase in hematocrit (P less than 0.05 at 1 ATA; P less than 0.01 at 3 ATA). Hemorrhaged rats treated with oxygen also exhibited a significantly longer survival time (P less than 0.01 at both doses), and higher survival rates (50% at 1 ATA and 100% at 3 ATA; P less than 0.05 and P less than 0.01, respectively) than untreated shock rats. No significant effect on any of the above mentioned variables was found in hemorrhaged rats treated with 7% oxygen at 3 ATA (oxygen pressure 0.2 ATA), indicating that all salutary effects can be attributed to oxygen and not to the increased ambient pressure per se. Our results indicate that 100% oxygen in normobaric and hyperbaric conditions exerts important beneficial effects in hemorrhagic shock and may be a useful drug for the treatment of this condition.
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PMID:Oxygen therapy in hemorrhagic shock. 204 10

We studied the effects of hyperbaric oxygen in a severe model of circulatory shock induced by occlusion and reperfusion of major splanchnic arteries (splanchnic artery occlusion (SAO) shock). Pentobarbital-anesthetized rats subjected to total occlusion of the superior mesenteric and the celiac arteries for 40 min developed a severe shock state, resulting in a uniformly fatal outcome after release of the occlusion. Exposure to hyperbaric oxygen at 2 ATA (atmosphere absolute) (1 ATA = 0.1 MPa) was initiated immediately after reperfusion. SAO shock rats exposed to hyperbaric oxygen maintained mean arterial blood pressure at significantly higher values throughout the postreperfusion period compared with untreated SAO shock rats (p less than 0.01), with final mean arterial blood pressures of 88 +/- 9 and 51 +/- 4 mmHg, respectively. Treatment with hyperbaric oxygen attenuated the increase in plasma activities of the lysosomal hydrolase cathepsin D (p less than 0.05), and diminished the increase of hematocrit (p less than 0.01 from untreated shock rats). Splanchnic occlusion shock rats treated with hyperbaric oxygen also exhibited a significantly higher survival rate than the untreated shock group (77 vs. 0%, respectively; p less than 0.01). Our results suggest that the beneficial effects of exposure to hyperbaric oxygen immediately after reperfusion of the splanchnic region outweigh its possible deleterious effect.
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PMID:Effects of hyperbaric oxygen in circulatory shock induced by splanchnic artery occlusion and reperfusion in rats. 259 28