Biomedical subjects

Jarle Vaage

Publications and source records attributed to Jarle Vaage.

22 records · Page 2Linked to original sources

PubMed2003

Preconditioning and cardiac surgery.

Preconditioning is in experimental studies the most powerful mode of cardioprotection known. The signal transduction pathways involve a variety of trigger substances, mediators, receptors, and effectors. The studies of preconditioning in cardiac surgery provide conflicting results but the majority of studies show that ischemic preconditiong is an effective adjunct to myocardial protection. However, ischemic preconditioning with repeated clamping of the aorta will never get widespread use. If the "preconditioning response" is to be exploited in cardiac surgery, targeting the underlying molecular mechanisms must provide easily applicable techniques or drugs, which are shown in large scale clinical studies to be beneficial.

Animals↗

PubMed2003

Protective effect of antioxidants on pulmonary endothelial function after cardiopulmonary bypass.

OBJECTIVES: Pulmonary endothelium-dependent vasodilation is impaired after cardiopulmonary bypass. One explanation might be the generation of reactive oxygen species during the period without flow in the pulmonary artery. The aim of the current study was to investigate if treatment with antioxidants could improve pulmonary endothelial function after cardiopulmonary bypass and influence the blood oxidative status. DESIGN: A prospective, randomized, double-blind study. SETTING: The operating room, intensive care unit, and the biochemistry laboratory in University Hospitals. PARTICIPANTS: Patients scheduled for cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: Treatment with vitamin E, vitamin C, allopurinol, and acetylcysteine (n = 12) or placebo (n = 10). MEASUREMENTS AND MAIN RESULTS: The pulmonary reactivity to an infusion of acetylcholine and markers of oxidative stress in blood were measured before and after cardiopulmonary bypass. Sixteen control patients received saline instead of acetylcholine. Before surgery the pulmonary vascular resistance index decreased during infusion of acetylcholine by 24% and 21% in the treatment and placebo groups. After surgery the decrease was 20% and 8%, respectively, (p = 0.422 and p = 0.026) compared with preoperative response. Pulmonary vasodilation induced by acetylcholine was better maintained in the group treated with antioxidants (p = 0.048). In the treatment group, the blood concentrations of early intermediates of lipid peroxidation were higher, but not that of the end products. Glutathione and oxidized glutathione increased after cardiopulmonary bypass in the treatment group. CONCLUSION: The better maintained endothelium-dependent vasodilation after cardiopulmonary bypass in the treatment group indicated that antioxidant therapy reduced endothelial dysfunction.

Acetylcholine↗

PubMed2003

Biochemical markers of cerebrospinal ischemia after repair of aneurysms of the descending and thoracoabdominal aorta.

OBJECTIVE: To investigate the clinical potential of several markers of spinal cord ischemia in cerebrospinal fluid (CSF) and serum during aneurysm repair of the descending thoracic or thoracoabdominal aorta. DESIGN: Observational study of consecutive patients. Nonblinded, nonrandomized. SETTING: University hospital thoracic surgical unit. PARTICIPANTS: Eleven consecutive elective patients. INTERVENTIONS: Distal extracorporeal circulation and maintenance of CSF pressure <10 mmHg until intrathecal catheter removal. MEASUREMENTS AND MAIN RESULTS: CSF and serum levels of S100B (and its isoforms S100A1B and S100BB), neuronal-specific enolase (NSE), and the CSF levels of glial fibrillary acidic protein (GFAp) and lactate were determined. Two patients had postoperative neurologic deficit. One with a stroke showed a 540-fold increased GFAp, a 6-fold NSE, and S100B increase in CSF. One with paraplegia had a 270-fold increase in GFAp, a 2-fold increase in NSE, and 5-fold increased S100B in CSF. One patient without deficit increased GFAp 10-fold, NSE 4-fold, and S100B 23-fold in CSF. CSF lactate increased >50% in 6 of 9 patients without neurologic deficit. Serum S100B increased within 1 hour of surgery in all patients without any concomitant increase in CSF. S100A1B was about 70% of total S100B in both serum and CSF in patients with or without neurologic defects. S100B in CSF increased 3-fold in 3 of 9 asymptomatic patients. CONCLUSIONS: In patients with neurologic deficit, GFAp in CSF showed the most pronounced increase. Biochemical markers in CSF may increase without neurologic symptoms. There is a significant increase in serum S100B from surgical trauma alone without any increase in CSF.

Adult↗

PubMed2003

Hyperoxia elicits myocardial protection through a nuclear factor kappaB-dependent mechanism in the rat heart.

OBJECTIVE: Hyperoxia has been previously shown to protect the heart from ischemia-reperfusion injury. In the present study we investigated whether the cardioprotective effects of hyperoxia were dependent on the redox-sensitive transcription factor nuclear factor kappaB. METHODS: Rats were kept in a hyperoxic (> or =95% O(2)) environment for 60 minutes. Their hearts were isolated immediately afterward, buffer perfused in a Langendorff apparatus, and subjected to 25 minutes of global ischemia and 60 minutes of reperfusion. Cardiac pressures and coronary flow were measured, and infarct size was determined by means of triphenyl tetrazolium chloride staining. Activation of nuclear factor kappaB was assessed by means of the electrophoretic mobility shift assay, whereas the inhibitor IkappaBalpha was evaluated by means of immunoblotting. Pharmacologic inhibition of nuclear factor kappaB was achieved with 2 different agents, SN50 and pyrrolidine dithiocarbamate. RESULTS: Preischemic exposure to hyperoxia improved postischemic recovery of myocardial contractile function and coronary flow and reduced infarct size. Hyperoxia activated pulmonary and myocardial nuclear factor kappaB. Pretreatment with SN50 (400 microg/kg administered intraperitoneally) or pyrrolidine dithiocarbamate (100 mg/kg administered intraperitoneally) before hyperoxia abolished the functional and infarct-limiting protection. Hyperoxia reduced nuclear factor kappaB activation in the heart during sustained ischemia and reperfusion and increased the cytoplasmatic inhibitory factor IkappaBalpha. Administration of pyrrolidine dithiocarbamate or SN50 during ischemia and reperfusion to isolated hearts from normoxic control animals improved postischemic contractile function and coronary flow and reduced infarct size. CONCLUSIONS: Hyperoxia protects the rat heart against ischemia-reperfusion injury. The cardioprotection depends on myocardial activation of the transcription factor nuclear factor kappaB. Our results support evidence for a dual role of nuclear factor kappaB in the heart.

Analysis of Variance↗