Biomedical subjects

G Valen

Publications and source records attributed to G Valen.

58 records · Page 4Linked to original sources

PubMed1993

Ischaemia-reperfusion and toxic oxygen metabolites do not induce release of immunoreactive atrial natriuretic factor from isolated rat hearts.

Secretion of immunoreactive atrial natriuretic factors (ANF) after injury by ischaemia-reperfusion and toxic oxygen metabolites (TOM) was investigated in the following groups of Langendorff-perfused rat hearts: 1.1., control perfusion; 1.2., hearts perfused with H2O2 (200 mumol l-1) as a TOM-generating agent for 10 min, followed by recovery for 30 min; 1.3., thiourea (10 mmol l-1), a hydroxyl radical scavenger, was given together with H2O2; 2.1., control perfusion; 2.2., ischaemia (37 degrees C) for 20 min followed by reperfusion for 40 min. Ischaemia-reperfusion and TOM temporarily decreased left ventricular developed pressure and increased left ventricular end-diastolic pressure. The cardiac effects of H2O2 were inhibited by thiourea. Coronary flow (CF) was increased by TOM and decreased by ischaemia-reperfusion. Immunoreactive ANF was measured sequentially in the coronary effluent by radioimmunoassay. Basal secretion of immunoreactive ANF for all groups pooled was 0.45 +/- 0.02 pmol min-1 (mean +/- SEM), and did not change significantly with time in any group. In conclusion, ischaemia-reperfusion and TOM do not influence secretion of immunoreactive ANF.

Animals↗

PubMed1993

Pathophysiology and mediators of ischemia-reperfusion injury with special reference to cardiac surgery. A review.

Although necessary for the ultimate tissue survival, reperfusion may paradoxically exacerbate the ischemic injury. Ischemia and reperfusion injury is intimately woven together. The relative role of reperfusion injury is not clarified and probably varies with the ischemic insult: Reperfusion is always preceded by ischemia, and some of the reperfusion-related events may represent a process continuing from the ischemic period; thus the proper designation should be ischemia-reperfusion injury. The reperfusion-related events are: arrhythmias, myocardial stunning with both systolic and diastolic dysfunction, and low reflow and microvascular stunning. Of pathogenetic importance are the mode and speed of reperfusion as well as the initiation of an intracoronary inflammatory reaction during reperfusion, including endothelium-leukocyte interaction, platelets, generation of oxygen free radical, generation and release of arachidonic acid metabolites, platelet activating factor, endothelium derived relaxing factor, endothelins, kinins, and histamine, complement activation, disturbances in calcium homeostasis, and disturbances in lipid and fatty acid metabolism.

Animals↗

PubMed1993

Toxic oxygen metabolites and leukocytes in reperfusion injury. A review.

Toxic oxygen metabolites (TOM) are generated by activated leukocytes and ischemic tissue upon reperfusion, and are cardiotoxic in vitro. Generation of TOM during reperfusion in vivo has been measured directly and indirectly. TOM contribute to myocardial stunning, causing systolic and diastolic dysfunction. TOM may also play a role in the pathogenesis of reperfusion arrhythmias. It is uncertain if TOM cause cell death during reperfusion. Inhibition of TOM with antioxidants may be important for myocardial protection during cardiac surgery.

Cardiac Surgical Procedures↗

PubMed1991

Could treatment with scavengers of oxygen free radicals minimize complications in cardiac surgery?

Cardiac surgical complications may be caused by a plethora of events. Oxygen free radicals may participate in the pathophysiology of cardiopulmonary bypass and myocardial ischaemia-reperfusion injury. The evidence of free radical production during bypass is limited, and studies of the effect of free radical scavengers even more limited. Experimental work points towards a role of oxygen free radicals in reperfusion damage of the ischaemic myocardium, but clinical data are lacking. Hitherto the clinical availability of free radical scavengers/antioxidants has been scarse. At present more such drugs are becoming clinically applicable, and trials on their effect are highly warranted, in particular as an adjuvant in myocardial protection.

Animals↗