Panax ginseng administration in the rat prevents myocardial ischemia-reperfusion damage induced by hyperbaric oxygen: evidence for an antioxidant intervention

• Published in: Planta medica Vol. 65; no. 7; p. 614
• Main Authors: Maffei Facino, R, Carini, M, Aldini, G, Berti, F, Rossoni, G
• Format: Journal Article
• Language: English
• Published: Germany 01.10.1999
• Subjects: Administration, Oral; Angiotensin II - pharmacology; Animals; Blood Pressure - drug effects; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiopathology; Free Radical Scavengers - administration & dosage; Free Radical Scavengers - pharmacology; In Vitro Techniques; Male; Myocardial Reperfusion Injury - chemically induced; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - physiopathology; Myocardial Reperfusion Injury - prevention & control; Myocardium - chemistry; Myocardium - metabolism; Oxygen - toxicity; Panax - chemistry; Plant Extracts - administration & dosage; Plant Extracts - pharmacology; Plants, Medicinal; Rats; Rats, Sprague-Dawley; Vasoconstrictor Agents - pharmacology; Ventricular Function, Left - drug effects; Ventricular Pressure - drug effects
• ISSN: 0032-0943
• DOI: 10.1055/s-1999-14034

The aim of this work was to investigate in the rat the protective effect of an oral administration (one week) of Panax ginseng (PG) extract (10 mg/ml in drinking water; 1.6 g/kg/day) on myocardial post-ischemic damage induced by hyperbaric oxygen (HBO) and on the loss in functionality of the endothelium in aorta ring preparations. The hearts from control rats (no-HBO and no-HBO-PG), and from rats exposed to HBO and to HBO after PG treatment were isolated and subjected to mild ischemia and then reperfused. HBO greatly worsens the post-ischemic damage in controls, as demonstrated by the rise of left ventricular end diastolic pressure (LVEDP) and coronary perfusion pressure (CPP). PG significantly restrained the increase of LVEDP and CPP in respect to HBO-untreated rats, as well as that of CPP induced by injection of angiotensin II during pre-ischemia. In HBO control rats the reduction of the vasorelaxant effect of acetylcholine on norepinephrine precontracted aortic rings, was markedly recovered by PG; a similar trend was observed in aortic rings challenged with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (56% recovery). These results strongly indicate that PG prevents the myocardial ischemia/reperfusion damage and the impairment of endothelial functionality induced by reactive oxygen species arising from HBO exposure, through an antioxidant intervention. The in vitro radical scavenging activity of PG seems to be too weak (0.05-0.5 mg/ml) to explain by itself the cardiac and extra-cardiac protective effects, and this suggests a role also for an indirect antioxidant action of the drug (endothelial nitric oxide synthase stimulation).