Lecithinized Cu, Zn-Superoxide Dismutase Limits the Infarct Size Following Ischemia-Reperfusion Injury in Rat Hearts in Vivo

Critical timing of -arginine treatment in post-ischemic myocardial apoptosis?role of NOS isoforms

“…The infarct size in the vehicle group from the current study is relatively small compared with previously reported results, although even a smaller infarct size has been found in this model [27]. In most myocardial ischemia and reperfusion models used to date, animals are anesthetized during the entire ischemia/reperfusion period and the chest remains open.…”

Loss of plasma membrane integrity, complement response and formation of reactive oxygen species during early myocardial ischemia/reperfusion

“…While several animal studies found that SOD1 could reduce infarction in both regional (Gross et al, 1986; Hangaishi et al, 2001; Kanamasa et al, 2001) and global heart ischemia (Ambrosio and Flaherty, 1992; Nishikawa et al, 1991; Otani et al, 1986; Wang et al, 1998), others found that it failed to protect against infarction in various ischemia models (Gallagher et al, 1986; Jones et al, 2003; Klein et al, 1988; Matsuda et al, 1991; Nejima et al, 1989; Ooiwa et al, 1991; Patel et al, 1990; Przyklenk and Kloner, 1989; Richard et al, 1988; Uraizee et al, 1987; Watanabe et al, 1993). Downey et al suggested that SOD1 might interfere with the ability of TTC to differentiate between living and dead cells (Downey et al, 1991), with the result that TTC produced an artifactually reduced infarct size in SOD1-treated animals (Shirato et al, 1989).…”

Silymarin protects neurons from oxidative stress associated damages in focal cerebral ischemia: A behavioral, biochemical and immunohistological study in Wistar rats

“…ROS productions are more pronounced during reperfusion than ischemia [4,5]. In relevance with the above point, many different radical scavengers have been used both in vivo and in vitro to target this critical moment of ROS burst [6,7].…”