vital alpha testo being the aorta that the pressure-volume loop responds in such a way that there's a significant reduction in pressure and volume and in fact if you look at this pressure volume loop which may or may not play and if we tried to shorten it by around 15 minutes we can see that there was less less consistent effect and if you open the artery analyse reperfusion injury and then unload that actually you lost the benefit of the beneficial effect so what we learned from the kinetics with that you had to unload and in fact ideally you could wait and allow the cardioprotective pathways to be activated and then see the effect on infarct size now 30 minutes of delay is still not palatable to a lot of folks so we still wanted to take a deeper dive into mechanism so one of the things we did and again I like the idea of using omics based platforms especially because it takes the the bias out of our hands we deliver these samples and in an unbiased

vital alpha testo canada Sham uninjured heart but actually the unloaded pattern started to look more like a sham or uninjured heart and when we looked at the pathway analysis many many things started to point towards the mitochondria and so when we looked more Pacifica Lee at the mitochondria from the in Foggs own with primer and reperfusion you see the classic swelling and rupture and the blurbs that are forming in the mitochondria but in Freud's own actually the mitochondria here and the alone parts looked quite intact and actually look very similar to an uninjured myocardium so this pushed us further and we started to look again at that question of signaling and when we looked more specifically at SPF one alpha again we confirmed our previous finding that in fact protein levels of SDF one alpha were significantly increased in the infarct tone compared to of the unloaded hearts compared to non unloaded hearts and in fact this SDF signal was fairly profound we wanted to understand why you're getting higher concentration