Microdialysis separately monitors myocardial interstitial myoglobin during ischemia and reperfusion

Abstract

Direct monitoring of myoglobin efflux during ischemia and reperfusion has been limited because of inherent sample collection problems in the ischemic region. Recently, the cardiac dialysis technique has offered a powerful method for monitoring myocardial interstitial levels of low-molecular-weight compounds in the cardiac ischemic region. In the present study, we extended the molecular target to high-molecular-weight compounds by use of microdialysis probes with a high-molecular-mass cutoff and monitored myocardial interstitial myoglobin levels. A dialysis probe was implanted in the left ventricular free wall in anesthetized rabbits. The main coronary artery was occluded for 60 or 120 min. We examined the effects of myocardial ischemia and reperfusion on myocardial interstitial myoglobin levels. Interstitial myoglobin increased within 15 min of ischemia and continued to increase during 120 min of ischemia, whereas blood myoglobin increased at 45 min of ischemia. Lactate and myoglobin in the interstitial space increased during the same period. At 60 min of ischemia, reperfusion markedly accelerated interstitial myoglobin release. The interstitial myoglobin level was fivefold higher at 0-15 min of reperfusion than at 60-75 min of coronary occlusion. The dialysis technique permits earlier detection of myoglobin release and separately monitors myoglobin release during ischemia and reperfusion. Myocardial interstitial myoglobin levels can serve as an index of myocardial injury evoked by ischemia or reperfusion.

Efferent vagal nerve stimulation induces tissue inhibitor of metalloproteinase-1 in myocardial ischemia-reperfusion injury in rabbit

“…A microdialysis probe was implanted into the LV anterior wall. Heparin sodium (200 U/kg) was administered intravenously to prevent blood coagulation (19).…”

“…The materials and properties of the dialysis probe have been described (19). Briefly, we designed a hand-made long transverse dialysis probe.…”

“…We therefore investigated the effects of electrical stimulation of vagal nerve on myocardial expression of MMP-2/9 and TIMP-1/2 in a rabbit model of myocardial ischemia-reperfusion (I/R) injury. We also investigated the direct action of acetylcholine (ACh), a neurotransmitter released by vagal nerve stimulation (VNS), on myocardial release of TIMP-1 using a cardiac microdialysis technique (19). Our results indicated that VNS induced expression of TIMP-1 from cardiomyocytes and reduced active MMP-9 in myocardial I/R injury in rabbit.…”

Detection of endogenous acetylcholine release during brief ischemia in the rabbit ventricle: A possible trigger for ischemic preconditioning

“…In the case of myocardial interstitial myoglobin levels, the reperfusion further increases the myoglobin levels, suggesting an occurrence of reperfusion injury to the myocardium (Kitagawa et al 2005).…”

Monitoring Changes in the Redox State of Myoglobin in Cardiomyocytes by Raman Spectroscopy Enables the Protective Effect of NO Donors to Be Evaluated

“…There is evidence reported in the literature that this takes place following ischemia but it might not be a process that is specific to myoglobin. 33,34,35,36 Monitoring cardioprotection by NO-donor compounds during simulated reperfusion In figures 6 (c) and 8 (c), there are significant changes in the Raman spectrum following perfusion of the substrate-free buffer subsequent to pre-conditioning of cardiomyocytes with DEA and SNP, respectively: (i) there is a small shift in ν 4 from 1375 cm -1 to 1372 cm -1 ; (ii) the overlapping ν 2 and ν 19 bands at 1585 cm -1 are much weaker and the ν 10 band at 1637 cm -1 is not resolved (these disappearing bands originate from low-spin heme complexes); (iii) a ν 2 band band appears at 1565 cm -1 , which indicates the formation of a high-spin heme complex; and (iv) a ν(C a =C b ) band appears at 1615 cm -1 . In summary, the spectra in figure 6 (c) and 8 (c) …”