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Thorsten Reffelmann

Publications and source records attributed to Thorsten Reffelmann.

20 records · Page 2Linked to original sources

Relationship between no reflow and infarct size as influenced by the duration of ischemia and reperfusion.

No reflow after acute myocardial infarction is an important predictor of infarct size and clinical outcome. However, the exact relationship between no reflow and infarct size remains to be determined, particularly because no reflow may progress during the time course of reperfusion. Control groups of five previous protocols using the anesthetized, open-chest rabbit model of coronary artery occlusion and reperfusion were retrospectively analyzed with respect to the correlation between regional myocardial blood flow (RMBF; radioactive microspheres) and infarct size (triphenyltetrazolium chloride) in the course of reperfusion. After 30 min of occlusion, reflow (defined as the ratio of RMBF in the risk area divided by the nonischemic area) declined from hyperemic values after 30 min of reperfusion (reflow ratio: 1.33 +/- 0.81; RMBF in the risk area at the same time point: 2.25 +/- 1.04 ml x g(-1) x min(-1)) to 0.47 +/- 0.22 after 120 min and 0.46 +/- 0.13 after 180 min of reperfusion. After 120 min of ischemia, reflow at 30 min of reperfusion was 0.49 +/- 0.24 and deteriorated by 120 min of reperfusion (0.26 +/- 0.15). In every group, there was a strong correlation between infarct size and reflow (correlation coefficients: -0.62 to -0.82). The lines of regression for the groups with assessment of RMBF after 120 or 180 min of reperfusion were nearly identical regardless of the duration of ischemia. Thus microvascular reperfusion injury led to a striking decrease in RMBF within the first 2 h of reperfusion, with infarct size as the major determinant of reflow at a given time point of reperfusion.

Animals↗

Transplantation of fetal cardiomyocytes into infarcted rat hearts results in long-term functional improvement.

Studies have demonstrated the feasibility of transplanting cardiomyocytes after myocardial infarction (MI). However, persistence and effects on left ventricular (LV) function have not been elucidated in long-term studies. Ventricular fetal cardiomyocytes from embryos of both sexes were injected into marginal regions of MI 4 weeks after suture occlusion of the left anterior descending artery in adult female rats. Two and 6 months after transplantation (Tx), engrafted cells were traced by immunohistochemical in situ hybridization for Y chromosomes or bromodeoxyuridine (BrdU) staining, LV dimensions and function were assessed by echocardiography, and LV pressure was assessed ex vivo in a Langendorff perfusion system. Immunohistochemistry for alpha-sarcomeric actin and Y chromosomes revealed the presence of transplanted cells in infarcted host myocardium at both 2 and 6 months. End-diastolic LV diameter markedly decreased after Tx and fractional shortening gradually increased after Tx (31.3 +/- 4.5% before Tx, 45.4 +/- 4.2% at 6 months; p<0.005). Wall area fraction and MI size were unaffected by Tx. In hearts with MI, but not in normal hearts, Tx led to the development of higher pressures (87 +/- 18 versus 38 +/- 8 mmHg, 6 months post-Tx versus nontreated). After catecholamine stimulation, both infarcted and normal hearts developed higher pressures after Tx (p<0.005), ultimately associated with reduced mortality after Tx versus nontreated. Transplanted cardiomyocyte-rich graft cells persist in host myocardium and mediate continuous improvement of LV function and survival in a rat model of MI even during long-term follow-up, possibly involving a catecholamine-sensitive mechanism.

Animals↗