gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Transgenic human tissue kallikrein rats are not protected after induction of myocardial infarction

Transgene hKLK1-Ratten sind nicht geschützt nach operativer Anlage eines Myokardinfarktes

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker M. Koch
  • D. Westermann
  • M. Wendorf
  • A. Dendorfer
  • F. Spillmann
  • corresponding author M. Bader
  • T. Walther
  • H.P. Schultheiss
  • C. Tschöpe

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP42

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Koch et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Increased endogenous levels of kallikrein (KLK) and bradykinin (BK), and an upregulation of BK B1 and B2 receptors in response to cardiac ischemia might belong to an endogenous myocardial protection system. In this study we compared coronary BK outflow levels (ex vivo) and left ventricular (LV) function of wild type Spraque Dawley and transgenic rats harbouring the human tissue KLK gene TGR(hKLK1).


We studied BK coronary outflow in buffer-perfused isolated working hearts before and after global ischemia in both strains (n=6). To investigate the significance of changes in BK outflow levels, we analyzed LV function in vivo by using a conductance-micromanometry catheter (1.4 F) to obtain pressure-volume loops under basal and under isoproteronol stress conditions 6 days after indcuction of myocardial infaction (MI) or sham operation in all groups (n=6). In addition, we analyzed LV function and cardiac morphology by echocardiography 3 weeks post MI (n=6).


Basal coronary BK outflow of TGR(hKLK1) was 3.5-fold increased compared to controls (0.94+/-0.18 pg/ml vs. 0.24+/-0.05 pg/ml; p < 0.01). In contrast to controls we found no further increase in BK outflow after global ischemia (1.40+/-0.25 vs. 4.53+/-1.24 pg/ml). However, LV function of control vs. TGR(hKLK1) (Stroke volume: 132+/-23 vs. 140+/-20 µl; LVdP/dtmax 2605+/-131 vs. 2632+/-292 mmHg/s; Tau: 19.1+/-0.8 vs. 22.2+/-1.2 ms) and LV diameter (enddiastolic diameter: 9.5+/-2.4 vs. 7.7+/-2.6 mm) did not differ 6 d and 3 w after induction of MI or sham operation under basal conditions and without significant differences between both groups under stress conditions.


Despite a chronic increase in cardiac BK levels, TGR(hKLK1) are not protected after induction of MI.