Biomedical subjects
R Cornelussen
Publications and source records attributed to R Cornelussen.
Inability of the heat-shocked heart to adjust its pre-ischemic and post-ischemic performance to variable loading conditions.
The aim of the present study was to investigate whether the pre-ischemic and post-ischemic hemodynamic function of the heat-shocked rat heart is affected by changes in afterload and extracellular calcium concentrations ([Ca2+]e). Experiments were performed on isolated, ejecting Lewis rat hearts 24h after in vivo heat shock (LewHS) or anesthesia alone (Lewc). In vitro hearts were subjected to 60 min normoxic perfusion, 45 min global ischemia, and 60 min of reperfusion. Pre-ischemic and post-ischemic left ventricular performance was evaluated at [Ca2+]e ranging between 0.65 and 3.0 mM at afterloads of 8.0 kPa and 16.0 kPa. At 8.0 kPa, pre-ischemic function was comparable in LewHS and Lewc at [Ca2+]e equal to or above 2.25 mM. At lower [Ca2+]e, i.e., 0.65 and 1.25 mM, cardiac output (CO) was significantly lower in LewHS than in Lewc hearts. At 16.0 kPa, significantly lower CO values were found in LewHS than Lewc hearts at all [Ca2+]e levels. During post-ischemic reperfusion under basal conditions (8.0 kPa; [Ca2+]e = 2.25 mM) a significantly better recovery was observed in LewHS than Lewc hearts, persisting at [Ca2+]e equal to 1.25 mM. However, either by lowering [Ca2+]e to 0.65 mM or increasing afterload to 16.0 kPa (at all [Ca2+]e), heat shock-associated improvement of post-ischemic performance disappeared. In conclusion, pre-ischemic left ventricular performance of the isolated heat-shocked heart is depressed when it performs at low [Ca2+]e or against a relatively high afterload. The heat shock-mediated improvement of post-ischemic function is only present at relatively low afterload levels in combination with normal extracellular calcium concentrations.
Heat shock improves ischemic tolerance of hypertrophied rat hearts.
The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoBHS and ShamHS, respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoBC) and nonheated (control) nonhypertrophied (ShamC) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoBHS and ShamHS hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoBHS hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoBHS hearts but was significantly increased in ShamHS hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.