Brief episodes of myocardial ischemia-reperfusion applied early in reperfusion may attenuate the reperfusion injury, strategy called ischemic postconditioning (IPO). Our objective was to examine the effects of IPO compared with ischemic preconditioning (IP) on postischemic myocardial dysfunction in spontaneously hypertensive rats (SHR). Isolated hearts from SHR and normotensive WKY rats were subjected to the following protocols: (1) Ischemic control (IC): global ischemia 20 min (GI20) and reperfusion 30 min (R). (2) IPO: three cycles of R30sec–IG30sec at the onset of R; (3) IP: a cycle of IG5–R10 previous to GI20, (4) IPO in the presence of chelerythrine, an inhibitor of protein kinase C (PKC). Systolic and diastolic function were assessed through developed pressure (LVDP) and end diastolic pressure (LVEDP), respectively. Lipid peroxidation was estimated by thiobarbituric reactive substance (TBARS) concentration. IPO significantly improved postischemic dysfunction. At the end of R, LVDP recovered to 87 ± 7% in WKY and 94 ± 7% in SHR vs. 55 ± 11% and 58 ± 12% in IC hearts. LVEDP reached values of 24 ± 6 mmHg for WKY and 24 ± 3 mmHg for SHR vs. 40 ± 8 and 42 ± 5 mmHg in IC hearts. Similar protection was achieved by IP. TBARS contents of SHR hearts were significantly diminished by IP and IPO. PKC inhibition aborted the protection of myocardial function and attenuated the diminution of lipid peroxidation conferred by IPO. These data show that IPO was as effective as IP in improving the postischemic dysfunction of hearts from SHR hearts, and that this cardioprotection appears to be associated with a diminution of ROS-induced damage involving the PKC activation.

Comparative effects of ischemic pre and postconditioning on ischemia-reperfusion injury in spontaneously hypertensive rats (SHR).

Objective : Parathyroid hormone-related peptide (PTHrP) improves heart function of post-ischemic and stunned myocardium and is released from the heart under ischemic conditions. Hypertrophic hearts from spontaneously hypertensive rats (SHR) develop a reduced ischemic tolerance, show reduced expression of PTHrP and develop paradoxical effects in regard to PTHrP. We hypothesized that PTHrP is causally involved in reduced ischemic tolerance of hypertrophied hearts. This hypothesis was tested by addition of a cardiac-specific PTHrP agonist or antagonist during ischemia and investigation of the functional recovery during the early phase of reperfusion.

Methods : Hearts from male normotensive adult (6 months) or old (12 months) Wistar and SHR rats were perfused at a constant flow for 20 min and then exposed for 30 or 15 min to global zero-flow ischemia followed by 30 min reperfusion. PTHrP agonist (PTHrP(1–36)) or antagonist (5Ile,23Trp,36Tyr-PTHrP(1–36)) (each 100 nmol/l) were added briefly before the onset of ischemia to ensure that they were present at the beginning of reperfusion. Heart function was determined by insertion of a balloon catheter into the left ventricle. Left ventricular developed pressure (LVDP), d P /d t max, d P /d t min, left ventricular end-diastolic pressure (LVeDP), heart rate (HR) and coronary resistance (CR) were recorded.

Results : Reduced post-ischemic recovery in old SHR was confirmed. Hearts from all four groups responded normally to exogenous PTHrP with a positive chronotropic effect under non-ischemic conditions. In hearts from adult normotensive rats, a beneficial effect of released endogenous PTHrP was confirmed. However, addition of the cardiac-specific PTHrP antagonist during ischemia significantly improved post-ischemic recovery in hearts from old normotensive rats and SHR. This beneficial effect of the antagonist was accompanied by a significant reduction in post-ischemic LVeDP and was more pronounced in adult SHR. This effect was also observed when the hearts were paced (4 Hz). Upon short-term ischemia (15 min), in the absence of ischemia-induced rigor contraction, the antagonist improved LVDP recovery in hearts from old normotensive rats.

Conclusion : In summary, a protective effect of released endogenous PTHrP was confirmed for hearts from adult normotensive rats. This effect is converted into an opposite effect in hearts from SHR and old normotensive rats. Therefore, released endogenous PTHrP can contribute to reduced ischemic tolerance in hypertrophied hearts and during aging.

/pdf/cardiac-specific-effects-of-parathyroid-hormone-related-18us4iy0fx.pdf

Cardiac-specific effects of parathyroid hormone-related peptide: modification by aging and hypertension.

Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: Role of NO and mitoKATP

Aim: 18F-fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET) provides information about myocardial glucose metabolism to diagnose myocardial viability. Additional information about the functional status is necessary. Comparison of tomographic metabolic PET with data from other imaging techniques is always hampered by some transfer uncertainty and scatter. We wanted to evaluate a new Fourier-based ECG-gated PET technique using a high resolution scanner providing both metabolic and functional data with respect to feasibility in patients with diseased left ventricles. Methods: Forty-five patients with coronary artery disease and at least one left ventricular segment with severe hypokinesis or akinesis at biplane cineventriculography were included. A new Fourier-based ECG-gated metabolic 18F-FDG-PET was performed in these patients. Function at rest and 18F-FDG uptake were examined in the PET study using a 36-segment model. Results: Segmental comparison with ventriculography revealed a high reliability in identifying dysfunctional segments (>96%). 18F-FDG uptake of normokinetic/hypokinetic/akinetic segments was 75.4 ± 7.5, 65.3 ± 10.5, and 35.9 ± 15.2% (p < 0.001). In segments ≥70% 18F-FDG uptake no akinesia was observed. No residual function was found below 40% 18F-FDG uptake. An additional dobutamine test was performed and revealed inotropic reserve (viability) in 42 akinetic segments and 45 hypokinetic segments. Conclusion: ECG-gated metabolic PET with pixel-based Fourier smoothing provides reliable data on regional function. Assessment of metabolism and function makes complete judgement of segmental status feasible within a single study without any transfer artefacts or test-to-test variability. The results indicate the presence of considerable amounts of viable myocardium in regions with an uptake of 40–50% 18F-FDG.

ECG-gated 18F-FDG positron emission tomography.

Background We tested the hypothesis that decreased calcium responsiveness is responsible for the reduction in contractile function in regional hibernating and stunned myocardium in situ. Methods and Results In 19 anesthetized swine, the left anterior descending coronary artery flow was reduced to decrease anterior myocardial work index (sonomicrometry) by ≈60%. During 90 minutes of hypoperfusion, creatine phosphate recovered (as determined by biopsy specimens and bioluminescence) and no necrosis developed (as determined by staining with triphenyl tetrazolium chloride). In 10 swine, changes in the intracellular calcium concentration were induced by systematic variation of the postextrasystolic time interval at a constant prematurity. In 9 additional swine, a graded IC calcium infusion was performed. Under control conditions, anterior myocardial work increased with a fully compensated postextrasystolic time interval from 380±93 (mean±SD) to 523±98 mm Hg·mm. IC calcium infusion increased anterior myocardial ...

Calcium Responsiveness in Regional Myocardial Short-term Hibernation and Stunning in the In Situ Porcine Heart

Objective : Severely hypertrophied myocardium was described to have a reduced tolerance towards ischemia. For non-hypertrophied hearts inconclusive findings on the Ca2+-responsiveness are reported. Information on sensitivity to reversible ischemia and on postischemic Ca2+-responsiveness of hearts with clinically common moderate hypertrophy is lacking. Thus, the responsiveness of hypertrophied and normal postischemic myocardium to positive inotropic stimulation should be investigated in the present study. Methods and results : Hearts from spontaneously hypertensive rats (SHR, 4 months old) with significant LV-hypertrophy (+50%) and hearts from normotensive 4 months old Wistar rats were investigated using an isovolumic beating isolated heart model (8 hearts/each of the 8 groups). Functional recovery after 30 min of no-flow ischemia was 78±1% and 77±3% of preischemic control data in hypertrophied and non-hypertrophied hearts assessed as developed left ventricular pressure (non-ischemic controls: 95±2% in hypertrophied and 93±3% in non-hypertrophied controls). Maximum short-term stimulation with Ca2+ revealed a decreased peak left ventricular pressure of 124±4% in hypertrophied and 120±5% in non-hypertrophied postischemic hearts, as compared with non-ischemic controls 138±3% and 157±5%, respectively ( p <0.01). A maximum dose of dopamine stimulated hypertrophied and non-hypertrophied postischemic hearts comparable to Ca2+. Analysing the dose–response curve for Ca2+-stimulation, the sensitivity expressed as fraction of the maximum was identical in non-ischemic and postischemic myocardium of hypertrophied and non-hypertrophied ventricles in spite of the reduced peak values. Conclusion : The findings demonstrate that after moderate reversible ischemia the steady-state function is similarly decreased in hypertrophied and non-hypertrophied postischemic myocardium. The maximum response to Ca2+ is significantly reduced in both types of myocardium, while the Ca2+ sensitivity is unchanged. Identical results after maximum dopamine stimulation as after Ca2+ indicate that the releasibility of Ca2+ and the β-adrenoceptors are not the critical causes for the postischemic dysfunction in hypertrophied or non-hypertrophied myocardium.

/pdf/inotropic-response-of-stunned-hypertrophied-myocardium-8hz828r0tt.pdf

Inotropic response of stunned hypertrophied myocardium: responsiveness of hypertrophied and normal postischemic isolated rat hearts to calcium and dopamine stimulation

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Inotropic response of stunned hypertrophied myocardium: responsiveness of hypertrophied and normal postischemic isolated rat hearts to calcium and dopamine stimulation