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ABSTRACT: There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfusion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts (P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts (P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts.
Physiological research / Academia Scientiarum Bohemoslovaca 01/2008; 58(1):29-38. · 1.55 Impact Factor
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ABSTRACT: It is now recognized that changes occurring during cardiac remodeling
may influence the tolerance of the myocardium to ischemic stress.
Therefore, the present study investigated the response of the post-infarcted
heart to ischemia in an experimental model of ischemia and reperfusion injury
and the possible underlying mechanisms. Acute myocardial infarction
(AMI) was induced in Wistar male rats by ligating the left coronary artery
(AMI, n = 13), while sham-operated rats were used as controls (SHAM,
n = 11). At 2 weeks, cardiac dysfunction was observed in AMI, as indicated by
the reduction of the left ventricular EF%. Isolated hearts were then subjected
to 30 min of zero-flow global ischemia followed by 45 min of reperfusion.
Ischemic contracture was significantly depressed in AMI hearts. Postischemic
left ventricular end diastolic pressure (LVEDP45) in mmHg and
LDH release in IU/g were markedly decreased; LVEDP45 was 52.1 (7.5) for
AMI vs 96.6 (7.5),P < 0.05 and LDH release was 7.5 (1.0) in AMI vs 11.4 (0.56)
in SHAM, P < 0.05. This response was associated with 2-fold increase in
HSP70 expression in AMI hearts (noninfarcted segment), P < 0.05 vs SHAM
and 1.7 fold increase in the expression of the phospho-HSP27, P < 0.05, while
the expression of PKCε was shown to be 1.4-fold less in AMI, P < 0.05. In conclusion,
the post-infarcted heart seems to be resistant to ischemiareperfusion
injury and heat shock protein 70 and 27 may be involved in this
response.
Archiv für Kreislaufforschung 06/2007; 102(4):327-333. · 7.35 Impact Factor
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ABSTRACT: Hyperthyroid hearts are shown to display a phenotype of cardioprotection against ischemic stress, but the underlying signaling mechanisms remain largely unknown. The present study investigated the possible relation of HSP70 to the thyroid hormone induced cardioprotection. HSP70 is a redox-regulated molecular chaperone, and enhances cell survival under stress. Thyroxin (25 microg/100 g body weight) was administered to Wistar male rats for four days (THYR-4d) and two weeks (THYR-14d), respectively, while untreated animals served as controls (CON-4d, CON-14d). Isolated hearts from control and thyroxin treated rats were subjected to 20 min zero-flow ischemia followed by 45 min of reperfusion (I/R). The amount of HSP70 in the myocardium for THYR-14d was 1.85 times the levels of CON-14d (p < 0.05). The levels of HSP70 expression were no different between THYR-4d and CON-4d, p > 0.05. This was only accompanied by an increase in MDA levels (used as an index of oxidative stress) in THYR-14d compared to untreated hearts. These changes corresponded to a differential response of the heart to I/R; post-ischemic recovery of function was significantly increased in THYR-14d compared to CON-14d, and was no different between the THYR-4d and CON-4d hearts. In conclusion, long-term thyroxin administration results in increased tolerance of the myocardium to I/R and enhances the expression of HSP70 which may, at least in part, account for this response.
Hormone and Metabolic Research 05/2006; 38(5):308-13. · 2.19 Impact Factor
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ABSTRACT: Motion of the carotid atheromatous plaque may be responsible for plaque rupture and cerebrovascular symptoms. B-mode ultrasound allows non-invasive recording of arterial wall and plaque motion. Our aim was to analyze quantitatively patterns of arterial wall motion with different techniques. Temporal sequences of digitized B-mode ultrasound images of the carotid arteries of 10 young healthy subjects were interrogated. Arterial wall motion was analyzed using: a/ block-matching, and b/ optical flow. The motion of selected regions of the luminal surface of the arterial wall was estimated using region tracking and block-matching. The motion of areas of the arterial wall was estimated using optical flow. Waveforms showing radial and axial displacements, as well as radial and axial velocities were produced for the selected ROIs using both techniques. Both techniques produced waveforms with peaks, corresponding to cardiac cycle events, that occurred at similar time points. To study the similarity of the waveforms obtained from the two techniques, a cross-correlation coefficient was calculated. Cross-correlation coefficients were 0.72..0.22 and 0.70..0.19 for displacements and velocities, respectively, in the radial direction. In the axial direction, the coefficients were 0.32..0.39 and 0.24..0.22 for displacements and velocities, respectively. On the basis of this relative comparison of methods, we conclude that significant observations can be made for each motion analysis technique in terms of characterization of the mechanical properties of the tissue.
Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 02/2005; 5:4469-72.
