scholarly journals High Mobility Group Box 1 Induces a Negative Inotropic Effect on the Left Ventricle in an Isolated Rat Heart Model of Septic Shock

2008 ◽  
Vol 72 (6) ◽  
pp. 1012-1017 ◽  
Author(s):  
Satoshi Hagiwara ◽  
Hideo Iwasaka ◽  
Tomoko Uchino ◽  
Takayuki Noguchi
2003 ◽  
Vol 66 (1) ◽  
pp. 157-161 ◽  
Author(s):  
Gustavo Guevara-Balcázar ◽  
Enrique Querejeta-Villagómez ◽  
Oskar Nuevo-Adalla ◽  
Alejandra Orozco-Guillen ◽  
Ivan Rubio-Gayosso ◽  
...  

2018 ◽  
Vol 22 (4) ◽  
pp. 88
Author(s):  
R. A. Knyazev ◽  
N. V. Trifonova ◽  
A. V. Ryabchenko ◽  
M. V. Kotova ◽  
A. R. Kolpakov ◽  
...  

<p><strong>Background.</strong> It was shown earlier that high-density lipoproteins of rat blood plasma increased the frequency and strength of contraction of an isolated rat heart. The main protein component of high-density lipoproteins, apolipoprotein A-I, isolated from human blood plasma, increased the force of cardiac contractions, with little effect on the frequency. A method for obtaining recombinant apolipoprotein A-I developed at the Institute of Biochemistry allows for facilitating the research into cardiotropic properties of this protein.<br /><strong>Aim.</strong> The purpose of this experiment was to study the effect of recombinant apolipoprotein A-I on the performance of an isolated rat heart and to compare it with the action of native apolipoprotein A-I.<br />Methods. The experiment was performed on Wistar male rats weighing 230–250 g. Isolated hearts of the rats were routinely perfused retrograde, and isovolume pressure in the left ventricle was measured. Recombinant apolipoprotein A-I was obtained in <em>E. coli</em> cells in the form of a chimeric polypeptide followed by the conversion of protein into a mature form of recombinant apolipoprotein A-I.<br /><strong>Results.</strong> It was shown that recombinant apolipoprotein A-I with a concentration of 20 μg/ml caused a stable increase in pressure in the left ventricle, while the magnitude of the coronary flow and heart rate changed insignificantly. The maximum inotropic effect was registered for 20 min from the beginning of perfusion and amounted to 147.5% relative to the reference values. It was found out that in the presence of recombinant apolipoprotein A-I, the maximum rate of contraction of the left ventricle increased. At the same time, the diastole had a tendency to increase and was larger in comparison with the initial data at 10 and 20 minutes of perfusion.<br /><strong>Conclusion.</strong> The recombinant apolipoprotein A-I under study has cardiotonic properties similar to its native form. However, the mechanism for implementing the inotropic effect requires further study.</p><p>Received 3 September 2018. Revised 8 October 2018. Accepted 11 October 2018.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Conflict of interest:</strong> Authors declare no conflict of interest.</p><p><strong>Author contributions</strong><br />Conception and study design: A.R. Kolpakov, R.A. Knyazev<br />Data collection and analysis: N.V. Trifonova, A.V. Ryabchenko, M.V. Kotova<br />Critical revision of the article: R.A. Knyazev<br />Drafting the article R.A. Knyazev<br />Critical revision of the article: A.R. Kolpakov, L.M. Polyakov <br />Final approval of the version to be published: R.A. Knyazev, N.V. Trifonova, A.V. Ryabchenko, M.V. Kotova, A.R. Kolpakov, L.M. Polyakov</p>


2003 ◽  
Vol 285 (1) ◽  
pp. H316-H324 ◽  
Author(s):  
Richard Southworth ◽  
Pamela B. Garlick

The clinical hallmarks of hibernating myocardium include hypocontractility while retaining an inotropic reserve (using dobutamine echocardiography), having normal or increased [18F]fluoro-2-deoxyglucose-6-phosphate (18FDG6P) accumulation associated with decreased coronary flow [flow-metabolism mismatch by positron emission tomography (PET)], and recovering completely postrevascularization. In this study, we investigated an isolated rat heart model of hibernation using experimental equivalents of these clinical techniques. Rat hearts ( n = 5 hearts/group) were perfused with Krebs-Henseleit buffer for 40 min at 100% flow and 3 h at 10% flow and reperfused at 100% flow for 30 min (paced at 300 beats/min throughout). Left ventricular developed pressure fell to 30 ± 8% during 10% flow and recovered to 90 ± 7% after reperfusion. In an additional group, this recovery of function was found to be preserved over 2 h of reperfusion. Electron microscopic examination of hearts fixed at the end of the hibernation period demonstrated a lack of ischemic injury and an accumulation of glycogen granules, a phenomenon observed clinically. In a further group, hearts were challenged with dobutamine during the low-flow period. Hearts demonstrated an inotropic reserve at the expense of increased lactate leakage, with no appreciable creatine kinase release. PET studies used the same basic protocol in both dual- and globally perfused hearts (with 250MBq18FDG in Krebs buffer ± 0.4 mmol/l oleate). PET data showed flow-metabolism “mismatch;” whether regional or global,18FDG6P accumulation in ischemic tissue was the same as (glucose only) or significantly higher than (glucose + oleate) control tissue (0.023 ± 0.002 vs. 0.011 ± 0.002 normalized counts · s-1· g-1· min-1, P < 0.05) despite receiving 10% of the flow. This isolated rat heart model of acute hibernation exhibits many of the same characteristics demonstrated clinically in hibernating myocardium.


2011 ◽  
Vol 25 (8) ◽  
pp. 560-565
Author(s):  
Kenji Fukushima ◽  
Mitsuru Momose ◽  
Chisato Kondo ◽  
Nobuhisa Hagiwara ◽  
Shuji Sakai

2006 ◽  
Vol 14 (5) ◽  
pp. 273-280 ◽  
Author(s):  
Daya D. Verma ◽  
Tatyana S. Levchenko ◽  
Eugene A. Bernstein ◽  
Dmitriy Mongayt ◽  
Vladimir P. Torchilin

2003 ◽  
Vol 41 (6) ◽  
pp. 331
Author(s):  
Ofer Merin ◽  
Eyal Atias ◽  
Ari Zimran ◽  
Debbie Elstein ◽  
Gerhard Wasser ◽  
...  

2013 ◽  
Vol 36 (10) ◽  
pp. 1270-1278 ◽  
Author(s):  
L. Figueroa-Valverde ◽  
F. Díaz-Cedillo ◽  
E. García-Cervera ◽  
E. Pool Gómez ◽  
M. López-Ramos ◽  
...  

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