Kancirova 2016 Nove Strategicke Pristupy v experimentalnej Kardioprotekcii: Difference between revisions

Latest revision as of 13:22, 23 January 2019

Kancirová I, Jašová M (2016) Mitochondrie ako hlavné efektory mechanizmov endogénnej ochrany myokardu. Nove Strategicke Pristupy v experimentalnej Kardioprotekcii 72-89.

» Open Access PDF

Kancirova I, Jasova M (2016) Nove Strategicke Pristupy v experimentalnej Kardioprotekcii 72-89

Abstract: Ischemic heart disease is one of the most frequent causes of severe myocardial injury occuring in the developed countries. Therefore, the emphasis is focused on the new possibilities of the cardioprotection usage in order to avoid the lethal heart injury and to improve its functional parameters. Different types of preconditioning preparing heart on the increased load induce protective functional and structural changes participating in processes of endogenous protection. The aim of our study was to elucidate the role of heart mitochondria as the final effector of noninvasive form of remote ischemic preconditioning applied at the distance location from the heart. Remote ischemic preconditioning consisted of three cycles of 5-minutes ischemia and 5-minutes reperfusion (200 mmHg) of the right hind limb using a pressure cuff. Mitochondria were isolated by differential centrifugation using the protease (P 6141) from the excited hearts subjected to ischemia-reperfusion Langendorff test (15 minutes of stabilization, 30 minutes of global ischemia, 40 minutes of reperfusion). Following parameters were determined in the isolated heart mitochondria: the activity of mitochondrial respiration using respirometer Oxygraph-2k (Oroboros Instruments, Austria), the mitochondrial ATP synthase activity determined as the amount of inorganic phosphate released by ATP splitting per unit of time, the mitochondrial membrane fluidity by spectrofluorometry using the fluorescent probe 1,6-diphenyl-1,3,5-hexatrien and the content of oxidised isoforms coenzyme Q(CoQ9ox) by HPLC method. Isolated heart exposed to ischemic-reperfusion injury resulted in a reduction of the mitochondrial ATP synthase activity as well as decrease in the ADP-stimulated respiration without affecting the basal mitochondrial respiration. Increase the content of coenzyme CoQ9ox oxidised isoforms reflecting respiratory chain damage during heart global ischemia and reperfusion accompanied by the mitochondrial membrane fluidity decrease. Remote ischemic preconditioning partly prevented the decrease of mitochondrial ATP synthase activity as well as decrease of ADP-stimulated respiration due to ischemia-reperfusion injury whereas the content of coenzyme CoQ9ox oxidized isoforms was increased after 15 minutes stabilization of ischemiareperfusion test. Mitochondrial membrane fluidity was increased in all phases of ischemia-reperfusion test. Despite of increased generation of free oxygen radicals during the stabilization phase, rigidization of the mitochondrial membrane was not observed. This findings suggest a signallig role of free oxygen radicals. Our results confirm damaging consequence of ischemia-reperfusion test on the functional and structural properties of the heart mitochondria. Remote ischemic preconditioning trought the generation of free oxygen radicals by the mitochondrial respiratory chain probably indicates the mechanisms of heart endogenous protection that lead to the alleviation of the lethal damaged induced by ischemic-reperfusion injury. • Keywords: Remote ischemic preconditioning, Ischemia-reperfusion injury, Heart mitochondria, Respiratory chain, Free oxygen species, Mitochondrial membrane fluidity

Labels: MiParea: Respiration Pathology: Cardiovascular Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart Preparation: Isolated mitochondria Enzyme: Complex V;ATP synthase

Coupling state: OXPHOS

HRR: Oxygraph-2k

2016-02

@@ Line 1: / Line 1: @@
 {{Publication
-|title=Kancirová I, Jašová M (2016) Mitochondrie ako hlavné efektory mechanizmov endogénnej ochrany myokardu. Nove Strategicke Pristupy v experimentalnej Kardioprotekcii p:92.
+|title=Kancirová I, Jašová M (2016) Mitochondrie ako hlavné efektory mechanizmov endogénnej ochrany myokardu. Nove Strategicke Pristupy v experimentalnej Kardioprotekcii 72-89.
 |info=[http://www.preveda.sk/media/var/files/NOV%C3%89%20STRATEGICK%C3%89%20PR%C3%8DSTUPY%20V%20EXPERIMENT%C3%81LNEJ%20KARDIOPROTEKCII_PREVEDA%202016.pdf#page=72 Open Access PDF]
 |authors=Kancirova I, Jasova M
 |year=2016
-|journal=Nove Strategicke Pristupy v experimentalnej Kardioprotekcii
+|journal=Nove Strategicke Pristupy v experimentalnej Kardioprotekcii 72-89
-|abstract=Vedecká monografia pod názvom „Nové strategické prístupy v experimentálnej kardioprotekcii“
+|abstract=Ischemic heart disease is one of the most frequent causes of severe myocardial injury occuring in the developed countries. Therefore, the emphasis is focused on the new possibilities of the cardioprotection usage in order to avoid the lethal heart injury and to improve its functional parameters. Different types of preconditioning preparing heart on the increased load induce protective functional and structural changes participating in processes of endogenous protection. The aim of our study was to elucidate the role of heart mitochondria as the final effector of noninvasive form of remote ischemic
-ponúka prehľad aktuálnych, vysoko odborných štúdií z oblasti základného kardiovaskulárneho
+preconditioning applied at the distance location from the heart. Remote ischemic preconditioning consisted of three cycles of 5-minutes ischemia
-výskumu. Experimentálny výskum v oblasti srdcovo-cievnych ochorení
+and 5-minutes reperfusion (200 mmHg) of the right hind limb using a pressure cuff. Mitochondria were isolated by differential centrifugation using
-tvorí nosný pilier pre úspešnú liečbu a prevenciu kardiovaskulárnych ochorení. Vedecká
+the protease (P 6141) from the excited hearts subjected to ischemia-reperfusion Langendorff test (15 minutes of stabilization, 30 minutes of global ischemia, 40 minutes of reperfusion). Following parameters were determined in the
-monografia je prierezom nových poznatkov, ktoré v sebe zahrňujú výskum adaptačných
+isolated heart mitochondria: the activity of mitochondrial respiration using respirometer Oxygraph-2k (Oroboros Instruments, Austria), the mitochondrial ATP synthase activity determined as the amount of inorganic phosphate released by
-odpovedí a mechanizmov ochrany patologicky ovplyvneného myokardu s prihliadnutím
+ATP splitting per unit of time, the mitochondrial membrane fluidity by spectrofluorometry using the fluorescent probe 1,6-diphenyl-1,3,5-hexatrien
-na vek a pohlavné rozdiely. Prezentované výsledky poskytujú informácie o aktivácii protektívnych
+and the content of oxidised isoforms coenzyme Q(CoQ9ox) by HPLC method. Isolated heart exposed to ischemic-reperfusion injury resulted in a reduction
-procesov, vedúcich k zvýšeniu tolerancii srdca voči ischemickému poškodeniu.
+of the mitochondrial ATP synthase activity as well as decrease in the ADP-stimulated respiration without affecting the basal mitochondrial respiration. Increase the content of coenzyme CoQ9ox oxidised isoforms reflecting respiratory chain damage during heart global ischemia and reperfusion accompanied by the mitochondrial membrane fluidity decrease.
-Zároveň poukazuje na dôležitosť detailného poznania vplyvu rizikových faktorov zodpovedných
+Remote ischemic preconditioning partly prevented the decrease of mitochondrial ATP synthase activity as well as decrease of ADP-stimulated respiration
-za vznik srdcovo-cievnych ochorení, súvisiacich so životným štýlom.
+due to ischemia-reperfusion injury whereas the content of coenzyme CoQ9ox oxidized isoforms was increased after 15 minutes stabilization of ischemiareperfusion test. Mitochondrial membrane fluidity was increased in all phases of ischemia-reperfusion test. Despite of increased generation of free oxygen radicals during the stabilization phase, rigidization of the mitochondrial membrane was not observed. This findings suggest a signallig role of free oxygen radicals. Our results confirm damaging consequence of ischemia-reperfusion test on the functional and structural properties of the heart mitochondria. Remote ischemic preconditioning trought the generation of free oxygen radicals by the mitochondrial respiratory chain probably indicates the mechanisms of heart endogenous protection that lead to the alleviation of the lethal damaged induced by ischemic-reperfusion injury.
-Vedecká monografia poskytuje aktuálny prehľad strategických postupov využívajúcich
+|keywords=Remote ischemic preconditioning, Ischemia-reperfusion injury, Heart mitochondria, Respiratory chain, Free oxygen species, Mitochondrial membrane fluidity
-ku kardioprotekcii procesy endogénnej ochrany, akými sú ischemický preconditioning,
-ako aj neinvazívny spôsob zvýšenia ischemickej tolerancie srdca, pri ktorom sa spúšťací
-ischemický impulz aplikuje na mieste vzdialenom od miesta očakávaného protektívneho
-efektu, klinicky aplikovateľný preconditioning “na diaľku“, tzv. „remote“ ischemický preconditioning.
-Významná časť monografie je venovaná štúdiu energetickej udržateľnosti myokardu
-počas jeho patologickej záťaže so zreteľom na funkciu mitochondrií. Dôležitou súčastou
-sú informácie o možnosti prevencie kardiovaskulárnych ochorení ovplyvnením endotelu –
-spoločného miesta, kde pôsobia rôzne rizikové faktory kardiovaskulárnych chorôb.
-Autori jednotlivých kapitol prihliadali pri vytvárani tohto súborného diela na významnú
-vlastnosť, akou je schopnosť myokardu čiastočne sa adaptovať na patologický podnet.
-Prihladajúc na tento dôležitý poznatok prebieha v myokarde oproti patogickým podnetom
-celý rad kompenzačných mechanizmov, ktorých výsledkom je udržanie funkcie srdca a následne
-jeho prežívanie.
-Oblasť výskumu kompenzačných mechanizmov účinných v procesoch endogénnej
-ochrany myokardu, ku ktorému prispieva i táto monografia sa ukazuje byť ako perspektívna
-metóda v podmienkach zvýšených energetických nárokov patologicky zaťaženého
-myokardu.
-Prezentované poznatky sú vhodné ako podporný študijný materiál pre študentov lekárskych
-a prírodných vied. Na svoje si prídu nadšenci experimentálnej kardioprotekcie, fyziológie,
-patofyziológie, molekulárnej biológie, biochémie, ale aj biofyziky.
 }}
 {{Labeling
 |area=Respiration
+|organism=Rat
+|tissues=Heart
+|preparations=Isolated mitochondria
+|enzymes=Complex V;ATP synthase
+|injuries=Ischemia-reperfusion
+|diseases=Cardiovascular
+|couplingstates=OXPHOS
 |instruments=Oxygraph-2k
-|additional=Labels, 2016-02
+|additional=2016-02
 }}