Energy transduction in myocardial myofibrils in thyrotoxicosis

Energy transduction in myocardial myofibrils in thyrotoxicosis

J Mel Cell Cardiol 21 (Supplement IV) (1989) Pi'9KNKRGY TRLNSDUCTI~ IK MYOCARDIAL MYOFIBRILS IN THYROTCKICOSIS. N.V.Karsanov,D.R.Tatulashvili, G...

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J Mel

Cell

Cardiol

21 (Supplement

IV) (1989)

Pi'9KNKRGY TRLNSDUCTI~ IK MYOCARDIAL MYOFIBRILS IN THYROTCKICOSIS. N.V.Karsanov,D.R.Tatulashvili, G.V.Suko an. The Republican Reseati Center of Medical Biophysics, Tbilisi, 9;SSR The work was carried out on skinned fibers and purified myofibrils from dog hearts. In 2-week thyrotoxicosis (induced by injection of L-thyroxine,O.7 mg/kg) decrease in max&nnna force generated by skinnsd muscle fibers is assooiated with a sharp increase in free energy release per generated force unit and a sharp increase in wastefulness of energy utilization during contraotion. It is especially visible in ehrinkage force maintenanoe phase, In 2-5-month thyrotoxicosis the same decrease in force generated by skinned fibre is accompanied by a sharp decrease in ATP hydrolysis enthalpy and efficiently utilized energy by contractile protein system to the restin state level, with the heat production rate being relatively high, i.e. the economy of contractile process is markedly reduoed. It is concluded that energy transduction disturbance in the contractile protein system in t$y$)toxicosis is due to the failure of actin to activate myosin rillar ATPase and disturbed couplin@; of generated force and 7A P hyirolysis free energy release by aotomyosin.

P8OOm THE STRUWJJRK OF THIN FILAMENT AND ACTIN PRUl'OMERKS FROM NORMAL

KYCCARDIUM. T.G.Ssmsonidze, O.N.Zograf, D.G.Khachidze, D.D.Eristavi, N.V.Karsanov. The Mpublioan Research Center of Medioal Biophysics of the Georgian SSR, Tbilisi, USSR Three-dimensional reoonstruotion of thin filament from a normal rabbit myooardial cell was performed based on electron miCrOf%Opy, optical and oomputer diffraction and filtration data. It was found that the parameters of a thin filament helix were subjected to changes due to transfer constant instability. In those filament sites for which athree-d nsional reoonstruotion was o ried out transfer onstant was 27.5 8"", the period of helix was 770 K diameter was 100 I;z p/q=28/13. Reconstruction showed that actin protomeres were packed into a thin filament within a single-stranded helix, the tropomyosin filament being located at the outer side of the small domain at a distame of40 from its axis and forming a two-started helix with a period of I % snd p/q=2/I, The actin protomere had the dimensions of of two domains, the tan@ntial components of 65x45x4C F and consisted the slope of the large domain to the helioal axis being 70°. The a&in rotomere resemblea a kidney by shape situated in a thin filament so i hat its bent end follewa helical rotation direction.

P~~MODIFICATION OF NEUTROPHIL FUNCTIONS AFTER TI@rATMENT WITH ISOSORBIDE DINITRATE AND MOLSIDOMINE Tomasz Siminiak, Henryk Wysocki, Academy of Medicine, Institute of Internal Medicine, Dept. Intensive Therapy, Przybyszewskiego 49, PL-60 355, Poznan, Poland There is evidence, that polymorphonuclear neutrophils (PMN) increase irreversible tissue injury during acute myocardial infarction, through its mechanical properties as well'as through release of free oxygen radicals and proteolityc enzymes. We investigated the effect of oral treatment with vasodilator drugs, isosorbide dinitrate and molsidomine (M), on neutrophil migration in viva. 26 patients with ischemic (ISDN), heart disease, were investigated using the "skin chamber technique". After skin scarification on volar surface of forearm, we placed a chamber with autologous serum, and calculte the number of migrated neutrophils. After or@ tseatment with ISDN,6the2 number of PMN in the chamber increased from 27.6f9.0 x 10 /cm to 69.0f11.4 x 10 /cm (p
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