Contractility of smooth muscles and ultrastructure of their microfilaments in restriction of physical activity.
BACKGROUND
Depending on the intensity of hypodynamics (as a factor of ischemic heart disease) the aim of our investigation was to determine the contractility of smooth muscles of thoracic aorta with and without endothelium by biological active substances (prostaglandin F2 alpha and acetylcholine) and to compare with ultrastructural alterations of microfilaments.


METHODS
A hypodynamic stress of 48-days duration was provoked via permanent and periodically recurrent intervention (when the hypodynamic state was altered with physical activity) in Chinchilla rabbits by placing them in metal hutches (according to B. M. Fiodorov). The relaxing effect of endothelium--dependent vasodilatator agonist (acetylcholine in concentration 10(-7) M, 10(-6) M, 10(-5) M, 10(-4) M) on smooth muscles (treated with vasoconstrictor prostaglandin F2 alpha) was detected by means of a mechanotron 6 MXIC in isometric regime. The contraction force was expressed in percentage. One hundred percent was the maximum contraction that developed after administration of 2 x 10(-5) M prostaglandin F2 alpha solution to the smooth muscles preparation. For ultrastructure studies of microfilaments semithin sections of smooth muscles were examined with electron microscope 'Philips--300'.


RESULTS
The research findings show that under the influence of acetylcholine the relaxing of endothelium of thoracic aorta smooth muscles (treated with prostaglandin F2 alpha) is more expressed in periodically recurrent intervention.


CONCLUSIONS
Permanent hypodynamic stress of 48 days duration caused strongly expressed contractility of smooth muscles with is associated with ultrastructural damage of microfilaments (such as irregular formation, drop out in flakes, microfilaments becoming shorter and thicker).
Kusleikaite
M
M
Institute of Cardiology of Kaunas Medical University, Kaunas, Lithuania. sstonkus@takas.it
Stonkus
S
S
Kusleika
S
S
D000109:Acetylcholine / Q000494:pharmacology; D008841:Actin Cytoskeleton / Q000187:drug effects / Q000648:ultrastructure*; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D015237:Dinoprost / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000502:physiology*; D007103:Immobilization / Q000502:physiology*; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000502:physiology* / Q000648:ultrastructure; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
D015237:Dinoprost; D000109:Acetylcholine