ABSTRACT
Ruptures of the rotator cuff tendons of the human shoulder are a common incidence and lead to functional impairment of the four muscles connected to the cuff, entailing profound changes of their cellular tissue composition. Most importantly, such tendon tears lead to atrophy, fatty degeneration and fibrosis of the corresponding muscles. The muscle most commonly affected with such changes is the M. supraspinatus. The present study uses biopsy samples from the supraspinatus muscle of 12 elderly patients and 6 controls to examine the rupture-induced muscle change at both the cellular and the intracellular (ultrastructural) levels. Amounts of fatty tissue, connective tissue and muscle were assessed by light microscopy-based morphometry and stereology. Stereology of electron micrographs was employed to determine volume densities of muscle fibre mitochondria, myofibrils and intracellular lipid. Results demonstrate that the supraspinatus muscles of patients with a massive rupture contain significantly higher amounts not only of fatty tissue but also of intracellular lipid than those of control subjects. These patients further exhibit a major decrease in relative amounts of myofibrils, thus confirming that change of intracellular composition is a major component of the observed muscle degeneration. The results contribute to establish the true spectrum of supraspinatus muscle damage in humans induced by tendon rupture.
Subject(s)
Muscle, Skeletal/injuries , Muscle, Skeletal/pathology , Muscular Atrophy/pathology , Rotator Cuff Injuries , Rotator Cuff/pathology , Tendon Injuries/complications , Adipose Tissue/pathology , Aged , Aging/pathology , Biopsy , Blood Vessels/pathology , Connective Tissue/pathology , Disease Progression , Female , Fibrosis/etiology , Fibrosis/pathology , Fibrosis/physiopathology , Humans , Lipids , Male , Microscopy, Electron, Transmission , Middle Aged , Mitochondria/pathology , Muscle Fibers, Skeletal/pathology , Muscle, Skeletal/physiopathology , Muscular Atrophy/physiopathology , Rotator Cuff/physiopathology , Severity of Illness IndexABSTRACT
The isoprostanes, 8-iso-prostaglandin F2alpha and 8-iso-prostaglandin E2, which are released in vivo by free radical-catalyzed peroxidation of arachidonic acid, are potent vasoconstrictors. Increased formation of 8-iso-prostaglandin F2alpha has been detected in human cardiovascular diseases, in which enhanced plasma levels of noradrenaline and angiotensin II have harmful vasoconstrictor effects. Therefore, we investigated the influence of perfusions with the thromboxane A2 mimetic, U 46619, and with the isoprostanes, 8-iso-prostaglandin F2alpha, 8-iso-prostaglandin E2, 8-iso-prostaglandin E1 and 8-iso-prostaglandin F3alpha, on the vasoconstrictor effects of noradrenaline and angiotensin II in the isolated perfused rabbit ear. Our results demonstrate that perfusions with U 46619, 8-iso-prostaglandin E2 and 8-iso-prostaglandin F2alpha, at a subthreshold concentration (30 nM), amplified the vasoconstrictions induced by noradrenaline or angiotensin II significantly. In addition, the results show that U 46619, 8-iso-prostaglandin F2alpha, 8-iso-prostaglandin E2 and 8-iso-prostaglandin E1, which were applied as a bolus, induced much more pronounced vasoconstrictions than prostaglandin F2alpha, prostaglandin E2 and prostaglandin F3alpha. Prostaglandin E1 and 8-iso-prostaglandin F3alpha, showed no effects. In conclusion, it can be assumed that the powerful vasoconstrictions induced by 8-iso-prostaglandin E2 and 8-iso-prostaglandin F2alpha and their potentiating effects on vasoconstrictions induced by noradrenaline or angiotensin II might be of pathophysiological relevance in cardiovascular diseases.