Mechanical properties of the vascular smooth muscle from normal and dystrophin-deficient (mdx) mice were examined. Changes in resting and developed tensions in response to stretch were recorded in isolated portal vein. The vascular segments were elongated in 5% increments of the 'in situ' length (L(r)) up to 1.30 L(r). The resting length-tension curves in male mdx mice were similar to normal mice, while a marked decrease in the slope of the curve was noted in female mdx mice. These findings were not affected by atropine, phentolamine, tetrodotoxin or [CA2+] in the surrounding media. At L(r), the tension of isolated portal vein was characterized by spontaneous synchronized uniform force waves in normal mouse. In contrast, the mdx mouse portal veins an irregular motor pattern characterized by desynchronized force waves with a decrease of amplitude and an increase in frequency was recorded. Extension of the length of the portal vein segment did not increase the spontaneous phasic activity developed in female mdx mice although this was noted with male mdx mice and normal mice. Experiments with chemical depolarizing agents indicated that spontaneous myogenic excitation activated the great majority of vascular smooth muscle cells in normal mouse portal vein, whereas in mdx mice only a reduced number of these cells were excited suggesting that in the mdx mouse the intercellular electronic coupling is altered. In conclusion this study provides the first description of the mechanical activities of portal vein longitudinal muscle and shows that in mdx mice the motor activity is severely disrupted.

Mancinelli, R., Tonali, P., Romani, R., Tringali, A., Vargiu, R., Azzena, G. B., Mechanical properties of smooth muscle portal vein in normal and dystrophin-deficient (mdx) mice, <<EXPERIMENTAL PHYSIOLOGY>>, 1999; 84 (5): 929-940. [doi:10.1017/S0958067099018709] [http://hdl.handle.net/10807/194294]

Mechanical properties of smooth muscle portal vein in normal and dystrophin-deficient (mdx) mice

Mancinelli, R.;Tringali, A.;Azzena, G. B.
1999

Abstract

Mechanical properties of the vascular smooth muscle from normal and dystrophin-deficient (mdx) mice were examined. Changes in resting and developed tensions in response to stretch were recorded in isolated portal vein. The vascular segments were elongated in 5% increments of the 'in situ' length (L(r)) up to 1.30 L(r). The resting length-tension curves in male mdx mice were similar to normal mice, while a marked decrease in the slope of the curve was noted in female mdx mice. These findings were not affected by atropine, phentolamine, tetrodotoxin or [CA2+] in the surrounding media. At L(r), the tension of isolated portal vein was characterized by spontaneous synchronized uniform force waves in normal mouse. In contrast, the mdx mouse portal veins an irregular motor pattern characterized by desynchronized force waves with a decrease of amplitude and an increase in frequency was recorded. Extension of the length of the portal vein segment did not increase the spontaneous phasic activity developed in female mdx mice although this was noted with male mdx mice and normal mice. Experiments with chemical depolarizing agents indicated that spontaneous myogenic excitation activated the great majority of vascular smooth muscle cells in normal mouse portal vein, whereas in mdx mice only a reduced number of these cells were excited suggesting that in the mdx mouse the intercellular electronic coupling is altered. In conclusion this study provides the first description of the mechanical activities of portal vein longitudinal muscle and shows that in mdx mice the motor activity is severely disrupted.
Inglese
Mancinelli, R., Tonali, P., Romani, R., Tringali, A., Vargiu, R., Azzena, G. B., Mechanical properties of smooth muscle portal vein in normal and dystrophin-deficient (mdx) mice, <<EXPERIMENTAL PHYSIOLOGY>>, 1999; 84 (5): 929-940. [doi:10.1017/S0958067099018709] [http://hdl.handle.net/10807/194294]
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10807/194294
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