Properties of soleus muscle Z-lines and induced Z-line analogs revealed by dissection with Ca2+-activated neutral protease.

Rat soleus muscle Z-lines and Z-line anomalies induced by neostigmine methyl sulfate (NMS) and cat soleus muscle Z-lines and Z-line anomalies induced by tenotomy were examined by electron microscopy before and after dissection of muscle fibers with Ca2+-activated neutral protease (CAF) to elucidate structural properties of Z-lines and related Z-line-type structures. In both normal and treated muscles, interdigitation of thin (6-7 nm) filaments, which were continuous with I-filaments (actin) from adjacent sarcomeres, was observed at the Z-line in longitudinal section. Both neostigmine methyl sulfate and tenotomy treatments induced muscle atrophy associated with Z-line degradation, streaming, and irregular distribution and accumulation of Z-line material and Z-rod formation. Tenotomized muscle also was characterized by the presence of N-line-like bands and I-Z-I brushes. CAF digestion removed the electron-dense covering material from Z-rods and revealed a backbone of actin filaments. The origin of Z-rods, their structural similarity to Z-lines in longitudinal and cross section, and their susceptibility to CAF indicate that Z-rods are directly related to native Z-lines and are probably lateral polymers of a basic Z-line unit. The regular square net alignment (22 nm) of I-filaments (actin) in cross sections of I-Z-I brushes which contain no N-lines suggests that the I-square net arrangement near the Z-line is determined by Z-filament-actin filament interaction rather than by the N-line or other factors. The results suggest that I-filaments (actin) penetrate the mammalian Z-line and are Z-line constituents and that the width of Z-lines and the length of Z-rods are determined by the amount of overlap of actin filaments. The perpendicular periodicity of Z-rods and the zigzag-oblique arrowheadlike appearance seen in longitudinal sections of Z-lines are attributed to alpha-actinin.

Hemodynamics of arterial stenoses at elevated flow rates.

This study is concerned with the pressure drop that develops across an arterial stenosis, with particular emphasis on the effect of the stenosis at high blood flow rates induced by a locally administered vasodilator drug. Stenoses, ranging in severity from 55.7% to 91.0% reduction in lumen area were artificially induced in the femoral and carotid arteries of large mongrel dogs. Instantaneous flow rates and pressure drops were measured over a wide range of flow conditions. Mean velocities varied from 3.9 to 88.8 cm/sec. Experimental data support the applicability of a relatively simple equation for predicting the pressure drop over this wide range of velocities and stenosis geometries. Results show that blood flow through a particular artery can increase by a large factor, in the range of 4-5, under conditions of vasodilation with a corresponding large decrease in pressure distal to the stenosis. The pressure drop increases in a nonlinear manner with velocity and thereby accentuates the importance of the stenosis at elevated flow rates. We suggest that a critical stenosis be defined in terms of its effect on maximal flow rather than resting flow.

Pressure drop across artificially induced stenoses in the femoral arteries of dogs.

Stenoses were artificially induced in 13 large mongrel dogs by implanting small hollow cylindrical plugs in their femoral arteries. The instantaneous pressure drop across the stenosis and the flow rate were measured for a series of stenoses varying in severity from 52.3 to 92.2%. Mean pressure drops ranged from approximately 2 to 30 mm Hg with peak pressure drops ranging from 9 to 53 mm Hg. The pressure drop could be estimated from a relatively simple equation that was originally developed for flow through model stenoses. With this equation, the effects of several factors that contribute to the pressure drop, including stenosis size and shape, artery lumen diameter, blood density, blood viscosity, and velocity and acceleration of flow, could be clearly delineated. For severe stenoses, unsteady flow effects were small and flow could be treated as quasi-steady. Calculations based on data obtained from the dog experiments revealed that the mean pressure drop across a stenosis increased nonlinearly with percent stenosis and showed quantitatively that the value of critical stenosis decreased with increasing demand for blood flow.