Proliferation Of Sarcoplasmic Reticulum Research Articles

Sound production, hearing sensitivity, and in-depth study of the sound-producing muscles in the cowfish (Lactoria cornuta).

The ability to produce sounds has been reported in various Ostraciidae but not deeply studied. In some Ostracion species, two different sound-producing muscles allow these boxfishes to produce two different kinds of sounds in a sequence. This study investigates sound production in another Indo-Pacific species, the longhorn cowfish Lactoria cornuta that also possesses two pairs of sonic muscles associated with the swim bladder: extrinsic sonic muscles (ESMs) and intrinsic sonic muscles (ISMs). The cowfish produces two kinds of sounds called hums and clicks. Hums are made of trains of low amplitude pulses that last for long periods of time, suggesting that they are produced by fatigue-resistant muscles, whereas clicks correspond to shorter sounds with greater amplitude than the hums, suggesting that they result from more powerful contractions. Ultra-structural differences are found between extrinsic and intrinsic sonic muscles. According to features such as long sarcomeres, long I-bands, a high number of mitochondria, and a proliferation of sarcoplasmic reticulum (SR), ESMs would be able to produce fast, strong, and short contractions corresponding to clicks (the shortest sounds with the greatest amplitude). ISMs have the thinnest cells, the smallest number of myofilaments that have long I-bands, the highest volume of mitochondria, and well-developed SR supporting these muscles; these features should generate fast and prolonged contractions that could correspond to the hums that can be produced over long periods of time. A concluding figure shows clear comparisons of the different fibers that were studied in L. cornuta. This study also compared the call features of each sound with the cowfish's hearing ability and supports L. cornuta was more sensitive to frequencies ranging between at least 100 and 400Hz with thresholds of 128-143dBre1µPa over this range, meaning that they are sensitive to the frequencies produced by conspecifics.

Morphologic changes in extraocular muscles of the dystrophic hamster.

Cardiomyopathic hamsters (UM-X7.1 strain) have demonstrable myopathy involving both skeletal and cardiac muscle. In addition, they have multiple ocular abnormalities. In this study, extraocular muscles were examined by light and electron microscopy. Changes observed within affected muscle fibers were variable and included coagulation necrosis, lysis of myofibrils, mitochondrial changes, and infiltration by phagocytic cells. Regenerative changes included duplication of myoblast nuclei, proliferation of sarcoplasmic reticulum, and myofibrillogenesis. The lesions are presumably myogenic in origin. The cardiomyopathic hamster may be useful as an animal model for certain types of ocular myopathy in man.

ULTRASTRUCTURAL ASPECT OF LEFT VENTRICULAR HYPERTROPHY IN SPONTANEOUSLY HYPERTENSIVE RATS : A QUALITATIVE AND QUANTITATIVE STUDY

The morphology of the left ventricular myocardium of spontaneously hypertensive rats (SHR) (Okamoto and Aoki) was studied with light and electron microscopes, with special reference to a quantitative analysis of subcellular organelles and a description of the characteristics of the capillaries in myocardium. Paired groups of SHR and control Wistar-Kyoto rats were sacrificed at 3, 5, 9, 11, 15 and 21 weeks and one year of age. In the left ventricular lateral wall of SHR, starting at the age of 11 weeks, the cardiocytes became progressively thicker as the blood pressure rose and exhibited various ultrastructural alterations. In these cardiocytes, the proliferation of Z-band materials was occasionally present in the myofibrils, and was closely associated with the subsarcolemmal area and intercalated discs. Convolutions and extensive foldings of the intercalated discs were prominent. Mitochondrial abnormalities consisted of fragmentation and stacks of cristae, aggregates of small mitochondria and intramitochondorial α-glycogen rosettes. In one-year-old SHR, malaligned cardiocytes as well as myofibrils were seen in certain areas of the myocardium. In some cardiocytes, streaming and clumping of Z-band material, myofibrillolysis and proliferation of sarcoplasmic reticulum appeared. In addition, there were clusters of spherical microparticles, tubular aggregates and intramitochondrial inclusions, suggestive of degenerative changes. Stereological analysis of subcellular organelles in the hypertrophied cardiocytes of SHR revealed an increase of myofibrillar volume fractions and a decrease of mitochondrial volume fractions, resulting in an increase in the ratio of myofibrils to mitochondria. These findings differed from those in the posterior papillary muscle of the left ventricle in the same animal hearts. Thus, it is apparent that myocardial hypertrophy varies in each area of the myocardium due to different stresses during the course of its development. In the hypertrophied myocardium of SHR, the capillaries were seen to proliferate with the appearance of a "tunnel capillary", while interstitial fibrosis and hypertensive vascular lesions progressed with aging. The capillary proliferation maintained a constant diffusion distance from the capillary to the cardiocyte, probably as one of adaptation in cardiac hypertrophy in SHR.

Myocardial ultrastructure in patients with chronic aortic valve disease

Light and electron microscopic observations were made on left ventricular myocardium removed at operation from 16 patients with chronic aortic valve disease. In all 16 patients most cardiac muscle cells were hypertrophid, and surrounded by small amounts of fibrous tissue. In two of the six patients with pure aortic regurgitation and in four of the five patients with combined aortic stenosis and regurgitation, cardiac muscle cells with evidence of degeneration were present in addition to hypertrophied, nondegenerated cells. Degenerated cardiac muscle cells were not observed in the six patients with predominant aortic stenosis. Cardiac muscle cells with mild degeneration showed focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. More severely degenerated muscle cells showed a marked decrease in the numbers of myofibrils and T tubules and proliferation of sarcoplasmic reticulum or mitochondria, or both. Severely degenerated cells usually were present in areas of marked fibrosis, often were atrophic, had thickened basement membranes and had lost their intercellular connections. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic aortic valve disease.

Ultrastructure of crista supraventricularis muscle in patients with congenital heart diseases associated with right ventricular outflow tract obstruction.

Ultrastructural studies were made of operatively resected crista supraventricularis muscle in 59 patients with congenital heart diseases, or whom 54 had obstruction to right ventricular outflow. Relationships of anatomic diagnosis, age, peripheral arterial oxygen saturation (PAO2), peak right ventricular systolic pressure gradient and right ventricular end-diastolic pressure (RVEDP) to hypertrophic changes, abnormalities of cellular and myofibrillar orientation, and degenerative alterations were determined. Changes directly related to hypertrophy were: cell diameters greater than 20 mu, irregular cell shape, lobulated nuclei, multiple intercalated discs, dilated T tubules, abnormal Z bands, and increased numbers of ribosomes. Abnormalities of cellular or myofibrillar orientation were focal in distribution and occurred in 12 patients, most of whom had elevated RVEDP, decreased PAO2, markedly enlarged cells, and interstitial fibrosis. Interstitial fibrosis was prominent in 19 patients and was associated with cellular hypertrophy, elevation of RVEDP, and increased age of the patients. Degenerative changes (myofibrillar lysis, abnormally small mitochondria, myelin figure formation, and proliferation of sarcoplasmic reticulum in cardiac muscle cells ocurred in six patients and correlated with increased age, decreased PAO2, and elevated RVEDP. Mitochondria containing glycogen deposits were present in 17 patients, most of whom had decreased PAO2. The variability of morphologic manifestations of chronic cardiac hypertrophy and the relationships of hypertrophic changes to orientation abnormalities and degenerative alterations are discussed.