Chronic massive rotator cuff tear in rats: in vivo evaluation of muscle force and three-dimensional histologic analysis.

BACKGROUND: Massive rotator cuff tear repair is frequently complicated by unsatisfactory clinical results due to possible tendon retraction, muscle atrophy, and fatty degeneration. The objective of this study was the development of a chronic massive tear in a rat model and the evaluation of the muscle force in vivo and of the histologic changes in a 3- dimensional manner. METHODS: To simulate massive rotator cuff tears, both the supraspinatus (SS) and the infraspinatus (IS) tendons were surgically detached from the right humerus of 15 male adult Sprague-Dawley rats. Twelve weeks postoperatively, all animals underwent isometric tension recordings of both the SS and IS muscles. Histologic analysis and image deconvolution processing were performed to estimate the presence and the distribution of atrophy in 3 dimensions. RESULTS: An overall 30% and 35% reduction in muscle force of the SS and IS muscles, respectively, was observed compared with the left uninjured shoulder (P < .005). Histologic analysis revealed that the degeneration and the fatty infiltration were more evident near the tendon and at the dorsal side in both muscle groups. CONCLUSIONS: These results show that functional impairment of SS and IS muscles after chronic massive tendon tears could be attributed to the decrease in muscle force production during their repair on the greater tuberosity and, second, to the comparatively greater degeneration of their dorsal part.

Three-dimensional morphometric mapping of rat muscle fibers.

INTRODUCTION: Quantitative descriptions of fiber type organization in hind limb muscles are incomplete or rare. METHODS: Fiber morphometrics for both rat tibialis anterior (TA) muscles were measured in 3 dimensions. RESULTS: Slow oxidative fiber area and perimeter varied in all zones. Fast oxidative glycolytic fibers (FOG) were predominant in the mediolateral and posterior zones, and fast glycolytic fibers (FG) predominated in the anterior zone. The mean area of FOG and succinate dehydrogenase intermediate fibers was lowest in the anterior zone. Mean area of FG was highest in the proximal and distal parts of the muscle. The area and perimeter of fast fibers differed significantly between the right and left limbs in the medial zone. In the middle and lateral zones, they differed at the proximal and distal parts. CONCLUSIONS: This detailed analysis in a high resolution, 3-dimensional map provides an essential tool for understanding the structure and function of TA muscles.

Assessment of motoneuron death during development following neonatal nerve crush and Mg2+ treatment.

BACKGROUND: Sciatic nerve injury in neonatal rats impairs muscle recovery and significantly reduces the number of surviving motoneurons. We examined the rate of motoneuron death after sciatic nerve crush in neonatal rats, as well as the neuroprotective effect of systemic MgSO4 administration, by assessing the number of horseradish peroxidase -labelled motoneurons in the spinal cord ventral horn, after injecting EDL and TA muscles. MATERIAL/METHODS: Left sciatic nerve crush was performed on the 2nd postnatal day. MgSO4 (0.05 ml of 1 M solution/10 g body weight) was administered subcutaneously, daily for twelve days. Animals were examined for the number of motoneurons of EDL and TA muscles, in the spinal cord ventral horns at 14, 21, and 28 days postnatally (P) and adulthood. 24 h to 48 h after intramuscular HRP injection, the animals were perfused transcardially with a fixative containing glutaraldehyde. Serial sections of the spinal cords were cut and processed for Hanker-Yates staining, and the number of labeled motoneurons was measured under a camera lucida. RESULTS: Nerve crush resulted in 37% motoneuron survival at P14, 33% at P21, 28% at P28 and 21% in adult rats. Following MgSO4 administration motoneuron survival rates of 51%, 47%, 44% and 39% were observed respectively, for the different age groups. The values obtained in magnesium-treated rats proved to be significantly different (p<0.05), compared to non-treated rats of the same age group. CONCLUSIONS: Nerve crush after birth resulted in significant motoneuron death, established already at P14. MgSO4 administration induced significant motoneuron survival.

Serum estradiol, progesterone, testosterone, FSH and LH levels in postmenopausal women with Alzheimer's dementia.

Several studies have suggested that estrogen replacement therapy lowers the risk of Alzheimer's dementia (AD) among postmenopausal women. Other studies have evaluated serum levels of sex hormones and gonadotropins in women with AD. Estrogens (E(1) and E(2)), luteinizing hormone (LH) and follicular stimulating hormone (FSH), dihydroepiandrosterone and sex hormone binding albumin, which normally responds to circulating testosterone, have been investigated by others using the same protocol in postmenopausal women with AD, older than 65 years. Others have studied in elderly women with AD, also using one protocol, fewer sex hormones and/or gonadotropins. We have studied the serum levels of estradiol, progesterone, testosterone, LH and FSH in the same serum sample of postmenopausal women with AD and other dementias and compared them to a group of controls. We are not aware of a similar study in the literature. All patients were diagnosed on clinical grounds and screened by the mini mental score examination (MMSE). Forty eight women had AD (Group A), mean age 72 years and age range 60-84 years, s even had other types of dementia (Group B), mean age 63.5 years and age range 53-74 years and 33 women had no cognitive impairment and were studied as controls (Group C). Group C women had mean age of 65 years and their age ranged between 55-73 years. Estradiol, progesterone and testosterone were measured by radioimmunoassay (RIA), while FSH and LH by radioimmunometric assay (IRMA). Our results showed that estradiol was significantly lower in Group A as compared to Group C (P=0.04). There was no significant difference in the levels of the other four hormones in the three Groups as studied by the Mann-Whitney U and the Pearson's statistical test. Our results were not influenced by differences due to sex, age, ethnic group or education since these factors were either similar or comparable in all Groups studied. All but two of the subjects, with mild alcoholism, smoking, increased BMI and chronic diseases, had all five hormones studied within reference limits. We consider that the absence of difference we found in the four hormone levels, in Groups A, B and C may be related to free hormones, to the different stage of AD of our patients, to intra assay variability, to assay sensitivity or to other non specified factors. Future study may be directed towards whether a primary or secondary hypogonadism exists in AD and whether hormones are contributing to or are the result of brain degeneration in AD.