Significant Increase In Cross-sectional Area Research Articles

Vasoactive intestinal peptide regulates embryonic growth through the action of activity-dependent neurotrophic factor.

Activity-dependent neurotrophic factor is a potent, neuroprotective protein released from astroglia by VIP and accounts in part for the neuroprotective properties of this neuropeptide. The growth-regulatory actions of VIP during embryogenesis may also occur indirectly through the release of activity-dependent neurotrophic factor. Whole cultured day-9 mouse embryos treated with activity-dependent neurotrophic factor (10(-13) M) for 4 hr grew 3.1 somites, compared with 1.6 somites in control embryos. Treated embryos appeared morphologically normal and exhibited significant increases in cross-sectional area, protein, and DNA content and bromodeoxyuridine incorporation. Anti-activity-dependent neurotrophic factor significantly inhibited growth. Co-treatment of embryos with anti-activity-dependent neurotrophic factor inhibited VIP-stimulated growth; however, anti-VIP did not inhibit activity-dependent neurotrophic factor-induced growth. These data indicate that an activity-dependent neurotrophic factor-like substance is an endogenous embryonic growth factor and that VIP-regulated growth occurs, at least in part, through activity-dependent neurotrophic factor.

TREATMENT OF EXERCISE INDUCED MUSCLE INJURY VIA HYPERBARIC OXYGEN THERAPY

206 This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise induced muscle injury. 21 college-aged male volunteers were assigned to three groups: control, immediate HBO (iHBO), and delayed HBO (dHBO). All subjects performed 6 sets (10 repetitions per set) of eccentric repetitions with a load equivalent to 120% of their concentric maximum. HBO treatments consisted of 100 minutes exposure to 2.5 ATA with intermittent breathing of 100% oxygen (30 min. on, 5 min. off). HBO treatments began either 2 (iHBO) or 24 hours (dHBO) post-exercise, and were administered daily through day 4 post-exercise. Dependent variables (cross-sectional area (CSA) and T2 relaxation time via MRI, isometric strength, and perceived soreness for the forearm flexors along with serum creatine kinase (CK)) were assessed at baseline, 24 hours, 7 and 15 days postinjury. Mean baseline CSA values were: 2016.3, 1888.5, and 1972.2 mm2 for control, iHBO and dHBO respectively. All groups showed significant increases in CSA in response to injury (21% @ 24 hours, 18% @ 7 days) (P<0.0001), but there were no significant differences between groups (P=0.438). Mean baseline T2 relaxation times were: 26.18, 26.28, and 27.43 msec for control, iHBO and dHBO respectively. Significant increases for T2 relaxation time were observed for all groups (64% @ 24 hours, 66% @ 7 days, and 28% @ 15 days) (P<0.0001), but there were no significant differences between groups (P=0.692). Isometric strength (P<0.001), serum CK levels (P=0.007), and perceived soreness (P<0.001) also indicated significant muscle injury for all groups but there were no differences between groups (P=0.459, P=0.943, and P=0.448 respectively). These results suggest that hyperbaric oxygen therapy was not effective in the treatment of muscle injury as indicated by the markers evaluated. Supported by a grant from The Hyperbaric Partnership, Denver, CO

Hormone replacement therapy increases isometric muscle strength of adductor pollicis in post-menopausal women

A randomized open trial of hormone replacement therapy was used to assess changes in adductor pollicis muscle strength during 6-12 months of treatment with Prempak C 0.625(R) in comparison with an untreated control group. Muscle strength (maximal voluntary force; MVF), muscle cross-sectional area and bone mineral density were measured. Women entering the trial had oestrogen levels below 150 pmol.l-1, confirming their post-menopausal hormonal status. In the treated group, MVF increased by 12.4+/-1.0% (mean+/-S.E.M.) of initial MVF over the duration of treatment, while it declined slightly (2.9+/-0.9%) in the control group. This increase in strength could not be explained by an increase in muscle bulk, there being no significant increase in cross-sectional area during the study. Those subjects who were weakest at enrolment showed the greatest increases in muscle strength after treatment. Bone mineral density in total hip, Ward's triangle and total spine increased in the treated group, in agreement with previous studies. There was no correlation between the individual increases in bone mineral density and those in MVF.

The influence of angiotensin II-induced increase in aortic wall mass on compliance in rats in vivo.

This study was undertaken to examine the effects of angiotensin II-induced structural changes in the aortic wall on the dynamic mechanical properties of the vessel in the rat. Wistar rats were infused s.c. with 250 ng/kg/min angiotensin II (Ang II) for 14 days (ANG). Both ANG and control rats (CON) were equipped with an arterial catheter for measurement of arterial blood pressure. Thoracic aorta diameter, compliance coefficient (CC), and distensibility coefficient (DC) were determined non-invasively in pentobarbital-anesthetized animals using a B-mode imager attached to a vessel wall tracking system. After sacrifice, medial cross-sectional area (CSA), and elastin and collagen densities were determined by morphometry on cross-sections. Media thickness (Mt) and wall-to-lumen ratio (W/L) were subsequently calculated. Ang II infusion significantly increased mean arterial blood pressure in conscious rats (122 +/- 3 mmHg CON vs. 157 +/- 4 mmHg ANG). This was normalized when the rats were anesthetized, thus making it possible to determine CC and DC under isobaric conditions where the diastolic diameters were also similar. Two-week infusion of Ang II induced a significant increase in CSA from 0.48 +/- 0.02 mm2 in CON to 0.61 +/- 0.03 mm2. Mt and W/L were likewise increased, but collagen and elastin densities remained unchanged. CC and DC were not effected by this increase in aortic wall mass (CC: 0.143 +/- 0.009 CON, 0.147 +/- 0.014 mm2/kPa ANG; DC: 0.052 +/- 0.005 CON, 0.051 +/- 0.004 kPa-1 ANG). An increase in aortic wall mass resulting from chronic infusion of angiotensin II does not alter the dynamic compliance of the vessel under isobaric conditions.

Testosterone induces dilation of canine coronary conductance and resistance arteries in vivo.

Although estrogens have been shown to be vasoactive hormones, the vascular effects of testosterone are not well defined. Like estrogen, testosterone causes relaxation of isolated rabbit coronary arterial segments. We examined the vasodilator effects of testosterone in vivo in the coronary circulation and the potential mechanisms of its actions. Using simultaneous intravascular two-dimensional and Doppler ultrasound, we examined the effect of intracoronary testosterone in coronary conductance and resistance arteries in 10 anesthetized dogs (5 male, 5 female). We also assessed the contribution of NO, prostaglandins, ATP-sensitive K+ channels, and classic estrogen receptors to testosterone-induced vasodilation. Testosterone induced a significant increase in cross-sectional area, average coronary peak flow velocity, and calculated volumetric coronary blood flow at the 0.1 and 1 mumol/L concentrations. This effect was independent of sex. Pretreatment with N omega-nitro-L-arginine methyl ester to block NO synthesis decreased testosterone-induced increase in cross-sectional area, average coronary peak flow velocity, and coronary blood flow. Pretreatment with glybenclamide to assess the role of ATP-sensitive K+ channels did not influence testosterone-induced dilation in epicardial arteries but did attenuate its effect in the microcirculation. Pretreatment with indomethacin or the classic estrogen-receptor antagonist ICI 182,780 did not alter testosterone-induced changes. Short-term administration of testosterone induces a sex-independent vasodilation in coronary conductance and resistance arteries in vivo. Acute testosterone-induced coronary vasodilation of epicardial and resistance vessels is mediated in part by endothelium-derived NO. ATP-sensitive K+ channels appear to play a role in the vasodilatory effect of testosterone in resistance arteries.

Changes in satellite cell mitotic activity during acute period of unilateral diaphragm denervation.

The acute period of unilateral diaphragm denervation (DNV) is associated with increases in cell mitotic activity, protein synthesis, and muscle fiber hypertrophy. Our purpose was to determine whether acute unilateral diaphragm DNV is associated with changes in muscle isometric contractile properties, cross-sectional area of different muscle fiber types, mitotic activity of muscle fiber satellite cells, and muscle fiber ultrastructural properties indicative of injury. Adult male Fischer 344 rats underwent a right phrenicotomy, and DNV and intact (INT) hemidiaphragms were studied 72 h later. DNV hemidiaphragm displayed a significant decline in maximal isometric force (8.7 vs. 24.3 N/cm2) and a prolonged time to peak twitch force (47.8 vs. 37.5 ms) and time to half relaxation (72.3 vs. 44.3 ms) compared with INT contralateral hemidiaphragm (P < 0.05). DNV resulted in a significant increase in cross-sectional area of types I (33%), IIa (35%), and IIb (28%) fibers relative to INT hemidiaphragm (P < 0.05). Satellite cell mitotic activity (assessed by incorporation of bromodeoxyuridine) was approximately 5.5 times greater in DNV than in INT muscle (DNV 25.0 +/- 3.8, INT 4.5 +/- 1.4 labeled satellite cell nuclei/1,000 nuclei; P < 0.05). Ultrastructural examination of electron micrographs revealed alterations in Z-line and sarcomeric structure indicative of muscle injury. Cellular infiltration and segmental necrosis were also noted in some fibers. We conclude that acute unilateral diaphragm DNV results in muscle fiber injury that induces satellite cell activation. We also speculate that the specific force decrement associated with DNV is at least partially the result of muscle injury.

Effects of Exhaustive Concentric and Eccentric Exercise on Murine Skeletal Muscle

C57BL/10SnJ mice were run to exhaustion on a treadmill at a 20 degrees incline, uphill or downhill. Contractility, morphology, and histology were evaluated in the soleus and extensor digitorum longus (EDL) muscles at days 0, 3, and 7 postexercise. Serum creatine kinase was elevated immediately postexercise (681% increase downhill and 225% increase uphill). After uphill running, the soleus had a significant increase in cross-sectional area (CSA) and decreased tetanic tension/CSA and twitch contraction time through day 7. The EDL showed increased CSA, decreased tetanic and twitch tension, and increased fatigue at day 0 only, with no other contractile abnormalities. After downhill running, the EDL showed reduced tetanic and twitch tension, but no fatigue or morphometric differences, whereas the soleus showed no significant abnormalities. No significant muscle histopathology was observed at any time following uphill or downhill running. This study indicates that both exhaustive eccentric and concentric exercise may produce significant impairments in muscle contractility without inducing histopathology. Exhaustive concentric exercise also induces muscle swelling and may preferentially impair slow twitch fibers.

Elastic behaviour of the carotid artery in intact spontaneously hypertensive rats.

Intact spontaneously hypertensive rats (SHR) were studied to assess the effect of prolonged antihypertensive treatment on the elastic behaviour of the external carotid artery. Thirty-week-old SHR received the ACE inhibitor captopril, the arteriolar dilator hydralazine or their vehicle for 6 weeks. These rats were compared to normotensive, vehicle treated WKY rats. The internal diameter of the carotid artery was measured continuously in halothane-anaesthetized rats using an echo-tracking device, and intra-arterial pressure was also monitored continuously, on the contralateral side. Captopril- and hydralazine-treated SHR as well as normotensive controls had similar blood pressure values. No significant shift in the distensibility-pressure curves was observed among vehicle-treated SHR and WKY rats or the SHR which had received captopril or hydralazine. Histological examination of the carotid artery fixed ex vivo with paraformaldehyde showed a significant increase in cross-sectional area in vehicle-treated SHR as compared to their normotensive counterparts. These results therefore suggest that the elastic behaviour of elastic arteries is not necessarily altered by the structural changes developing in response to hypertension.

Biomechanical and histological observations of the dog patellar tendon after removal of its central one-third

The use of a central one-third patellar tendon as an autograft for surgical reconstruction of a damaged cruciate ligament is common. Few complications of its use have been reported. However, recent clinical studies indicate that decreased quadriceps strength, decreased range of motion, decreased thigh circumference, and patellofemoral problems can be associated with this procedure. Some of these complications may result from alterations in the biomechanical properties of the remaining patellar tendon. The objective of this study was to examine biomechanically and histologically the fate of the remaining patellar tendon after removal of its central one-third. Three groups of dogs were used for this study. On one knee the central third of the patellar tendon was removed, while the contralateral side was used as a control. One group was immediately euthanized, while the other two groups were euthanized at 3 and 6 months. Control and operated patella-patellar tendon-tibia preparations were harvested and stretched to failure at 100% strain per second. The 3 and 6 month groups had a 10% decrease in length of the operated patellar tendon versus the contralateral control. There was a very significant increase in cross-sectional area of the patellar tendon at 3 months, and a further increase at 6 months. The failure load was 70% of the controls at 3 months and 60% of the controls at 6 months. The stiffness and modulus of the operated tendon within the physiologic range were dramatically reduced to 70% and 33% of controls at 6 months, respectively. These overall results were observed with the central one-third defect closed or left open in surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Influences of physical conditioning and deconditioning on coronary vasculature of dogs.

To investigate the effects of physical conditioning and deconditioning on the coronary vasculature, eight dogs were exercised by treadmill running. Five dogs were deconditioned by confinement in cages following the conditioning period. A technique was developed and validated for measuring circumflex coronary artery diameter from magnified projections of standardized coronary angiograms. Myocardial capillary density, perimeter, and basement membrane thickness were determined from electron microscopy of serial ventricular septal biopsy samples. Physical conditioning caused a small but statistically significant increase in cross-sectional area of the circumflex artery. Although physical conditioning caused no statistically significant changes in the myocardial capillaries, trends were apparent for increases in density and perimeter of myocardial capillaries and a decrease in basement membrane thickness. Physical deconditioning caused statistically significant reductions in cross-sectional area of the circumflex artery and in myocardial capillary density but little change in perimeter or basement membrane thickness of myocardial capillaries. The results suggest that physical conditioning may be associated with an improvement in coronary vascular capacity which may regress rapidly with deconditioning.

Instantaneous Dimensional Changes of the Left Ventricle in Dogs

The cardiac cycle in dogs starts with an isovolumic period in which there is shortening of the base-to-apex length with an increase in cross-sectional area. Total shortening is about one-fourth of that in open-chest dogs. Minimal changes in base-to-apex length occur during the ejection phase, and there is a typical pattern of decrease in cross-sectional area. During isovolumic relaxation, the left ventricular base-to-apex length increases. Rapid filling is characterized by a sudden increase in cross-sectional area and is followed by a diastasis of varying lengths. Atrial systole is associated with a sudden significant increase in cross-sectional area and a decrease in base-to-apex length. The magnitude of change in cross-sectional area about the left ventricle during ejection may be used as an index of stroke volume. Our studies suggest that the ventricle contracts in an "eccentric manner," and relaxes in a "concentric fashion." Simultaneous monitoring of the instantaneous changes in cross-sectional area and circumference about the middle of the left ventricle may be used as an index of its efficiency of contraction in awake, intact dogs.