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Myomesin and M-protein: expression of two M-band proteins in pectoral muscle and heart during development.

The expression of the myofibrillar M-band proteins myomesin and M-protein was studied in chicken pectoral muscle and heart during differentiation using monoclonal antibodies in a double-antibody sandwich enzyme-linked immunosorbent assay, immunoblotting, and immunocytochemistry. In presumptive pectoral muscle, myomesin accumulated first, increasing from 2% of the adult concentration at day 7 to 70% by day 16 in ovo. M-protein accumulation lagged 6-7 d behind that of myomesin attaining only 40% of the adult concentration in ovo. The molecular masses of myomesin (185 kD) and M-protein (165 kD) remained constant during embryogenesis. In cultured myogenic cells the accumulation and M-band localization of myomesin preceded that of M-protein by 1.5 d. Chicken heart was shown, in addition to M-protein, to contain unique isoforms of myomesin. In hearts of 6 d embryos, a 195-kD myomesin isoform was the major species; throughout development, however, a transition to a mixture of 195 and 190 kD was observed, the latter being the major species in the adult tissue. During heart differentiation the initial accumulation of myomesin again preceded that of M-protein, albeit on an earlier time scale than in pectoral muscle with M-protein reaching adult proportions first.

Animals↗

Immunofluorescent and histochemical localization of AMP deaminase in skeletal muscle.

Fluorescent antibody staining experiments with both isolated myofibrils and muscle fibers grown in culture show that AMP deaminase is bound to the myofibril in the A band. The strongest staining occurs at each end of the A band. The approximate width of the fluorescent stripes and their relation to the A band remains constant as a function of sarcomere length. Removal of enzyme from the myofibrils leads to loss of staining, and readdition of purified enzyme restores the original staining pattern. A histoenzymatic method for the detection of AMP deaminase activity in cultured fibers gives comparable localization. The results are consistent with the previous observation (Ashby, B. and C. Frieden. 1977.J. Biol. Chem. 252:1869--1872) that AMP deaminase forms a tight complex in solution with subfragment-2 (S-2) of myosin or with heavy meromyosin (HMM).

AMP Deaminase↗

Breast muscle development in commercial broiler chickens.

Genetic and gender-related variations in breast muscle yield of broiler chickens may be attributed to differences in number and size of muscle cells (myofibers). In this study, male and female broilers from eight commercial strain crosses (SC) were compared for body and breast muscle weight with adjustment of the Gompertz function. Additionally, breast fillet dimensions (length, width, and depth) and myofiber density (myofiber number/area; MFD) were assessed. Live weight and breast muscle development was determined to 56 d of age at weekly intervals. MFD was assessed at 8 d of age. As expected, SC differed in BW, breast weight and yield, and breast fillet dimensions and had variations in growth curves. Maximal growth rate for breast weight was reached approximately 4 d after that of BW. Males and females showed different growth curves, with males having slower growth rate maturity parameter and reaching the maximal growth rate later than females for BW and breast weight. Breast depth was the breast measure with highest positive correlation to breast yield. SC differences could not be explained by MFD, but males had higher MFD density than females. The possible relationship of the MFD observations to total myofiber number is discussed.

Animals↗

Monochromatic light stimuli during embryogenesis enhance embryo development and posthatch growth.

Photostimulation with green light accelerated BW and muscle development of broilers. In experiment 1, temperature sensors were inserted into 50 broiler eggs. The eggs were placed under 5 green light-emitting diode (LED) lamps at an intensity of 0.1 W/m2 at eggshell level for 5, 10, 15, 20, and 25 min (n = 10). Egg temperatures were recorded continuously. A high correlation was found between lighting period and egg temperature elevation, and an intermittent light regimen of 15 min on and 15 min off was found to eliminate light-induced egg overheating. In experiment 2, the effect of in ovo green light photostimulation on embryonic development was studied. Five hundred fertile eggs were divided into 2 groups: the first was photostimulated with green light from 5 d of incubation until hatch (0.1 W/m2 intensity) and the second was incubated in the dark. In ovo green light photostimulation caused a significant elevation in BW and breast muscle weight during embryo development and posthatch until 6 d of age. In experiment 3, 240 fertile broiler eggs were divided into 2 groups as described in experiment 2. At hatch, chicks from each in ovo light treatment were divided into 2 subgroups: the first was reared under green light and the second under white light. In ovo photostimulation with green light enhanced BW and breast muscle weight. However, rearing under green light did not have any synergistic effect on BW. Collectively, the results suggest that stimulation with green light enhances development and growth in chicks and that the best effect is achieved when this stimulus is provided during incubation.

Animals↗

DDD/DDT pacemakers in the treatment of ventricular tachycardia.

The possibility of adapting multimode dual-chamber pacemakers for programmed and burst stimulation was explored in a group of patients with ventricular tachycardia. The potential usefulness and pitfalls of these pacemakers were exemplified in one patient, presented in detail. The implanted DDD pacemaker was programmed to an all-synchronous mode (DDT), permitting programmed ventricular stimulation through synchronization with chest wall stimulation provided by a standard external programmable stimulator. With the ventricular sensing refractory period shortened to 200 ms, both programmed electrical stimulation and burst pacing for termination of induced tachycardias were possible. When medications failed to offer protection against the patient's tachycardias, the ventricular sensing refractory period (and minimum stimulation interval) was increased to 300 ms, thereby permitting burst pacing at up to 200 beats/minute for termination of spontaneous episodes. After many trials to confirm the efficacy of such stimulation, and the lack of muscle potential triggering, the patient was discharged home with the pacemaker in the DDT mode. He was instructed to go to his local emergency room, and was equipped with a portable device to trigger his implanted unit. Subsequently, the patient had successful termination of several spontaneous episodes of ventricular tachycardia in an emergency room. Later, he began to experience palpitations during certain exercises, and it was found that the implanted unit was being triggered by pectoral myopotentials. The unit was therefore reprogrammed to decrease the sensitivity, and the patient was again discharged. The need for careful evaluation and close follow-up is emphasized to maximize the benefits and to minimize the very serious potential risks of this pacing mode.

Action Potentials↗

Myopotential interference inducing pacemaker tachycardia in a DVI programmed pacemaker.

A 67-year-old male, suffering from ventricular tachycardia unresponsive to drug therapy, received a universal AV sequential pacemaker (DDD,M). The pacemaker was programmed in the DVI mode, pacing rate 100 bpm, AV interval 250 ms. After implantation, the patient experiences two episodes of tachycardia that proved to be pacemaker tachycardia with a rate of 150 bpm. The first period was self-terminating, and the second had to be stopped by reprogramming the pulse generator. Pacemaker tachycardia could easily be provoked by instructing the patient to contract the pectoral muscle adjacent to the pulse generator. To our knowledge, this is the first report of pacemaker tachycardia provoked by myopotentials in a pulse generator programmed in the DVI mode.

Aged↗

Comparison of myopotential interference in unipolar-bipolar programmable DDD pacemakers.

Myopotential interference (MPI) can inhibit or trigger single and dual chamber unipolar pacemakers while bipolar pacemakers are resistant. Twenty units of two different models of dual chamber pacemaker, each capable of being programmed to single chamber or dual chamber and unipolar or bipolar function were tested to provoke myopotential interference. No patient had evidence of myopotential interference at any sensitivity setting in the bipolar configuration either in atrium or in ventricle. All patients (20/20) interfered with pacemaker function at the highest atrial or ventricular sensitivity settings in the unipolar configuration. T wave sensing occurred at the 0.25 mV sensitivity setting in four patients in pacemaker model 925, in both bipolar and unipolar configurations. Twenty-five percent of patients had myopotential interference at the unipolar atrial sensing threshold and did not allow a setting which would reject myopotential interference while providing satisfactory atrial sensing. Twenty percent (2/10) had myopotential caused ventricular inhibition at the least sensitive ventricular channel setting in model 240G so that myopotential interference could not be avoided in that unit no matter how large the electrogram.

Arrhythmias, Cardiac↗

The superfast atrial recharge pulse: a cause of pectoral muscle stimulation in patients equipped with a unipolar DDD pacemaker.

Pectoral muscle stimulation may cause serious discomfort to patients equipped with a pulse generator. Insulation defects of the lead, connector problems and defective coating of the pacemaker can are common causes of local muscle contractions. This report describes pectoral muscle stimulation caused by the atrial superfast recharge pulse incorporated into the atrial channel of a commercially available unipolar DDD pacemaker. As pectoral muscle stimulation could not be eliminated by reprogramming the pacemaker to a lower atrial output in some patients a redesign of the pacemaker is highly required.

Cardiac Pacing, Artificial↗

Pacemaker and defibrillator lead entrapment: case studies.

Cadavers and cineradiographic analysis have been used to document the effects of the medial subclavicular musculotendinous complex (MSMC) upon lead function. Four cadavers with pacemakers were dissected and photographed to demonstrate the course a lead takes as it passes through the costoclavicular region. One lead had been placed into the cephalic vein. In the other three cadavers, leads placed by currently accepted techniques of subclavian venipuncture were all found to pass through the soft tissues of the subclavicular region before entering the venous system. Cineradiographic results from a patient with a defibrillator, taken before and after replacement of a broken lead, show the effect of clavicular motion on a lead that passes through the MSMC. Furthermore, cineradiography makes it possible to identify the point where the lead entered the vein, and whether or not it escaped being caught up in the soft tissues of the MSMC.

Cadaver↗

Interaction between motor axons from two different nerves reinnervating the pectoral muscle of Xenopus laevis.

1. An electrophysiological and morphological study of sprouting and regeneration of motor nerves has been performed in the dually innervated pectoral muscle of Xenopus laevis. 2. Section of one of the nerves induced axon sprouting in the intact nerve. Synapse formation by the sprouting axons was slow since the intact nerve took more than 3 months to increase its field of innervation by 70%. The rate of axon regeneration was faster than that of axon sprouting since the cut nerve reinnervated its former territory in less than 1 month. 3. At early stages of synapse formation the sprouted or regenerated endings were poorly branched but any terminal branches were, as a rule, longer than normal. Signs of degeneration and replacement of endings have been observed. 4. Low levels of transmitter release persisted for several months in newly formed endings. This depression was more pronounced at the endings formed outside the normal field of innervation of the nerve. 5. Poly-innervated muscle fibres have been observed during reinnervation by regenerated or sprouted axons. Their number decreases gradually in the months that follow the beginning of reinnervation. Synaptic efficacy was lower at poly than at mono-innervated muscle fibres. At doubly innervated spots and at separated spots on the same fibre average end-plate potential (e.p.p.) amplitude was 1/3 and 2/3 respectively of that recorded at singly innervated fibres. 6. Electrophysiological and morphological data have been compared at individual doubly innervated end-plate sites. End-plate potential amplitude was positively correlated with the degree of ending development. 7. Sprouted endings remain functional after periods of reinnervation of 30 months, although signs of regression have been observed. These are probably mediated by spontaneous degeneration of the terminals and replacement by endings from the regenerating nerve.

Animals↗