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At least 487 records · Page 27Linked to original sources
PubMed2005

Variation in course of cavernous nerve with special reference to details of topographic relationships near prostatic apex: histologic study using male cadavers.

OBJECTIVES: To study interindividual variation in the cavernous nerve course near the rhabdosphincter and the apex of the prostate as a basis for refining nerve-sparing radical prostatectomy. The varying anatomy of the cavernous nerve might account for the disparate potency rates after nerve-sparing radical prostatectomy. METHODS: We examined serial histologic sections from 20 male pelves (7 frontal, 8 sagittal, and 5 axial sections) and performed 5 fresh cadaver dissections. RESULTS: In the fresh dissections, the macroscopically identified neurovascular bundle consistently showed an almost straight proximal-to-distal course along the urethra. However, on histologic analysis, the types of the nerve course were classified as frontal (2 of 7 specimens), sagittal (3 of 8), and axial (2 of 5). In the frontal and sagittal courses, the nerves passed through the connective tissue of a narrow potential space between the rhabdosphincter and the levator ani. In the specimens showing an axial course, the nerves were spatially distinct from the prostate, coursing ventromedially in the pararectal space. Thus, the nerves could display a long, tortuous course, passing through the rectourethral muscle at its thickest portion. In addition, a nerve component supplying the area of the rhabdosphincter seemed to accompany the cavernous nerve. CONCLUSIONS: The neurovascular bundle, previously defined in terms of surgery, is likely to differ from the actual course of the cavernous nerve when this is axial, passing through the pararectal space and rectourethral muscle. To avoid cavernous nerve injury, the rectourethral muscle must be managed carefully in both the retropubic and the perineal approaches.

Aged↗
PubMed1998

Syndrome X and endothelial dysfunction.

OBJECTIVE: Syndrome X (angina, normal coronary arteriogram and positive exercise test) remains an enigma with unexplained features and apparent conflicts of evidence. The present study addressed whether (i) the Syndrome is characterised by generalised flow-related endothelial dysfunction, (ii) myocardial thallium201 defects reflect myocardial or microvascular dysfunction, (iii) endothelial dysfunction and its consequences can be improved by oral L-arginine. METHODS: Flow-mediated brachial artery dilatation was measured by ultrasonic 'wall-tracking' in 7 Syndrome X patients, further characterised as having thallium201 defects and no known cause of endothelial dysfunction, and a normal control group. Syndrome X patients entered a 4-week randomised double-blind placebo-controlled cross-over trial of oral L-arginine (7 g twice daily), with brachial artery studies, exercise tests and technetium99 tetrafosmin scans. RESULTS: Flow-mediated dilatation was absent in Syndrome X vs. normal. Stress technetium99 tetrafosmin and thallium201 scans showed similar defects. Flow-mediated dilatation, symptom-limited exercise duration and peak oxygen consumption (VO2max) were increased but rate-pressure-product (RPP) and radionuclide defects were unchanged after L-arginine vs. placebo. CONCLUSIONS: The study supports coronary microvascular rather than myocardial dysfunction and shows loss of flow-mediated dilatation in systemic arteries. Oral L-arginine improved flow-mediated dilatation, exercise capacity and VO2max (by ca. 17%) despite unchanged RPP. The findings support generalised endothelial dysfunction. The arginine effects imply NO-mediated improvement of skeletal muscle perfusion suggesting improved homogeneity of microvascular distribution.

Administration, Oral↗
PubMed1990

Spatially resolved changes in diabetic rat skeletal muscle metabolism in vivo studied by 31P-n.m.r. spectroscopy.

Phase-modulated rotating-frame imaging (p.m.r.f.i.), a localization technique for 31P-n.m.r. spectroscopy, has been applied to obtain information on the heterogeneity of phosphorus-containing metabolites and pH in the skeletal muscle of control and streptozotocin-diabetic rats. Using this method, the metabolic changes in four spatially resolved longitudinal slices (where slice I is superficial and slice IV is deep muscle) through the ankle flexor muscles have been investigated at rest and during steady-state isometric twitch-contraction at 2 Hz. At rest, intracellular pH was lower, and phosphocreatine (PCr)/ATP was higher, throughout the muscle mass in diabetic compared with control animals. The change in PCr/ATP in diabetic muscle correlated with a decrease in the chemically determined ATP concentration. During the muscle stimulation period, the decrease in pH observed in diabetic muscle at rest was maintained, but not exacerbated, by the contractile stimulus. Stimulation of muscle contraction caused more marked changes in PCr/(PCr + Pi), PCr/ATP and Pi/ATP in the diabetic group. These changes were most evident in slice III, which contains the greatest proportion of fast glycolytic-oxidative (type IIa) fibres, in which statistically significant differences were observed for all metabolite ratios. The results presented suggest that some degree of heterogeneity occurs in diabetic skeletal muscle in vivo with respect to the extent of metabolic dysfunction caused by the diabetic insult and that regions of the muscle containing high proportions of type IIa fibres appear to be most severely affected.

Adenosine Triphosphate↗
PubMed2005

Modifications of serum and cellular parameters in trotters after a race. Macrophage migration inhibitory activity reduction and serum beta-glucan elevation.

Trotters are exposed to a chronic prolonged stress, such as daily training and frequent races during their active lifespans. There is evidence that trotters undergo very often lethal lung infections after a race, and therefore, is likely that modifications of certain physiologic cellular parameters could account for the increased susceptibility to microbial diseases. Here, we demonstrate that in 7 trotters after a race either serum values (e.g., glycaemia, triglycerides, transaminases, gamma-glutamyltransferase, cholinesterase, amylase, alkaline phosphatase, total proteins, serum albumin, sodium, blood urea nitrogen, lactic dehydrogenase, creatine phosphokinase, and creatinine) or hematological parameters (red blood cell count, hemoglobin, lymphocyte and monocyte count) were increased. At the same time, in the same animals after a race, macrophage migration inhibitory factor activity was depressed, thus indicating an impaired T-lymphocyte response. Finally, increased levels of circulating beta-glucans in some horses, after a race, may suggest a reduced clearance of fungal cell wall components. Taken together, these findings indicate a condition of multiple organ dysfunction, such as the liver, the kidney, the pancreas, and skeletal muscles, as well as a reduced cell-mediated immune response in trotters, after a race.

Animals↗
PubMed1996

Physiologic changes in heart failure--"What's new".

The physiologic changes that accompany heart failure are complex and evolve over time. Adaptations to an initial insult include both central (myocardial) and peripheral mechanisms that attempt to maintain adequate cardiac output at rest, as well as during increased metabolic demands such as exercise. Physiologic models provide insight into these complex changes and are necessary to design and evaluate the efficacy of pharmacologic and nonpharmacologic interventions. Recent advances in ventricular remodeling and changes in myocardial adrenergic receptors are presented as are alterations in vasodilatory response, skeletal muscle structure, function, and metabolism.

Endothelium, Vascular↗
PubMed1990

Acetylcholine receptor antibodies in primary biliary cirrhosis: characterization of antigen and idiotypic specificity.

Auto-antibodies against the acetylcholine receptor of skeletal muscle are considered to be the cause of the neuromuscular dysfunction in myasthenia gravis. However, such auto-antibodies also occur in disease states not accompanied by neuromuscular symptoms. Patients with primary biliary cirrhosis have a high prevalence of different auto-antibodies, including antibodies against the acetylcholine receptor. In primary biliary cirrhosis, these anti-receptor antibodies are predominantly of IgM isotype. The IgM antibodies show a broader reactivity with receptors from other species than antibodies from myasthenic patients. Immunoglobulins from patients with primary biliary cirrhosis bear the same receptor antibody-associated idiotypes, but the repertoire is quantitatively different from that found in myasthenia gravis patients. The IgM receptor antibody activity in a serum from a patient with primary biliary cirrhosis could be inhibited by cardiolipin, poly[dT], poly[I], and ssDNA, whereas this antibody activity in serum from a patient with myasthenia gravis was slightly reduced only by cardiolipin. Generally, IgM antibodies from patients with primary biliary cirrhosis had a broader reactivity with polynucleotides and phospholipids than IgG antibodies and antibodies from patients with myasthenia gravis. These results indicate a difference in the fine specificity between acetylcholine receptor antibodies in primary biliary cirrhosis and in myasthenia gravis.

Animals↗
PubMedDate not supplied

Skeletal muscle used as experimental cardiac assist: Russian experience.

This manuscript presents experimental data in the area of biomechanical cardiac support obtained at the Bakulev Institute for Cardiovascular Surgery in Moscow, Russia. After creation of the left ventricular aneurysm and subsequent cardiomyoplasty, active functioning of the muscle-heart complex was observed. In the late postoperative stages (3-6 months) hemodynamic parameters did not reach original preoperative values, but were satisfactory to support decreasing heart function: Cardiac index was decreased by 9.8%, the pumping coefficient of the left heart (KLH) by 24.7%, and left ventricular stroke work index (LVSWI) fell by 25%. Acute aneurysm of the left ventricle is a good model to study the effectiveness of cardiomyoplasty. Determination of parameters for stimulation of the muscle autograft showed that from the point of view of hemodynamic parameters of the muscle-heart complex, the optimal initial training schedule is a burst of seven pulses, each from 0.07 to 0.6 ms in duration, with a frequency of 30-50 Hz an amplitude of 6 V, and a burst following frequency of 15-30 per minute.

Animals↗
PubMed1994

Circulation and sensation at the fingertips of claw hands.

Measurements of skin blood flow (by laser Doppler flowmetry) and temperature were made under environmental conditions promoting peripheral vasodilatation at the fingertips of a disfigured 'clawed' hand in 12 leprosy patients long-resident at Baba Baghi Leprosy Hospital, Tabriz, Iran. Sensory function was assessed by measuring the responses to light touch, pain and temperature of each finger, and peripheral autonomic function was gauged by estimating palmer sweating and by measuring skin vasomotor reflexes in response to inspiratory gasp. In 2 patients all measured fingers had laser Dopper flux (LDFlux) values and skin temperatures lower than the 95% confidence limits for the mean of 20 healthy controls, i.e. were impaired; in 2 patients all fingers had normal values for LDFlux and temperature; and in 8 patients there was a combination of impairment with most fingers normal for these parameters but with the small finger most commonly impaired. There were 10 (67%) fingers with impaired LDFlux and temperature values who had significant sensory impairment, whereas only 5 (18%) of the fingers with normal LDFlux values and temperatures had a similar sensory deficit. Overall, the fingers with the most impaired sensation had significantly (P < 0.05) lower LDFlux and temperature values than those with no sensory deficit. Microcirculatory impairment was not related to disordered skin vasometer reflexes or dysfunction of sweating. We concluded that the relationship between motor (skeletal muscle) nerve paralysis and any subsequent sensory neuropathy and/or microcirculatory impairment is more complex than might be expected from previous understanding of the disease.

Adult↗
PubMed2003

[Drug therapy and adjuvant therapy in heart failure. Exercise training--more effective than digitalis?].

Physical training is known to have a favorable effect on the extracardiac causes of intolerance of exertion associated with cardiac insufficiency. Randomized studies have shown an improvement in the oxidative capacity of the skeletal muscles, to an attenuation of chronic inflammation, correction of endothelial dysfunction, and to normalization of the frequently pathological ventilation under effort. The result is an increase in the maximum oxygen uptake--depending on the study--of between 15% and 29% (average 2 ml/kg min). An old worry that physical training might lead to a worsening of hemodynamics was not confirmed. As a result of the positive effect of training on the neurohumoral system and the peripheral endothelial function the resistance of peripheral vessels was lowered and the burden on the left ventricle reduced. The results of initial long-term observational studies also reveal a reduction in mortality.

Cardiovascular Agents↗
PubMed1990

Systemic and regional hemodynamic effects of alpha-adrenoceptor blockade in chronic left ventricular dysfunction in the conscious dog.

In seven dogs with long-standing left ventricular dysfunction induced 16 weeks earlier by repetitive transmyocardial direct current (DC) shock, the acute hemodynamic effect of the alpha 1-adrenoceptor antagonist urapidil was studied. Left ventricular end-diastolic pressure (LVEDP) was significantly increased from preshock levels at the time of study and cardiac output was reduced. Plasma norepinephrine was significantly increased from control levels and was not altered by urapidil infusion. The mean arterial pressure fell in response to alpha 1-blockade from 111 to 85 mm Hg, the LVEDP fell from 16 to 9 mm Hg, and cardiac output increased from 2.90 to 3.70 L/min (all p less than 0.01). Regional blood flows measured by microsphere injection revealed an increase in blood flow to skeletal muscle, which had not been significantly decreased by the left ventricular dysfunction in this model, and further decreases in splanchnic flow, which was already depressed compared with that in normal dogs. Therefore acute alpha-adrenoceptor blockade improves central hemodynamics in experimental heart failure but does not normalize the resting blood flow maldistribution in this model.

Adrenergic alpha-Antagonists↗
PubMed2003

On noxious desmin: functional effects of a novel heterozygous desmin insertion mutation on the extrasarcomeric desmin cytoskeleton and mitochondria.

Recent studies in desmin (-/-) mice have shown that the targeted ablation of desmin leads to pathological changes of the extrasarcomeric intermediate filament cytoskeleton, as well as structural and functional abnormalities of mitochondria in striated muscle. Here, we report on a novel heterozygous single adenine insertion mutation (c.5141_5143insA) in a 40-year-old patient with a distal myopathy. The insertion mutation leads to a frameshift and a truncated desmin (K239fs242). Using transfection studies in SW13 and BHK21 cells, we show that the K239fsX242 desmin mutant is incapable of forming a desmin intermediate filament network. Furthermore, it induces the collapse of a pre-existing desmin cytoskeleton, alters the subcellular distribution of mitochondria and leads to abnormal cytoplasmic protein aggregates reminiscent of desmin-immunoreactive granulofilamentous material seen in the ultrastructural analysis of the patient's muscle. Analysis of mitochondrial function in isolated saponin-permeablized skeletal muscle fibres from our patient showed decreased maximal rates of respiration with the NAD-dependent substrate combination glutamate and malate, as well as a higher amytal sensitivity of respiration, indicating an in vivo inhibition of complex I activity. Our findings suggest that the heterozygous K239fsX242 desmin insertion mutation has a dominant negative effect on the polymerization process of desmin intermediate filaments and affects not only the subcellular distribution, but also biochemical properties of mitochondria in diseased human skeletal muscle. As a consequence, the intermediate filament pathology-induced mitochondrial dysfunction may contribute to the degeneration/regeneration process leading to progressive muscle dysfunction in human desminopathies.

Adenine↗
PubMed1993

From Left Ventricular Dysfunction to Heart Failure in the Elderly Patient.

The pathophysiology of the syndrome of congestive heart failure (CHF) is different in elderly patients compared to middle-aged subjects. When the syndrome of CHF predominantly results from left ventricular (LV) systolic dysfunction, peripheral mechanisms in elderly patients are less apt to compensate for the decline in LV performance due to deconditioning of the skeletal muscles, decreased vasodilatory response to exercise, and reduced capacity to excrete sodium. These all develop with age. LV diastolic dysfunction, i.e., LV filling impairment, appears to be a more frequent cause of CHF in elderly patients than in middle-aged subjects. Hypertrophy of the cardiac myocyte is associated with a prolongation of the calcium transient which, in turn, results from a decreased concentration of the enzyme responsible for reuptake of calcium in the sarcoplasmic reticulum. Cardiac myocyte hypertrophy results from a steady loss of myocytes and a progressive rise in arterial impedance which are both observed with aging. Notwithstanding subendocardial myocardial ischemia which is frequently associated with LV wall hypertrophy, prolongation of the calcium transient leads to impaired LV wall relaxation and the syndrome of LV diastolic dysfunction. The goals of therapy are also different in elderly patients compared to middle-aged patients. In elderly patients, one is less concerned about restoring a near normal exercise capacity, and aims at preventing acute episodes of decompensation which frequently accompany excessive sodium intake. Therefore, strict adherence to diet and careful titration of the dosages of medication to renal function are important considerations when treating CHF in elderly patients. In particular, cardiac glycosides, which should be avoided with CHF due to LV diastolic dysfunction, should be carefully titrated to creatinine clearance and body weight when treating elderly patients with LV systolic dysfunction in sinus rhythm. Similarly, the dosages of most angiotensin-converting enzyme inhibitors should be reduced in elderly patients.

Journal Article↗
PubMed2001

[Female carrier of Duchenne muscular dystrophy presenting with secondary dilated cardiomyopathy: a case report].

A 48-year-old female carrier of Duchenne muscular dystrophy had developed congestive heart failure but had no skeletal muscle symptoms. She was admitted to our hospital complaining of palpitation in December 1998. Her three sons had Duchenne muscular dystrophy. Neurological examination was unremarkable with no evidence of muscle weakness. Serum creatine kinase level was slightly increased. Echocardiography showed severe left ventricular dysfunction. Coronary angiography showed no abnormalities. Left ventriculography showed generalized hypokinesis and left ventricular ejection fraction was 28%. Dystrophin immunostaining of the skeletal muscle biopsy specimen showed a mosaic pattern. The dystrophin negative fibers were scattered among positive fibers. Cardiomyopathy is the only clinical manifestation of dystrophin gene mutation in carriers. Beta-blocker therapy(carvedilol 5 mg/day) was effective in this patient.

Cardiomyopathy, Dilated↗
PubMed1993

[Congestive heart failure: from cardiac muscle to skeletal muscle].

It is well established that in patients with chronic heart failure, exercise capacity and clinical symptoms such as fatigue or dyspnea correlate poorly with the extent of left ventricular dysfunction. The increase in cardiac output caused by vasodilators, cannot be translated immediately into increased exercise capacity and peak oxygen consumption in patients with chronic heart failure. These observations have prompted the hypothesis that in chronic heart failure intrinsic abnormalities of skeletal muscle emerge that prevent acute improvement in peak VO2 and blood lactate accumulation. Studies using nuclear magnetic resonance demonstrate abnormal skeletal muscle metabolism during exercise, even in the absence of reduced flow or under ischaemic conditions. Histological examination of skeletal muscle reveals a variable extent of atrophy, increased interstitial cellularity and increase in type IIb fibres. Ultrastructural analysis shows abnormalities indicative of depressed oxidative capacity. Biochemical analysis of skeletal muscle biopsies demonstrates reduced activity of enzymes involved in aerobic metabolism and free fatty acid accumulation. These data indicate morphological, biochemical and metabolic alterations of skeletal muscle that should contribute significantly to the reduced muscle strength and rapid fatigue in patients with chronic heart failure. It has also been speculated that a generalized myopathy may occur in a subset of patients with dilated cardiomyopathy. These findings have clinical implications. Prolonged immobilization of patients with chronic heart failure was often suggested, is not practised anymore. Physical training in chronic heart failure has been shown to improve skeletal muscle function, exercise capacity and clinical symptoms in small controlled trials. Pharmacological treatment might be targeted for skeletal muscle disorders in patients with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed2000

Signaling mechanisms of altered cellular responses in trauma, burn, and sepsis: role of Ca2+.

Alterations in cellular responses in various organ systems contribute to trauma-, burn-, and sepsis-related multiple organ dysfunction syndrome. Such alterations in muscle contractile, hepatic metabolic, and neutrophil and T-cell inflammatory-immune responses have been shown to result from cell-signaling modulations and/or impairments in the respective cell types. Altered Ca(2+) signaling would seem to play an important role in the myocardial and vascular smooth muscle contractile dysfunction in the injury conditions; Ca(2+)-linked signaling derangement also plays a crucial role in sepsis-induced altered skeletal muscle protein catabolism and resistance to insulin-mediated glucose use. The injury-related increased hepatic gluconeogenesis and acute-phase protein response could also be caused by a pathophysiologic up-regulation of hepatocyte Ca(2+)-signal generation. The increased oxidant production by neutrophil, a potentially detrimental inflammatory response in early stages after burn or septic injuries, seems to result from an up-regulation of both the Ca(2+)-dependent as well as Ca(2+)-independent signaling pathways. The injury conditions would seem to cause an inappropriate up-regulation of Ca(2+)-signal generation in the skeletal myocyte, hepatocyte, and neutrophil, while they lead to a down-regulation of Ca(2+) signaling in T cells. The crucial signaling derangement that causes T-cell proliferation suppression seems to be a decrease in the activation of protein tyrosine kinases, which subsequently down-regulates Ca(2+) signaling. The delineation of cell-signaling derangements in trauma, burn, or sepsis conditions can lead to development of therapeutic interventions against the disturbed cellular responses in the vital organ systems.

Burns↗
PubMed2005

Overexpression of MyoD-inducible lysosomal sialidase (neu1) inhibits myogenesis in C2C12 cells.

Lysosomal sialidase, encoded by neu1, is required for the removal of terminal sialic acid residues from a variety of sialoglycoconjugates. In humans, deficiency of this enzyme results in the inborn error of metabolism sialidosis, characterized by the accumulation of sialoglycoconjugates within the nervous system and in peripheral organs. A subset of sialidosis patients present with symptoms of profound muscle dysfunction, including progressive muscular atrophy. We have previously shown that the 5' regulatory region of murine neu1 is typical of skeletal muscle-specific genes due to the presence of several E-boxes and its responsiveness to stimulation by muscle regulatory factors (MRFs) such as MyoD. Here, we report that sialidase activity is increased 6-fold during the first 24 h of differentiation of C2C12 myoblasts followed by an attenuation to pre-differentiation levels by 48 h. We demonstrate that the lysosomal sialidase promoter is highly upregulated by MyoD through a mechanism that is dependent on the MyoD chromatin remodeling domain. We also show that the sialidase promoter is repressed by activated MEK. Inappropriate overexpression of sialidase 48 h after the onset of differentiation results in downregulation of myogenin as well as myosin heavy chain expression and in a halt of the differentiation cascade. This study indicates that lysosomal sialidase is a potent regulator of the early stages of myogenesis.

Animals↗
PubMedDate not supplied

Dysfunctional metabolism induced by the systemic effects of burn trauma: the role of rates of polyinositol and glycerophosphate formation in diaphragm.

Common complications among patients with burns are respiratory problems. Inspiration for breathing normally is facilitated by diaphragmatic contractility. However, in burn trauma numerous factors impose on skeletal muscle activity and chest wall function. These present limitations to surgical procedures requiring anesthesia. The hypothesis of this study was that the systemic effects of increasing burn size may result in metabolic changes in the polyinositol part of the phosphatidyl inositol signal transduction system in diaphragm. In this report, rate changes in polyinositol phosphates (i.e., inositol triphosphate (IP3), inositol 1,4 biphosphate (I1,4P2), inositol 1 phosphate (I1P), and inositol) that occurred in diaphragm subjected to the systemic effects of burn trauma were examined. Third-degree burn injury was applied by scalding predefined areas (i.e., 0%, 20%, and 50% body surface area) on the dorsal and ventral surfaces of mice. At postburn day 21 tissues were harvested and the levels of the polyinositol phosphates were measured by incorporation of myo-[2-3H]-inositol with separation of the phosphates by anion-exchange chromatography. All actual levels and rates of formation were analyzed with standard statistical tests and curve-fitting routines. Rate changes of the labelled [3H]-polyinositol phosphates were determined for the control, 20%, and 50% groups. These data show that rate changes occur in the polyinositol part of the phosphatidyl signal transduction system and are caused by the systemic effects of large percent body surface area burns. The changes that occur in the polyinositol phosphates provide insight into dysfunctional processes that can affect skeletal muscle physiology. The long-term goal of these studies is that they will lead to therapeutic advancements in the treatment of respiratory dysfunction in patients with burns.

Animals↗