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At least 469 records · Page 26Linked to original sources

PubMed2003

Blockade of TGF-beta action ameliorates renal dysfunction and histologic progression in anti-GBM nephritis.

BACKGROUND: We tested whether the entire soluble extracellular domain of the human transforming growth factor-beta (TGF-beta) type II receptor, fused to the Fc portion of human immunoglobulin G (IgG1) (Tbeta-ExR) and expressed in skeletal muscles by adenovirus-mediated gene transfer (AdTbeta-ExR), can ameliorate renal dysfunction and histologic progression in a rat experimental anti-glomerular basement membrane (GBM) nephritis. METHODS: Anti-GBM nephritis was induced in Wistar Kyoto rats by an intravenous injection of anti-rat glomerular basement membrane (GBM) sera. At day 1 (24 hours after induction), AdTbeta-ExR (1 x 109 pfu/mL) was injected into the femoral muscle in the treatment group, and an adenovirus vector-expressing bacterial beta-galactosidase (AdLacZ) was injected into the control group. Then, clinical and histologic changes were examined for 3 weeks after the induction of anti-GBM nephritis. RESULTS: Tbeta-ExR was detected in the serum at day 7, but the serum concentration of Tbeta-ExR had decreased below the detectable level by day 14. Although blood pressure and the degree of proteinuria were similar in both groups, the deterioration of renal function was significantly blunted in the treatment group. Crescent formation and interstitial fibrosis were also ameliorated in the treatment group. These histologic improvements were accompanied by the decreased interstitial infiltration of macrophages and the decreased alpha-smooth muscle actin (alpha-SMA)-positive cells in the glomeruli and the interstitium. CONCLUSION: This study demonstrated for the first time that the blockade of TGF-beta action by AdTbeta-ExR in the early stage of anti-GBM nephritis ameliorates the clinical and histologic progression. In addition, this study shed light on the development of a specific gene therapy for human crescentic glomerulonephritis.

Actins↗

PubMedDate not supplied

Left ventricular function during strength testing and resistance exercise in patients with left ventricular dysfunction.

PURPOSE: Deterioration in left ventricular function is a more sensitive marker of myocardial ischemia during exercise than ST segment depression. The current study was designed to evaluate left ventricular function during one-repetition-maximum (1-RM) strength testing and resistance exercise in cardiac patients with moderate left ventricular dysfunction. METHODS: Using echocardiographic methods, left ventricular function was evaluated in 15 patients with left ventricular dysfunction (age, 65 +/- 6.5 years; ejection fraction, 42.1 +/- 5.8). Measurements were performed during 1-RM testing and resistance exercise (20%, 40%, and 60% of 1-RM using 10 to 15 repetitions) on the one-arm biceps curl (BIC) and bilateral knee extension exercises and compared with measurements of left ventricular function during the symptom-limited graded exercise test (SL-GXT). RESULTS: During the knee extension exercise, there was a slight but significant reduction (P< or =.05) in ejection fraction values at the end of 60% 1-RM, as compared with rest and previous workloads. Significant increases in systolic blood pressure and left ventricular end-systolic volume ratio values (P< or =.05) from rest to exercise were observed across test modes and for all workloads. The prevalence of new wall motion abnormalities during knee extension and BIC 1-RM strength testing was comparable with that observed during SL-GXT. The greatest increase in new wall motion abnormalities was seen during 60% 1-RM of knee extension exercise, as compared with prior workloads, BIC exercises, and SL-GXT. CONCLUSIONS: Despite an increase in occurrence of ischemic changes during the highest resistance exercise workloads and with larger muscle mass, the findings are small in magnitude and do not suggest reduced cardiac performance.

Aged↗

PubMed2005

The response of the flexor digitorum longus and posterior tibial muscles to tendon transfer and calcaneal osteotomy for stage II posterior tibial tendon dysfunction.

BACKGROUND: The purpose of this prospective study was to evaluate the response of the flexor digitorum longus (FDL) and posterior tibial (PT) muscles to FDL tendon transfer and medial displacement calcaneal osteotomy for stage II posterior tibial tendon dysfunction (PTTD). METHODS: Twelve patients were divided into two groups, depending on whether the PT tendon was excised (Excised Tendon Group) or left intact (Intact Tendon Group). The muscle volumes of the FDL and PT muscles in both legs were measured and compared, using cross-sectional area (CSA) analysis of preoperative and postoperative MRI. RESULTS: Preoperatively, there was an average 11% reduction in the PT muscle volume and a 17% increase in the FDL muscle volume from the normal contralateral side in both groups. One year after surgery (average 13.4 months) in both groups, the FDL muscle volume had increased by an average of 27% and the PT muscle volume had decreased by 23% compared to the contralateral normal side. The FDL volume increased by 44% in the Excised Tendon Group compared to 11% in the Intact Tendon Group. The PT muscle volumes were not assessed in the Excised Tendon Group because all PT muscle had been replaced by fatty infiltration. The PT volumes in the Intact Tendon Group decreased further from a 6% reduction preoperatively to a 23% reduction postoperatively compared to the normal contralateral side. The American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores increased from 50 preoperatively to 88 at 1 year after surgery. There was no difference in the scores between the Excised Tendon (47 to 87) and Intact Tendon (53 to 89) groups. CONCLUSION: We concluded that the FDL muscle hypertrophies in response to a failing PT muscle. This hypertrophy continues after FDL transfer and medial displacement calcaneal osteotomy. With excision of the PT tendon, the FDL undergoes greater hypertrophy than if the tendon is left attached. The PT muscle continues to atrophy and undergoes complete fatty replacement if the tendon is excised. Transfer of the FDL and medial displacement calcaneal osteotomy produce a satisfactory improvement in hindfoot function; the outcome was the same whether the PT tendon was sacrificed or left intact.

Adult↗

PubMed2001

Mice transgenic for the human myotonic dystrophy region with expanded CTG repeats display muscular and brain abnormalities.

The autosomal dominant mutation causing myotonic dystrophy (DM1) is a CTG repeat expansion in the 3'-UTR of the DM protein kinase (DMPK) gene. This multisystemic disorder includes myotonia, progressive weakness and wasting of skeletal muscle and extramuscular symptoms such as cataracts, testicular atrophy, endocrine and cognitive dysfunction. The mechanisms underlying its pathogenesis are complex. Recent reports have revealed that DMPK gene haploinsufficiency may account for cardiac conduction defects whereas cataracts may be due to haploinsufficiency of the neighboring gene, the DM-associated homeobox protein (DMAHP or SIX5) gene. Furthermore, mice expressing the CUG expansion in an unrelated mRNA develop myotonia and myopathy, consistent with an RNA gain of function. We demonstrated that transgenic mice carrying the CTG expansion in its human DM1 context (>45 kb) and producing abnormal DMPK mRNA with at least 300 CUG repeats, displayed clinical, histological, molecular and electrophysiological abnormalities in skeletal muscle consistent with those observed in DM1 patients. Like DM1 patients, these transgenic mice show abnormal tau expression in the brain. These results provide further evidence for the RNA trans-dominant effect of the CUG expansion, not only in muscle, but also in brain.

Animals↗

PubMed2004

Recovery of the posterior tibial muscle after late reconstruction following tendon rupture.

The purpose of this study was to determine the recovery potential of the posterior tibial muscle after late reconstruction following tendon rupture in stage II of posterior tibial tendon dysfunction. Fourteen patients (18 women, 6 men; mean age 59.8 years) were investigated 47 months (range, 24-76 months) after surgical reconstruction of a completely ruptured posterior tibial tendon (end-to-end anastomosis, side-to-side augmentation with the flexor digitorum longus tendon) in combination with a distal calcaneal osteotomy with a tricortical iliac crest bone graft for lengthening of the lateral column. At follow-up, clinical and radiological investigations were performed, including strength measurement and qualitative and quantitative MRI investigation. The overall clinical results were graded excellent in 12 patients, good in one, fair in one, and poor in none. The average ankle-hindfoot score (American Orthopaedic Foot and Ankle Society) improved from preoperatively 49.1 (range, 32-60) to 93.1 (range, 76-100) at follow-up. The functional result correlated with patient's satisfaction and sports activities (p <.05). All patients showed a significant strength of the posterior tibial muscle on the affected side, but it was smaller than on non-affected side (p <.05). The mean posterior tibial muscle strength was 75.1 N on affected and 104.9 N on nonaffected side, corresponding to a ratio of 0.73 between the two legs. The mean area of the posterior tibial muscle was 1.89 cm(2) on affected side, and 3.48 cm(2) on nonaffected side, corresponding to a ratio of 0.55 between the two legs. While fatty degeneration for the posterior tibial muscle was found in all patients, it was found to decrease with increasing strength of the posterior tibial muscle (p <.05) and muscular size (p <.05). On postoperative MRI, the posterior tibial tendon could be found to be intact in all patients. The recovery potential of the posterior tibial muscle was shown to be significant even after delayed repair of its ruptured tendon. A ruptured and/or diseased posterior tibial tendon should not be transected as it excludes any recovery possibilities of the posterior tibial muscle.

Adult↗

PubMed2002

Posterior tibial tendon dysfunction and MR imaging in rheumatoid arthritis.

We present the case of a patient with long-standing rheumatoid arthritis and an acute onset of total dysfunction of the posterior tibial tendon. On MRI, a rupture of the tendon was apparent. Intraoperatively, however, massive tenosynovitis with stricture of the tendon was identified as the cause of posterior tibial tendon dysfunction. This case illustrates a pitfall in MRI imaging with potential diagnostic and therapeutic consequences.

Arthralgia↗

PubMed2004

Evidence of electroconformational changes in membrane proteins: field-induced reductions in intra membrane nonlinear charge movement currents.

Experimental results are presented to show that a pulsed, intensive membrane potential can reduce intra membrane, nonlinear charge movement currents, which are the voltage-sensors in the voltage-dependent membrane proteins and in the excitation-contraction coupling of skeletal muscle fibers. The results indicate a possible mechanism involved in electrical injury: dysfunctions of the voltage-dependent membrane proteins caused by electroconformational damages in their voltage-sensors.

Animals↗

PubMed2005

Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6.

The primary gene mutated in Charcot-Marie-Tooth type 2A is mitofusin-2 (Mfn2). Mfn2 encodes a mitochondrial protein that participates in the maintenance of the mitochondrial network and that regulates mitochondrial metabolism and intracellular signaling. The potential for regulation of human Mfn2 gene expression in vivo is largely unknown. Based on the presence of mitochondrial dysfunction in insulin-resistant conditions, we have examined whether Mfn2 expression is dysregulated in skeletal muscle from obese or nonobese type 2 diabetic subjects, whether muscle Mfn2 expression is regulated by body weight loss, and the potential regulatory role of tumor necrosis factor (TNF)alpha or interleukin-6. We show that mRNA concentration of Mfn2 is decreased in skeletal muscle from both male and female obese subjects. Muscle Mfn2 expression was also reduced in lean or in obese type 2 diabetic patients. There was a strong negative correlation between the Mfn2 expression and the BMI in nondiabetic and type 2 diabetic subjects. A positive correlation between the Mfn2 expression and the insulin sensitivity was also detected in nondiabetic and type 2 diabetic subjects. To determine the effect of weight loss on Mfn2 mRNA expression, six morbidly obese subjects were subjected to weight loss by bilio-pancreatic diversion. Mean expression of muscle Mfn2 mRNA increased threefold after reduction in body weight, and a positive correlation between muscle Mfn2 expression and insulin sensitivity was again detected. In vitro experiments revealed an inhibitory effect of TNFalpha or interleukin-6 on Mfn2 expression in cultured cells. We conclude that body weight loss upregulates the expression of Mfn2 mRNA in skeletal muscle of obese humans, type 2 diabetes downregulates the expression of Mfn2 mRNA in skeletal muscle, Mfn2 expression in skeletal muscle is directly proportional to insulin sensitivity and is inversely proportional to the BMI, TNFalpha and interleukin-6 downregulate Mfn2 expression and may participate in the dysregulation of Mfn2 expression in obesity or type 2 diabetes, and the in vivo modulation of Mfn2 mRNA levels is an additional level of regulation for the control of muscle metabolism and could provide a molecular mechanism for alterations in mitochondrial function in obesity or type 2 diabetes.

Charcot-Marie-Tooth Disease↗

PubMed1986

Lactate transporter defect: a new disease of muscle.

New methods were used to identify the abnormality in a patient who showed evidence of neuromuscular dysfunction on extensive clinical examination. The methods revealed that the lactate content of the patient's skeletal muscle does not decline normally after exercise and that his red cells are defective in lactate transport. These results suggest that skeletal muscle and erythrocyte membranes share the same genetic lactate transporter (or a common subunit), which is deficient in this patient. This defect may be a common cause of elevated serum creatine kinase levels, as seen in the patient described here and of unexplained episodes of rhabdomyolysis and myoglobinuria.

Adult↗

PubMed2006

Influence of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on ubiquinone levels in rat skeletal muscle and heart: relationship to cytotoxicity and inhibitory activity for cholesterol synthesis in human skeletal muscle cells.

Although statins are prescribed as relatively safe and effective drugs for hypercholesterolemic patients, it has been reported that a significant side effect, myopathy, occurs infrequently during medication. Moreover, because statins decrease cardiac ubiquinone levels, the risk of cardiac dysfunction has been suggested. This study sought to evaluate and compare the cytotoxicity of statins (cerivastatin, pitavastatin, fluvastatin, simvastatin, atorvastatin and pravastatin) in cultured human skeletal muscle cells (HSkMCs) and the effects on ubiquinone levels in statin-treated rat skeletal muscle and heart. Cerivastatin, the most potent inhibitor of HMG-CoA reductase, showed the strongest cytotoxicity (over 10-fold) among the statins examined, while the effects of the others were in a similar range. In rat experiments, neither pitavastatin nor cerivastatin decreased ubiquinone levels in skeletal muscle, but both dose-dependently lowered ubiquinone levels in the heart. As the rates of reduction by pitavastatin (9.6% at 30 mg/kg) and cerivastatin (9.7% at 0.3 mg/kg) were almost equal, it was estimated that cerivastatin reduced ubiquinone levels in the rat heart approximately 100-fold more strongly than pitavastatin, based on the effective doses. We found that cerivastatin showed the most potent cytotoxicity in HSkMCs and strongly lowered ubiquinone levels in the rat heart.

Animals↗

PubMed2000

Lipotoxic diseases of nonadipose tissues in obesity.

It is proposed that an important function of leptin is to confine the storage of triglycerides (TG) to the adipocytes, while limiting TG storage in nonadipocytes. Excess TG deposition in nonadipocytes leads to impairment of functions, increased ceramide formation, which triggers nitric oxide-mediated lipotoxicity and lipoapoptosis. The fact that TG content in nonadipocytes normally remains within a very narrow range irrespective of excess caloric intake, while TG content of adipocytes rises, is consistent with a system of fatty acid (FA) homeostasis in nonadipose tissues. When leptin is deficient or leptin receptors are dysfunctional, TG content in nonadipose tissues such as pancreatic islets, heart and skeletal muscle, can increase 10-50-fold, suggesting that leptin controls the putative homeostatic system for intracellular TG. The fact that function and viability of nonadipocytes is compromised when their TG content rises above normal implies that normal homeostasis of their intracellular FA is critical for prevention of complications of obesity. FA overload of skeletal muscle, myocardium and pancreatic islets cause, respectively, insulin resistance, lipotoxic heart disease and adipogenic type 2 diabetes. All can be completely prevented by treatment with antisteatotic agents such as troglitazone. In diet-induced obesity, leptin signaling is normal initially and lipotoxic changes are at first prevented; later, however, post-receptor leptin resistance appears, leading to dysfunction and lipoapoptosis in nonadipose tissues, the familiar complications of obesity.

Adipocytes↗

PubMed2006

Diagnostic and therapeutic challenges in patients with coexistent chronic obstructive pulmonary disease and chronic heart failure.

Chronic obstructive pulmonary disease (COPD) and heart failure (CHF) are common conditions. The prevalence of COPD ranges from 20% to 30% in patients with CHF. The diagnosis of CHF can remain unsuspected in patients with COPD, because shortness of breath is attributed to COPD. Measurement of plasma B-type natriuretic peptide (BNP) levels helps to uncover unsuspected CHF in patients with COPD and clinical deterioration. Noninvasive assessment of cardiac function may be preferable to BNP to uncover unsuspected left ventricular (LV) systolic dysfunction in patients with stable COPD. Patients with COPD or CHF develop skeletal muscle alterations that are strikingly similar. Functional intolerance correlates with severity of skeletal muscle alterations but not with severity of pulmonary or cardiac impairment in COPD and CHF, respectively. Improvement of pulmonary or cardiac function does not translate into relief of functional intolerance in patients with COPD or CHF unless skeletal muscle alterations concomitantly regress. The mechanisms responsible for skeletal muscle alterations are incompletely understood in COPD and in CHF. Disuse and low-level systemic inflammation leading to protein synthesis/degradation imbalance are likely to contribute. The presence of COPD impacts on the treatment of CHF, as COPD is still viewed as a contraindication to beta-blockade. Therefore, COPD often deprives patients with CHF due to LV systolic dysfunction of the most beneficial pharmacologic intervention. A large body of data indicates that patients with COPD tolerate well selective beta-blockade that should not be denied to CHF patients with concomitant COPD.

Adrenergic Antagonists↗

PubMed1982

Stress and chronic headache: a psychophysiological analysis of mechanisms.

This study investigated the effects of three types of laboratory stressors (stressful imagery, mental arithmetic, pain) on temporal artery, skeletal muscle, general autonomic [digital blood volume pulse (DBVP), spontaneous resistance responses (SRR's)] and self-report measures of distress in chronic migraine, mixed, muscle contraction and non-headache controls. All subjects were female, free of medication at time of testing and equated for age. Headache subjects reported a 19 year history of headache. Results revealed a pattern of digital BVP (constriction), SSR's (increase) and frontal EMG (increase) indicative of a general autonomic-skeletal muscle arousal response to all three stressors in all groups, while the temporal artery response to the pain stimulus was vasodilation. Distress ratings were elevated during the stress periods for all four group. Pain threshold and tolerance and the tendency to utilize cognitive coping strategies during exposure to pain did not differ across the four groups. The results do not support the general autonomic dysfunction theory of migraine or the specificity hypothesis implicating an overreactive temporal artery or skeletal muscle response to stress in migraine and muscle contraction headache, respectively. Despite epidemiological research supporting the stress-headache relationship, the present results indicate that the psychophysiological mechanism underlying this relationship does not appear to involve abnormal tonic levels or phasic response to stress. It is argued that the temporal artery dilation response to pain questions the role of stress in triggering the two stage vasoconstriction-dilation mechanism of migraine and suggests the need to evaluate a four stage model as a potential psychophysiological mechanism underlying the stress-headache relationship.

Adult↗

PubMed1982

Cardiac function in Duchenne's muscular dystrophy. Results of 10-year follow-up study and noninvasive tests.

The purposes of this study were to: (1) evaluate the progression of cardiac involvement in Duchenne's muscular dystrophy using systolic time intervals (PEP/LVET); (2) determine if the degree of cardiac involvement bears a relation to the severity of skeletal muscle disease; and (3) describe the M-mode and two-dimensional echocardiographic findings. In 1970, systolic time intervals were studied in 16 patients. During the 10-year interim, two patients were lost to follow-up study, and five patients died. Nine remaining patients were re-studied in 1980 with M-mode and two-dimensional echocardiography as well as systolic time intervals. The PEP/LVET value of these nine patients increased from 0.37 +/- 0.05 (mean +/- SD) in 1970 to 0.47 +/- 0.07 (p less than 0.005) in 1980. Three patients remained ambulatory, and their PEP/LVET value (0.41 +/- 0.04) was significantly better than that of the nonambulatory patients (0.50 +/- 0.07, p less than 0.05). The M-mode echocardiography percentage diameter change was also worse in the nonambulatory group (21 +/- 4 percent versus 34 +/- 7 percent, p less than 0.02). The five patients who were nonambulatory in 1970 died in the intervening 10 years. This study demonstrated that the heart disease of Duchenne's muscular dystrophy is progressive and that the severity of skeletal muscle disease is probably associated with the degree of cardiac dysfunction.

Adolescent↗

PubMed1995

Impaired cholinergic peripheral vasodilation and its relationship to hyperemic calf blood flow response and exercise intolerance in patients with chronic heart failure.

This study examined the peripheral endothelium-dependent vasodilatory response to acetylcholine and the endothelium-independent vasodilatory response to nitroprusside in 19 patients with chronic heart failure and eight controls. These peripheral blood flow responses were compared with hyperemic calf blood flow changes after maximum leg exercise and 5-min femoral occlusion. The peripheral blood flow response to forearm intra-arterial infusion of acetylcholine and sodium nitroprusside, and reactive hyperemic calf blood flow changes were measured by plethysmography. All peripheral blood flow responses were significantly reduced in patients with chronic heart failure (P < 0.05). Reduction of acetylcholine-mediated changes in peripheral blood flow was correlated with exercise-induced calf blood flow response (r = 0.51, P < 0.05), but not with occlusion-induced calf blood flow response (r = 0.02, NS). Sodium nitroprusside-mediated changes were not correlated with any reactive hyperemic blood flow responses (exercise: r = 0.27, NS; occlusion: r = 0.11, NS). When the patients were divided into two subgroups based on the median exercise-induced calf blood flow change, the subgroup with the lower calf blood flow response showed a reduction in exercise capacity (anaerobic threshold: 11.8 +/- 0.6 vs. 14.6 +/- 1.0 ml/kg/min; P < 0.05). These findings suggest that endothelial dysfunction is related to a decrease in exercise-induced skeletal muscle blood flow and exercise capacity in patients with chronic heart failure.

Acetylcholine↗

PubMed2006

The ventricular septum: the lion of right ventricular function, and its impact on right ventricular restoration.

OBJECTIVE: To evaluate the structure-function relationships of the right ventricle (RV) and septum and determine if the helical ventricular band model would define fiber orientation for maximal force response. Implications were made for right ventricular function. METHODS: The right ventricular free wall and biventricular septum were studied by inserting sonomicrometer crystals at different angulations to determine the maximum response of fiber shortening. These reactions were compared to the lateral left ventricular (LV) wall and further tested by use of positive and negative inotropic drug infusions. RESULTS: The maximum contraction of the free wall was achieved by placing crystals in the transverse orientation angulations, whereas oblique orientation allowed the maximal septal response. Fiber orientation angulation was the same for the LV free wall and septum. These angulations correlate with the MRI-related twisting actions of septal motion needed for ejection and suction for rapid filling. These findings have important impact, because they imply that the septum is 'lion of right ventricular function,' since septal twisting is essential when pulmonary vascular resistance is increased. The incidence of postoperative right heart failure due to septal dyssyncrony, with loss of septal twisting action from inadequate myocardial protection, is explored relative to RV free wall and septum function. Furthermore, early studies of right ventricular restoration in patients with RV dysplasia and RV failure after chronic pulmonary insufficiency following repair of Tetralogy of Fallot are described, with predominant attention directed toward rebuilding normal septal architecture and function. CONCLUSIONS: This experimental and clinical overview indicates that the septum is 'the lion of right ventricular function,' and implies that the use of this knowledge can become an important guideline for planning novel surgical geometric interventions after RV failure.

Heart Septum↗

PubMed2006

Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.

BACKGROUND: High-dose clenbuterol (a selective beta2-adrenergic agonist) has been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown. METHODS: Seven subjects with heart failure (5 ischemic, 2 non-ischemic) were started on oral clenbuterol 5 to 46 weeks post-LVAD implantation and up-titrated to daily doses of 720 microg. The following procedures were performed at baseline and after 3 months of therapy: echocardiography at reduced support (4 liters/min); cardiopulmonary exercise testing; body composition analysis; and quadriceps maximal voluntary contraction (MVC). Myocardial histologic analysis was measured at device implantation and explantation. RESULTS: There were no serious adverse events or arrhythmias. Creatine phosphokinase (CPK) was elevated in 4 subjects, with no clinical sequelae. No change in ejection fraction was seen. End-diastolic dimension increased significantly (4.73 +/- 0.67 vs 5.24 +/- 0.66; p < 0.01), despite a trend toward increased LV mass. Body weight and lean mass increased significantly (75.5 +/- 17.9 vs 79.2 +/- 25.1 kg, 21.1 +/- 8.9 vs 23.6 +/- 9.7 kg, respectively; both p < 0.05). Exercise capacity did not change, but MVC improved significantly from 37.0 +/- 15.7 to 45.8 +/- 20.6 kg (p < 0.05). No significant change in myocyte size or collagen deposition was seen. CONCLUSIONS: Cardiac function did not improve in this cohort of LVAD patients treated with high-dose clenbuterol. However, clenbuterol therapy increased skeletal muscle mass and strength and prevented the expected decrease in myocyte size during LVAD support. Further study will clarify its potential for cardiac and skeletal muscle recovery.

Adrenergic beta-Agonists↗

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↗