[Arthroscopic tenodesis or tenotomy of the long head of the biceps tendon in preselected patients : Does it make a difference?] / Arthroskopische Tenodese oder Tenotomie der langen Bizepssehne bei vorselektionierten Patienten : Macht es einen Unterschied?

BACKGROUND: Are there clinical, cosmetic and/or structural differences between tenotomy and tenodesis of the long head of the biceps tendon (LHB) in patients selected according to commonly used indication criteria? MATERIAL AND METHODS: A total of 85 patients were included in this study. An LHB tenodesis (LHB-TD) was performed in 49 patients and a tenotomy (LHB-TT) in 36 patients. In addition to a standardized examination, the age and gender adjusted Constant score (aCS), the LHB score and the subjective shoulder value (SSV) were assessed. The cosmetic result was evaluated by both patient and examiner. In all patients the elbow flexion and supination strength were measured and compared between sides and sonography of the affected shoulder was performed. RESULTS: Both groups showed significant differences concerning age, body mass index (BMI) and requirements for shoulder function. The aCS and the LHB score showed good to excellent results without any significant differences between the groups and the SSV also did not reveal any significant differences between the two groups. In 34 patients of the LHB-TD group and 25 patients of the LHB-TT group a mild upper arm asymmetry could be detected (n. s.). Only three patients of the LHB-TD group and two patients of the LHB-TT group confirmed the presence of a subjective popeye deformity (n. s.). Both flexion and supination strength showed significantly better results for the LHB-TD group in comparison to the LHB-TT group. The LHB could not be sonographically detected in the bicipital groove in five patients of the LHB-TD group and in one patient of the LHB-TT group. CONCLUSION: In patients preselected according to routinely used indication parameters (e.g. age, BMI and functional requirements of the shoulder) both LHB-TD and LHB-TT can achieve good to very good functional and cosmetic results with high patient satisfaction.

Deuteron spectra, spin-lattice relaxation, and stimulated echoes in ice II.

(2)H NMR spectra, spin-lattice relaxation, and stimulated echoes have been measured in polycrystalline ice II in the temperature range of 84-145 K at ambient pressure. From the spectra we obtain the quadrupole coupling constant in ice II, e(2)qQ/h = (225.7+/-1.2) kHz, and the asymmetry parameter, eta = 0.118+/-0.006. At 145 K, a phase transition of ice II into ice I(c) is observed by a change of both, its spectral and relaxation behavior. The spin-lattice relaxation in ice II is bimodal, showing two components of approximately the same weight. The fast relaxing part of the recovery curve progresses monoexponentially and the temperature dependence of its mean relaxation time corresponds to an unusually low activation energy of 2.3 kJ mol(-1). The slowly relaxing part, displaying average relaxation times of about 4000 s, is significantly stretched with a Kohlrausch parameter of 0.6 and shows no temperature dependence. The stimulated echo experiments show a temperature independent correlation decay. The analysis of intermediate states indicates that no small-angle motions are involved in the underlying process. Both findings exclude an interpretation in terms of molecular motion. Instead, spin diffusion in the deuteron system has to be considered as the origin of the phenomena observed in the stimulated echo experiments.

Deuteron spin lattice relaxation in amorphous ices.

Temperature-dependent deuteron spin lattice relaxation times T(1) have been obtained from water in its three amorphous states at ambient pressure: low density amorphous (LDA), high density amorphous (HDA), and very high density amorphous (VHDA). It is found that in all of these states the magnetization recovery is essentially monoexponential and that T(1) of LDA is significantly longer than that of the higher density forms. Thus, T(1) can be used as a monitor parameter to study the kinetics of the transitions from HDA to LDA and from VHDA to LDA. During the transformation of VHDA to LDA an intermediate state is formed, which, according to its T(1) at low temperature, is clearly determined to be HDA-like. However, and most significantly, the transition from VHDA to this HDA-like state and further on to LDA occurs at temperatures significantly above the kinetic stability limit of native HDA produced at 77 K. These findings contribute to the current discussion on the nature of HDA and VHDA by strengthening the view that the annealing of VHDA at ambient pressure produces a relaxed HDA-like state.

Structure determination of CdS and ZnS nanoparticles: direct modeling of synchrotron-radiation diffraction data.

We introduce a modified method of powder-diffraction data analysis to obtain precise structural information on freestanding ZnS and CdS nanoparticles with diameters well below 5 nm, i.e., in a range where common bulk-derived approaches fail. The method is based on the Debye equation and allows us to access the crystal structure and the size of the particles with high precision. Detailed information on strain, relaxation effects, stacking faults, and the shape of the particles becomes available. We find significant size differences between our new results and those obtained by established methods, and conclude that a mixed zinc-blende/wurtzite stacking and significant lattice distortions occur in our CdS nanoparticles. Our approach should have direct impact on the understanding and modeling of quantum size effects in nanoparticles.

Nature of amorphous polymorphism of water.

We report elastic and inelastic neutron scattering experiments on different amorphous ice modifications. It is shown that an amorphous structure (HDA') indiscernible from the high-density phase (HDA), obtained by compression of crystalline ice, can be formed from the very high-density phase (vHDA) as an intermediate stage of the transition of vHDA into its low-density modification (LDA'). Both HDA and HDA' exhibit comparable small-angle scattering signals characterizing them as structures heterogeneous on a length scale of a few nanometers. The homogeneous structures are the initial and final transition stages vHDA and LDA', respectively. Despite their apparent structural identity on a local scale, HDA and HDA' differ in their transition kinetics explored by in situ experiments. The activation energy of the vHDA-to-LDA' transition is at least 20 kJ/mol higher than the activation energy of the HDA-to-LDA transition.

Differential lusitropic responsiveness to beta-adrenergic stimulation in rat atrial and ventricular cardiac myocytes.

Cardiac myocyte relaxation is brought about mainly through Ca2+ uptake into the sarcoplasmic reticulum (SR) by a Ca2+-ATPase isoform, SERCA2a. Its activity is modulated by another protein, phospholamban (PLB). The levels of both proteins differ in some mammals between atrial and ventricular myocardium and this may lead to differences in relaxation, especially under stimulatory conditions. At a concentration of 100 nM, the beta-adrenergic agonist isoprenaline (ISO) accelerates the relaxation of rat papillary muscle more than that of the left atria (16.4 versus 4.0% hastening of time to 50% relaxation, respectively). Ventricular myocytes were 24.7% quicker in reaching 50% of their diastolic length after contraction when treated with ISO compared to atrial myocytes, which were only 3.6% faster. Ca2+ fluorescence transients were also abbreviated in ventricular compared to atrial myocytes exposed to ISO (41.9 versus 25.2% hastening of time to 50% peak Ca2+ respectively). Ca2+ uptake into ventricular SR vesicles was increased by 13% in the presence of protein kinase A while that into atrial SR vesicles remained unaffected. Western blotting analysis revealed 23% less SERCA2a protein, but 76% more PLB in ventricular compared to atrial tissue. We conclude that the distinct levels of SERCA2a and PLB in ventricular and atrial myocardium are responsible for the differential modulation of the relaxation process arising from beta-adrenergic stimulation in single rat atrial and ventricular myocytes.

Angiotensin inhibition and atrial natriuretic peptide release after acute volume expansion in rats with aortocaval shunt.

OBJECTIVE: In heart failure atrial natriuretic peptide (ANP) release in response to volume expansion is impaired while the renin-angiotensin system is activated. This study was designed to test the hypothesis that ANP release in heart failure is dependent on an activated angiotensin system. METHODS: We studied the ANP and renin-angiotensin systems in a rat model of shunt-induced high-output heart failure, in which we rapidly increased circulating fluid volume with a 5 ml, hyperoncotic infusion, and evaluated the effects of acute inhibition of the angiotensin converting enzyme as well as of the blockade of the angiotensin II type 1 receptors on the ANP release and on renal excretory function. RESULTS: ANP and angiotensin II plasma concentrations prior to volume expansion were elevated (p < 0.05) in rats with aortocaval shunt compared to controls. The diuretic response to acute volume expansion (18.5 +/- 1.5 vs. 48.2 +/- 2.4 microliters/min, p < 0.001) was markedly blunted. ANP release was attenuated in rats with aortocaval shunt, as was the increase of its second messenger cGMP in plasma and urine. The blunted increase in ANP plasma levels was not due to depleted cardiac stores as cardiac ANP content, as well as ANP synthesis, were increased (p < 0.05). Acute inhibition of the angiotensin converting enzyme as well as blockade of the angiotensin II type 1 receptors restored ANP release in response to volume expansion (p < 0.01). Moreover, acute inhibition of the renin-angiotensin system completely normalized the diuretic response. CONCLUSIONS: Our data suggest that the ANP system is impaired in rats with aortocaval shunt. The activation of the angiotensin system contributes to the impairment of the ANP system. Acute inhibition of the angiotensin II system significantly improved the ability of the ANP system to respond to acute volume expansion. Our findings indicate a hitherto fore unappreciated interaction between both systems and suggest additional mechanisms for the beneficial effects of angiotensin converting enzyme inhibition or angiotensin II type 1 receptor antagonists in heart failure.

Acute hemodynamic and renal effects of adrenomedullin in rats with aortocaval shunt.

Heart failure is characterized by increased vascular resistance and water retention. Adrenomedullin is a peptide hormone with vasodilating and diuretic properties whose efficacy in heart failure has not been well established. We used an aortocaval shunt model of moderate heart failure in rats and infused increasing doses of adrenomedullin, both as bolus injections and 20-min infusions. In controls, a clear dose-dependent 4.8+/-1.0 to 13.6+/-2.3 mm Hg decrease in arterial blood pressure was observed after injection of 1 microg to 30 microg of adrenomedullin. In rats with aortocaval shunt, the hypotensive responses were significantly diminished. The urine flow rate, which was diminished at baseline in rats with aortocaval shunt, was increased and normalized by adrenomedullin administration. The glomerular filtration rate increased after infusion of adrenomedullin (0.5 microg/kg min(-1)) from 2.37+/-0.25 to 3.47+/-0.43 ml/min (P<0.01) in controls and from 1.79+/-0.33 to 2.58+/-0.49 (P<0.05) in rats with aortocaval shunt. Similarly, renal blood flow was significantly increased by adrenomedullin in both groups. Our results indicate a beneficial effect of adrenomedullin on renal function in rats with aortocaval shunt. These data suggest that adrenomedullin might be of potential therapeutic value in heart failure, without inordinately decreasing blood pressure.

Renal function in high-output heart failure in rats: role of endogenous natriuretic peptides.

The physiologic and pathophysiologic importance of natriuretic peptides (NP) has been imperfectly defined. The diminished renal responses to exogenous atrial NP in heart failure have led to the perception that the endogenous NP system might be less effective and thus contribute to renal sodium retention in heart failure. This study tests the hypothesis that in experimental heart failure, the renal responses to an acute volume load are still dependent on the NP system. The specific antagonist HS-142-1 was used to block the effects of NP in a model of high-output heart failure induced by an aortocaval shunt. Plasma cGMP levels and renal cGMP excretion were significantly lower in shunted and sham-operated rats receiving HS-142-1, compared with vehicle-treated controls, indicating effective blockade of guanylate cyclase-coupled receptors. Baseline sodium excretion and urine flow rate were lower in HS-142-1-treated sham-operated rats (15.2+/-1.1 microl/min versus 27.5+/-3.1 microl/min with vehicle, P < 0.001) and in HS-142-1-treated shunted rats (8.1+/-1.3 microl/min versus 19.9+/-2.3 microl/min with vehicle, P < 0.001). After an acute volume load, the diuretic and natriuretic responses were attenuated by HS-142-1 in control and shunted rats. The renal responses were reduced by HS-142-1 to a significantly greater extent in shunted rats than in control rats. HS-142-1 did not induce any significant systemic hemodynamic changes in either group, nor did it alter renal blood flow. However, the GFR in HS-142-1-treated shunted rats was lower than that in vehicle-treated shunted rats, both at baseline (0.6+/-0.3 ml/min versus 2.1+/-0.4 ml/min with vehicle, P < 0.05) and after an acute volume load (1.2+/-0.4 ml/min versus 2.6+/-0.4 ml/min with vehicle, P = 0.01), whereas no such effect was observed in control rats. These data indicate that the maintenance of basal renal function and the responses to acute volume loading are dependent on the NP system. The NP seem to be of particular importance for the maintenance of GFR in this model of experimental heart failure. These observations provide new insights into the importance of the renal NP system in heart failure.

Acute and chronic neutral endopeptidase inhibition and the natriuretic response to acute volume expansion.

Neutral endopeptidase inhibition (NEPI) provides a potential avenue to modulate the actions of atrial natriuretic peptide (ANP). We tested the hypothesis that acute and chronic NEPI increased the renal responses at baseline and after acute volume expansion in rats. ANP plasma levels and cGMP excretion were significantly increased with acute NEPI by SQ 28.603, whereas chronic inhibition with SCH 34826 did not lead to any changes. The ratio of cGMP excretion per plasma ANP, however, was significantly increased (6.2 +/- 0.9) by chronic treatment with SCH 34826 compared to chronic vehicle treatment (4.2 +/- 0.7) indicating an activated renal ANP receptor system. Baseline diuresis and natriuresis were enhanced with acute but not with chronic treatment. After acute volume expansion, ANP increased five-fold with acute NEPI, whereas it only increased about 70% in chronically inhibited rats. The natriuretic (497 +/- 62 vs. 329 +/- 42 micromol/60 min with vehicle, P < 0.05) and diuretic responses were significantly enhanced with chronic treatment. Together with an increased cGMP/ANP ratio, these data suggest that chronic activation of the renal ANP system after long-term NEPI facilitated the excretion of an acute volume load. These findings may have therapeutic implications in patients with chronic sodium retention.

Effect of chronic volume overload on baroreflex control of heart rate and sympathetic nerve activity.

Baroreceptor-heart rate reflex sensitivity is decreased in congestive heart failure. The reflex control of heart rate and sympathetic nerve activity in rats with chronic volume overload, an established model for moderate heart failure, is still unknown. Therefore, we investigated the regulation of humoral and neuronal sympathetic activity and the baroreflex control of heart rate and sympathetic nerve activity in conscious, unrestrained rats with aortocaval shunt. Rats with aortocaval shunts had larger hearts (388 +/- 11 vs. 277 +/- 4 mg/100 g body wt), elevated central venous pressures (14 +/- 4 vs. 4 +/- 3 mmHg), and higher atrial natriuretic peptide plasma levels (87 +/- 16 vs. 25 +/- 3 pmol/l) than controls but had similar systemic blood pressure and heart rate values. Plasma epinephrine (0.63 +/- 0.16 vs. 0.21 +/- 0.08 pmol/l, P < 0.05) and norepinephrine concentrations (0.27 +/- 0.03 vs. 0.16 +/- 0.02 pmol/l, P < 0.05) were elevated in shunted rats compared with controls. Nitroprusside-induced hypotension led to a significantly greater increase in efferent splanchnic sympathetic nerve activity in shunted rats than in controls (0.9 +/- 0.1 vs. 2.6 +/- 0.6 microV, P < 0.05), whereas the heart rate responses were not different between the groups. These results indicate that the regulation of the autonomic nervous system is altered in chronically volume-overloaded rats. The arterial baroreflex control of efferent splanchnic sympathetic nerve activity was dissociated from the control of heart rate. Therefore, analysis of the activation of sympathetic nervous system assessed by direct measurements of efferent sympathetic nerve activity appears to be more sensitive for the detection of altered autonomic nervous system function than the analysis of baroreflex control of heart rate.

Acute and chronic neutral endopeptidase inhibition in rats with aortocaval shunt.

In heart failure, sodium and water retention develop despite elevated plasma levels of atrial natriuretic peptide. Atrial natriuretic peptide is degraded in part by a neutral endopeptidase. Whether neutral endopeptidase inhibition improves sodium and water excretion in heart failure is unknown. We determined the effect of neutral endopeptidase inhibition on plasma levels of atrial natriuretic peptide and the renal response to acute volume expansion in rats with aortocaval shunts and in sham-operated controls. Acute endopeptidase inhibition with SQ 28,603 (30 mg/kg) elevated atrial natriuretic peptide plasma levels in both shunted rats (523 +/- 54 to 1258 +/- 330 pmol/L, P<.05) and controls (184 +/- 28 to 514 +/- 107 pmol/L, P<.05). Urinary cGMP excretion, which reflects renal action, increased in parallel. However, the diuretic and natriuretic responses to acute volume expansion were enhanced only in control rats and not in shunted rats. In contrast to the acute effects, chronic neutral endopeptidase inhibition with SCH 34826 (30 mg/kg twice daily) in shunted rats did not change atrial natriuretic peptide plasma levels or cGMP excretion. Nevertheless, the diuretic and natriuretic responses to acute volume load were increased by chronic endopeptidase inhibition in shunted rats (1789 +/- 154 to 2674 +/- 577 microL/80 min and 99 +/- 31 to 352 +/- 96 micromol/80 min, respectively; P<.05). Chronic endopeptidase inhibition attenuated the cardiac hypertrophic response to aortocaval shunt without changing arterial blood pressure. Our data show that the renal effects of neutral endopeptidase inhibition are not necessarily dependent on changes in atrial natriuretic peptide plasma levels but instead may be mediated by local inhibition of the neutral endopeptidase in the kidney. In addition, chronic endopeptidase inhibition may attenuate heart failure-induced cardiac hypertrophy independent of hemodynamic effects.