[Percutaneous liver biopsy. Overview of different techniques]. / Perkutane Leberbiopsie. Ubersicht über verschiedene Verfahren.

To classify a liver tumor, image-guided percutaneous biopsy of a liver lesion is indicated. Using ultrasound (US) to guide a biopsy needle into a liver lesion has been proven useful and safe. If a lesion cannot be seen on US or the access to a lesion has been complicated by its position, CT-guided biopsy can be performed. If a lesion cannot be delineated on US or CT, MR-guided biopsy is recommended. Using hepatospecific contrast agents, the time span to delineate tumor tissue can be prolonged. To differentiate diffuse liver disease, transvenous biopsy under fluoroscopic control can be performed if a percutaneous biopsy is contraindicated. In recent years fine-needle aspiration biopsy has been increasingly replaced by coaxial 14-20 G core biopsy, which is a safe and efficient technique to classify liver lesions and has a low complication rate.

Autocorrelation analysis of bone structure.

We propose a method called spatial autocorrelation analysis (SACA) to determine the spatial anisotropy of the trabecular bone in order to investigate osteoporosis. For demonstrating the potential of SACA we first evaluate the method on rectangular, simulated test patterns as a simple model for the anisotropic pore structure of the bone. As a next step towards biomedical application, photographic reference images of human vertebral bone were investigated by SACA. Osteoporotic bone structure could be clearly differentiated from non-osteoporotic sample images. Moreover, for demonstration of the applicability and potential of the method for in vivo characterization of osteoporosis, the microstructure of the human calcaneus was investigated by MR-microimaging on a young healthy male subject and an osteoporotic female. The measurements were performed using a high-field (3T) whole-body MR tomograph equipped with a special, strong head gradient system. The signal was acquired with a surface coil mounted on an in-house-built device for convenient immobilization of the subject's foot. Using a 3D gradient echo sequence a resolution of 0.254 x 0.254 x 2.188 mm3 was achieved in vivo. Selected images were inverted, gradient corrected for the inhomogeneous but sensitive detection by the surface coil, and subsequently analyzed by SACA. The anisotropy of bone structure detected by SACA is a possible candidate for noninvasive determination of the osteoporotic status, potentially complementing standard bone mineral density measurements.

Endothelin ETA receptor-subtype specific antagonism does not mitigate the acute systemic or renal effects of exogenous angiotensin II in humans.

BACKGROUND: Angiotensin II (Ang II) is assumed to play a pathophysiological role in a variety of vascular diseases. Animal studies indicate that these effects are partly attributed to stimulation of endothelin-1 (ET-1) release. The aim of the present study was to investigate whether the acute effects of Ang II on systemic and renal haemodynamics in healthy subjects can be influenced by endothelin ET(A)-receptor blockade. DESIGN: The study design was balanced, randomized, placebo-controlled, double blind, two-way cross-over, in 10 healthy male subjects. METHODS: Subjects received stepwise increasing intravenous doses of Ang II (0.65, 1.25, 2.5, 5 ng kg(-1) min(-1) for 15 min per dose level) in the presence or absence of BQ-123 (60 microg min(-1)), a specific ETA-receptor antagonist. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by the para-aminohippurate and inulin plasma clearance method, respectively. Renal vascular resistance (RVR) was calculated from mean arterial pressure (MAP) and renal plasma flow. RESULTS: Ang II decreased RPF by 34% and GFR by 9% and increased RVR by 94% and MAP by 27% (ANOVA, P < 0.001 vs. baseline, for all parameters). BQ-123 did not alter these renal and systemic haemodynamic responses to a significant degree. In addition, BQ-123 had no significant haemodynamic effect under baseline conditions. CONCLUSIONS: Short-term increase of circulating Ang II levels causes systemic and renal pressor effects, which are not mitigated by endothelin ETA-receptor blockade. This suggests that the pressor response to Ang II cannot be accounted for by the acute release of vasoactive ET-1.

Hypercapnia-induced cerebral and ocular vasodilation is not altered by glibenclamide in humans.

Carbon dioxide is an important regulator of vascular tone. Glibenclamide, an inhibitor of ATP-sensitive potassium channel (K(ATP)) activation, significantly blunts vasodilation in response to hypercapnic acidosis in animals. We investigated whether glibenclamide also alters the cerebral and ocular vasodilator response to hypercapnia in humans. Ten healthy male subjects were studied in a controlled, randomized, double-blind two-way crossover study under normoxic and hypercapnic conditions. Glibenclamide (5 mg po) or insulin (0.3 mU. kg(-1). min(-1) iv) were administered with glucose to achieve comparable plasma insulin levels. In control experiments, five healthy volunteers received glibenclamide (5 mg) or nicorandil (40 mg) or glibenclamide and nicorandil in a randomized, three-way crossover study. Mean blood flow velocity and resistive index in the middle cerebral artery (MCA) and in the ophthalmic artery (OA) were measured with Doppler sonography. Pulsatile choroidal blood flow was assessed with laser interferometric measurement of fundus pulsation. Forearm blood flow was measured with venous occlusion plethysmography. Hypercapnia increased ocular fundus pulsation amplitude by +18.2-22.3% (P < 0. 001) and mean flow velocity in the MCA by +27.4-33.3% (P < 0.001), but not in the OA (2.1-6.5%, P = 0.2). Forearm blood flow increased by 78.2% vs. baseline (P = 0.041) after nicorandil administration. Glibenclamide did not alter hypercapnia-induced changes in cerebral or ocular hemodynamics and did not affect systemic hemodynamics or forearm blood flow but significantly increased glucose utilization and blunted the nicorandil-induced vasodilation in the forearm. This suggests that hypercapnia-induced changes in the vascular beds under study are not mediated by activation of K(ATP) channels in humans.

Transcapillary insulin transfer in human skeletal muscle.

BACKGROUND: Transcapillary insulin transfer is considered a rate-limiting step in insulin action at supraphysiological insulin concentrations. However, it remains unclear whether this concept also applies for physiological conditions. MATERIALS AND METHODS: In the present study we set out to characterize transcapillary insulin transfer by measuring insulin concentrations in plasma and interstitial space fluid of skeletal muscle during an oral glucose tolerance test and euglycaemic hyperinsulinaemic clamp conditions, respectively. For this purpose we employed in vivo microdialysis of skeletal muscle in conjunction with an ultrasensitive insulin assay in eight healthy lean male volunteers (aged 25 +/- 1 years). RESULTS: Insulin concentrations at baseline were 48 +/- 8 pmol x L(-1) in plasma and 19 +/- 4 pmol x L(-1) in the interstitium (P = 0.002). The mean interstitium to plasma ratio at baseline was 0.48 +/- 0.09 pmol x L(-1). During the oral glucose tolerance test the interstitium to plasma ratio remained unchanged (0.43 +/- 0.12, P = NS vs. baseline), but was significantly reduced during euglycaemic hyperinsulinaemic clamp conditions at steady-state hyperinsulinaemia (0.12 +/- 0.01, P = 0.01 vs. baseline). CONCLUSION: In summary there is a substantial transcapillary insulin gradient in healthy human skeletal muscle under baseline and glucose-stimulated conditions. Our findings support the hypothesis of a saturable transcapillary insulin transport representing a partly rate-limiting step for insulin action.