Serum protein concentration and oncotic pressure relationship in the rat

Summary A formula relating oncotic pressure torat serum protein concentration was derived and found to be in complete agreement with the Landis-Pappenheimer formula derived from measurements onhuman plasma.This study was supported by the Danish Medical Research Council and Johan and Hanne Weimann's legacy.     

Developments in cardiovascular ultrasound. Part 2: Arterial applications

Many of the changes resulting from arterial disease can be measured, using Doppler ultrasound for measurement of blood velocity and B-scan imaging for measurement of tissue structure and composition. Wall thickness, the degree of arterial narrowing and plaque volume can be measured using B-scan imaging, and 3D ultrasound can be used to improve the accuracy of measurements of plaque volume and for improved visualisation of complex arterial geometries. Measurement of the dynamic properties of the arterial wall permits estimation of wall elasticity and plaque motion. From the Doppler signal, measurements of blood velocity are used to estimate the degree of arterial narrowing and volumetric flow, although measurement errors can be large. Wall shear stress can be estimated by measuring the velocity gradient at the vessel wall. The problems of inadequate spatial resolution and interference from overlying tissue are largely removed when intravascular systems are used, and these have superior capability in the assessment of arterial structure and tissue composition. However, measurement of quantities relating to blood flow is more difficult using the intravascular approach, as the indwelling cather disturbs the blood flow pattern, and currently, assessment of flow and vessel cross-section are not performed at the same site.     

人体组织中血液灌注率和动脉血温度的无损测量研究

由于人体组织中存在血液对流传热和代谢产热，当皮肤表面绝热后，皮肤表面的温度将上升，体表温升值是人体组织中血液灌注率和动脉血温度的函数，根据实际测量的体表温升与时间的关系就可以测出活体组织的血液灌注率和动脉血温度。根据一维Pennes生物传热方程，推导出了体表绝热后人体组织中及皮肤表面温度分布的解析解，并对人体组织中的血液灌注率及动脉血温度进行了实验测量。由于测量过程中利用的只是皮肤表面的温度信息，无须引入外加热源，对人体组织完全不会造成损伤，亦避免了干扰人体组织的正常生理状态，整个测量系统也比较简单。     

Learned control of heart rate during exercise in patients with borderline hypertension

Summary Twelve patients with borderline hypertension [⩽21.33/12.6, ⩾18.6/12.0 kPa (⩽160/ 95; ⩾ 140/90 mm Hg)] participated in an experiment aimed at testing whether they could learn to attenuate heart rate while exercising on a cycle ergometer. Six experimental (E) subjects received beat-to-beat heart-rate feedback and were asked to slow heart rate while exercising; six control (C) subjects received no feedback. Averaged over 5 days (25 training trials) the exercise heart-rate of the E group was 97.8 bt min⁻¹, whereas the C group averaged 107 bt min⁻¹ (P=0.03). Systolic blood pressure was unaffected by feedback training. Generally, changes in rate-pressure product reflected changes in heart-rate. Oxygen consumption was lower in the E than in the C group late in training. We conclude that neurally mediated changes associated with exercise in patients with borderline hypertension can be brought under behavioral control through feedback training.     

Nonhomogeneous Deformation in the Anterior Leaflet of the Mitral Valve

In the mitral valve, regional variations in structure and material properties combine to affect the biomechanics of the entire valve. Previous biaxial testing has shown that mitral valve leaflet tissue is highly extensible, and exhibits nonlinear, anisotropic material properties. In this study, experimental measurements of mitral valve leaflet deformation under quasi-static pressure loading were performed on isolated porcine hearts. Biplane video images of markers placed on the anterior leaflet surface were used to reconstruct the 3D position of the markers at several pressure levels over the physiological range. A least-squares finite-element method was used to fit parametric models to the markers and to calculate the deformation over the surface. The results showed that the leaflet deformations were anisotropic, exhibiting a large nonhomogeneous radial stretch and a small circumferential stretch. This information can be used to better understand how the valve deforms under physiological loading, and to help design treatments for valve problems, such as mitral regurgitation.     

The role of prostaglandins in the endothelium-mediated vasodilatory response to hypoxia

The effect of intraluminal hypoxia on vascular tone and the release of prostaglandins (PG) I₂ and E₂ were investigated in intact isolated segments of canine femoral and coronary arteries as well as in the rat tail artery. Perfusion with hypoxic Tyrode's solution (pO₂ 20–40 mm Hg) evoked a marked vasodilation of the segments, precontracted with norepinephrine or serotonin. Simultaneously, a 2–3-fold increase in the release of 6-keto-PGF₁ (the stable hydrolysis product of PGI₂) could be observed. In parallel to 6-keto-PGF₁, smaller quantities of PGE₂ were released. Removal of the endothelium as well as pretreatment with indomethacin abolished both, the dilatory response and the PG-release. After administration of verapamil as well as 3,4,5-trimethoxybenzoic acid 8-diethyl-aminooctylester (TMB-8) (which binds intracellular calcium) the PG-increase was abolished and hypoxic dilatation could no longer be elicited, although the vessel had still a capacity to dilate. Exogenous administration of PGI₂ and PGE₂ showed that in canine femoral and coronary arteries PGI₂ was the most effective vasodilating prostaglandin, while in the rat tail artery PGE₂ had a 10-fold higher dilating potency compared to PGI₂. At very high concentrations both PGI₂ and PGE₂ caused vasoconstriction. Our experiments suggest that the hypoxic endothelium-dependent dilatation may be mediated by an increased PG-release. Hypoxia-induced transmembrane calcium influx into the endothelial cells seems to be the trigger reaction.Supported by the Deutsche Forschungsgemeinschaft (Bu 436/2-1)     

Evaluation of antidecubitus mattresses

Pressure sores are a current problem in hospitals and care of the elderly, leading to protracted hospital stays and a high care burden. The trauma for the patients is severe, and the cost of pressure sore prevention and treatment, is considerable. Antidecubitus mattresses are used for prevention and in treatment, but they also contribute to the cost of treating pressure sores. The problem highlighted in the review is that the mattresses' effectiveness in preventing and treating pressure sores has not been sufficiently evaluated. When antidecubitus mattresses are evaluated, it is often only with regard to aspects of the interface pressure and the mattresses' ability to redistribute the pressure. The review points out the important observation that, to be able to evaluate the efficacy of the antidecubitus mattress, the mattress's effect on tissue viability needs to be studied. The parameters that ought to be considered when evaluating a support surface are: interface pressure, pressure and blood flow distribution, temperature and humidity in the skin-support surface interface. The authors propose that the effect on tissue viability of external loading can be assessed by simultaneous measurement of the interface pressure and tissue perfusion.     

Numerical Simulation and Experimental Validation of Blood Flow in Arteries with Structured-Tree Outflow Conditions

Blood flow in the large systemic arteries is modeled using one-dimensional equations derived from the axisymmetric Navier–Stokes equations for flow in compliant and tapering vessels. The arterial tree is truncated after the first few generations of large arteries with the remaining small arteries and arterioles providing outflow boundary conditions for the large arteries. By modeling the small arteries and arterioles as a structured tree, a semi-analytical approach based on a linearized version of the governing equations can be used to derive an expression for the root impedance of the structured tree in the frequency domain. In the time domain, this provides the proper outflow boundary condition. The structured tree is a binary asymmetric tree in which the radii of the daughter vessels are scaled linearly with the radius of the parent vessel. Blood flow and pressure in the large vessels are computed as functions of time and axial distance within each of the arteries. Comparison between the simulations and magnetic resonance measurements in the ascending aorta and nine peripheral locations in one individual shows excellent agreement between the two. © 2000 Biomedical Engineering Society. PAC00: 8719Uv     

舌粘膜及粘膜下血管网的构筑及其临床意义

本研究应用手术显微镜和扫描电镜观察了人舌粘膜的微血管构筑。舌深动脉长支和舌背动脉终支在舌粘膜下形成一完整的致密动脉网,跨越界沟和舌正中线,成为一整体。由动脉网发出微动脉支进入舌粘膜内,形成粘膜内的毛细血管网和各种乳头毛细血管丛。另外,还讨论了舌粘膜下馓血管构筑和舌瓣设计与临床舌诊的关系。     

Light and electron microscopic studies on rat arterial lesions induced by experimental arterial contraction

Summary Experimental contraction was produced in the rat mesenteric arteries and the arterial segments were studied morphologically. When the rat mesenteric artery was exposed in physiological saline solution at 37° C and 2–3 mg of methoxamine hydrochloride (10 mg/ml) was dripped onto it, intense contraction was observed for about 30 min but elevation in blood pressure was slight. During the contraction, numerous vacuoles were seen in the medial smooth muscle cells of the arterial segments, and these vacuoles were shown electron microscopically to have double unit membranes, indicating that they were formed by herniation of a part of the adjacent smooth muscle cell body. In the arteries 1–6 h after the end of the contraction, cellular, nuclear and vacuolar membranes and myofilaments of the medial muscle cells were partially lost. 12–24 h after the contraction the arteries exhibited necrosis and desquamation of endothelial cells and platelet adhesion. In the media, smooth muscle cells were completely deprived of cell membranes, myofilaments, nuclei, intracytoplasmic organelles other than mitochondria, and vacuolar membranes. The cytoplasm was filled with fine granular and granulo-vesicular material, and fibrin insudation was observed in these severely damaged cells. Arterial contraction may be an important factor in the induction of arterial lesions.