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.     

Oxygen-dependent mechanisms in cerebral autoregulation

Autoregulatory adjustments in the caliber of cerebral arterioles were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation. Increased venous pressure caused slight, but consistent, arteriolar dilation, at normal and at reduced arterial blood pressure and irrespective of whether or not intracranial pressure was kept constant or allowed to increase. Arterial hypotension caused arteriolar dilation which was inhibited partially by perfusion of the space under the cranial window with artificial CSF equilibrated with high concentrations of oxygen. This vasodilation was inhibited to a greater extent by perfusion of the space under the cranial window with fluorocarbon FC-80, equilibrated with high concentrations of oxygen. CSF or fluorocarbon equilibrated with nitrogen did not influence the vasodilation in response to arterial hypotension. The response to increased venous pressure was converted to vasoconstriction when fluorocarbon equilibrated with high concentrations of oxygen was flowing under the cranial window. The vasodilation in response to arterial hypotension was inhibited by topical application of adenosine deaminase. The results show that both metabolic and myogenic mechanisms play a role in cerebral arteriolar autoregulation. Under normal conditions, the metabolic mechanisms predominate. The presence of the myogenic mechanisms may be unmasked by preventing the operation of the metabolic mechanisms. The major metabolic mechanism seems to be dependent on changes in PO₂ within the brain with secondary release of adenosine.     

Pitfalls in acid/base experiments with conscious dogs

Arterial pH and blood gases were measured at intervals in conscious dogs after their first human contact of the day. Blood was sampled through an indwelling catheter in the aorta without disturbing the animals. It appeared that in the first 90 min arterial PO₂, oxygen saturation and haemoglobin concentration significantly declined. PCO₂ and pH changed less consistently when the acid/base status of the dogs was normal, but when a non-respiratory acidosis was present there was a significant decrease in pH and a significant increase in PCO₂. Arterial pH and blood gases were also measured before and after feeding the animals. It appeared that an appreciable metabolic alkalosis developed within 2 h after a meal. The alkaline tide was accompanied by a trend to higher values for PCO₂. It is concluded that, after a period of seclusion, renewed human contact causes behavioural changes in a dog, which may result in appreciable transitory changes in arterial pH and blood gas values. Blood sampling from conscious dogs should therefore take place after a proper period of habituation; preferably, a few samples should be taken at intervals to check that a steady state has been reached. If possible, blood should be collected before feeding; in any case the relationship in time of blood sampling to feeding should be constant throughout.     

Effects of reduced frequency breathing on arterial hypoxemia during exercise

Summary It is uncertain that exercise with reduced frequency breathing (RFB) results in arterial hypoxemia. This study was designed to investigate whether RFB during exercise creates a true hypoxic condition in arterial blood by examining arterial oxygen saturation (SaO₂) directly. Six subjects performed ten 30 s periods of exercise on a Monark bicycle ergometer at a work rate of 210 W alternating with 30 s rest intervals. The breath was controlled to use 1 s each for inspiration and expiration, and two trials with different breathing patterns were used; a continuous breathing (CB) trial and an RFB trial consisting of four seconds of breath-holding at functional residual capacity (FRC). Alveolar oxygen pressure during exercise showed a slight but significant (p<0.05) reduction with RFB as compared to CB. However, a marked increase in alveolar-arterial pressure difference for oxygen (A-aDO₂) (p<0.05) with RFB over CB resulted in a marked (p<0.05) reduction in arterial oxygen pressure. Consequently, SaO₂ fell as low as 88.8% on average. Additional examination of RFB with breath-holding at total lung capacity showed no increases in A-aDO₂ in spite of the same amount of hypoventilation as compared with that at FRC. These results indicate that RFB during exercise can result in arterial hypoxemia if RFB is performed with breath-holding at FRC, this mechanism being closely related to the mechanical responses due to lung volume restriction.     

Vergleichende Untersuchung von niedermolekularem Dextranoder Hydroxyäthylstärkelösungen als Volumenersatzmittel bei Hämodilutionstherapie

Summary Rheological therapy, as an immediate treatment in conjunction with physical therapy and the removal of risc factors, plays a significant role in the management of patients with peripheral vascular disease experiencing reduced walking tolerance. An essential element of rheological therapy is hemodilution. Currently, is still uncertain which plasma substitute solution would be the most appropriate in such cases. This study compared the effectiveness of low molecular hydroxyethyl starch to low molecular dextran during a 16-day hemodilution in combination to physical therapy. The clinical improvement observed with both plasma substitute solutions was comparable, yet in view of the cardiac volume overload, dextran demonstrates greater circulatory stress due to the transient pressure increase and more side effects. For this reason, we prefer to administer low or middle molecular hydroxyethyl starch in the dilution treatment of peripheral arterial occlusive disease as a chronic degenerative vascular disease.

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Abkürzungen A2M Alpha-2-Makroglobulin - D0 Meßzeitpunkt 0 der später mit Dextran behandelten Gruppe - D1 Meßzeitpunkt 1 der Dextran-Gruppe - D2 Meßzeitpunkt 2 der Dextran-Gruppe - Dextran 40 kleinmolekulares Dextran (mittleres Molekulargewicht 40000 Dalton) - ETA Plasmaviskosität - Fib Fibrinogen - Geh Gehstrecke - H0 Meßzeitpunkt 0 der später mit Hydroxyäthylstärke behandelten Gruppe - H1 Meßzeitpunkt 1 der HAES-Gruppe - H2 Meßzeitpunkt 2 der HAES-Gruppe - HAES 40 kleinmolekulare Hydroxyäthylstärke (mittleres Molekulargewicht 40000 Dalton) - Hkt Hämatokrit - LZ Leukozyten-Zahl - Pro Gesamteiweiß - SEA Erythrozyten-Aggregationsindex - SER Erythrozyten-Rigiditätsindex - TY Fließschubspannung - TZ Thrombozyten-Zahl     

载药纳米微球的制备和评价

含有有效药物的载药纳米粒子是一种新型的缓释系统,可改变常规的给药方式,有极广阔的发展前景。我们用超声的方法结合了不同的药物制成作用不同的纳米粒子,验证了纳米粒子对局部给药治疗的有效性,建立了良好的动物动脉摄取模型,为继续研究奠定了坚实的基础。     

Effects of active recovery on power output during repeated maximal sprint cycling

The effects of active recovery on metabolic and cardiorespiratory responses and power output were examined during repeated sprints. Male subjects (n = 13) performed two maximal 30-s cycle ergometer sprints, 4 min apart, on two separate occasions with either an active [cycling at 40 (1)% of maximal oxygen uptake; mean (SEM)] or passive recovery. Active recovery resulted in a significantly higher mean power output ( ) during sprint 2, compared with passive recovery [ ] 603 (17) W and 589 (15) W, P < 0.05]. This improvement was totally attributed to a 3.1 (1.0)% higher power generation during the initial 10 s of sprint 2 following the active recovery (P < 0.05), since power output during the last 20 s sprint 2 was the same after both recoveries. Despite the higher power output during sprint 2 after active recovery, no differences were observed between conditions in venous blood lactate and pH, but peak plasma ammonia was significantly higher in the active recovery condition [205 (23) vs 170 (20) μmol · 1⁻¹;P < 0.05]. No differences were found between active and passive recovery in terms of changes in plasma volume or arterial blood pressure throughout the test. However, heart rate between the two 30-s sprints and oxygen uptake during the second sprint were higher for the active compared with passive recovery [148 (3) vs 130 (4) beats · min⁻¹;P < 0.01) and 3.3 (0.1) vs 2.8 (0.1) 1 · min⁻¹;P < 0.01]. These data suggest that recovery of power output during repeated sprint exercise is enhanced when low-intensity exercise is performed between sprints. The beneficial effects of an active recovery are possibly mediated by an increased blood flow to the previously exercised muscle.     

Minimum realisations and modelling of biological systems

A state variable model in the canonical form of Bucy is constructed from the given impulse response of a finite-dimensional, discrete-time, linear constant dynamical biological (arterial circulatory) system.     

Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses

Recently, it was reported that acute hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s^–1 on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg (P<0.0001) at 30 s of maximal exertion, but further significant changes did not occur as exercise duration increased to 120 s [arterial oxygen tension 72.4 (2) mmHg]. A significant arterial hypoxemia also developed in galloping horses in the acute hypervolemia study [arterial oxygen tension at 30 and 120 s was 76.7 (1.7) and 71.9 (1.6) mmHg, respectively], but significant differences between treatments could not be demonstrated. In both treatments, a similar desaturation of arterial hemoglobin was also observed at 30 s of maximal exercise, which intensified with increasing exercise duration as hyperthermia, acidosis and hypercapnia intensified. Thus, acute expansion of plasma volume did not benefit arterial oxygenation in maximally exercising thoroughbred horses.