肾复康Ⅱ号胶囊对IgA肾病大鼠血清醛固酮及肾内小动脉病变的影响

目的:观察肾复康Ⅱ号胶囊对IgA肾病(IgAN)肾内小动脉病变大鼠醛固酮诱导的血管内皮细胞生长因子(VEGF)、增殖细胞核抗原(PCNA)、人基质金属蛋白酶-9(MMP-9)的表达,探讨肾复康Ⅱ号胶囊对IgAN小动脉病变的防治机制.方法:将70只健康雄性SD大鼠分为空白组、模型组、治疗组(肾复康组)、中药对照组(黄葵组...     

骨间后血管及其返支为蒂串连皮瓣的临床应用

目的为手部皮肤软组织缺损探寻一种新的修复方法.方法在40侧人体上肢标本上,对骨间后血管及其返支的来源、走行、分支、分布及吻合情况进行解剖观察的基础上,设计以前臂骨间后血管及其返支为蒂的串连皮瓣.1998年8月～2000年7月间临床应用此皮瓣逆行移位修复手背远侧及手指背侧皮肤缺损17例.皮瓣范围最大15cm×10cm,最小7cm×5cm.结果术后随访3周～6个月,除1例皮瓣远端有2cm×3cm坏死外,其余皮瓣全部成活,外观及功能满意.结论此皮瓣不损伤肢体主要血管,血管蒂较长,皮瓣切取面积较宽,厚薄适中,可用于修复拇指、手背至手指近节背侧的皮肤软组织缺损.手术简便,效果良好.     

食管壁微动脉及毛细血管的观测

目的;观察食管壁内动脉血供及微血管构筑的基础性研究资料。方法：随机选取新鲜胎尸25具,墨汁灌注,组织切片;家兔5只,钙钴法碱性磷酸酶染色。光学显微镜下观测。结果;食管壁内各层均存在动脉网,粘膜下层动脉网丰富,分深浅两层;各层毛细血管特点各异,外膜层稀,肌层有肌束间血管网,粘膜下层呈丛状,粘膜层最丰富;食管各段毛细血管密度差异不大,但颈段前壁纵形肌、胸上段后壁粘膜层有相对毛细血管贫乏区。结论：食管的各段各层均存在动脉网,毛细血管密度差异不大,能有限代偿食管壁外供血动脉的阻断。     

A quantitative ultrastructural study of juxtaglomerular arterioles in IDDM patients with micro- and normoalbuminuria

Summary Hyalinization of juxtaglomerular arterioles is prominent in advanced diabetic nephropathy and may have important functional consequences. We studied the early stages of diabetic renal disease using kidney biopsy material from insulin-dependent diabetic patients, 8 with normal albumin excretion rate (<15 /min) and 16 with microalbuminuria (15–200 g/min). Ten living non-diabetic kidney donors served as a control group. Median duration of diabetes was 9.5 years (range 5–31) in patients with normoalbuminuria, and 12 years (7–22) in patients with microalbuminuria (p=0.27). The tissue was sectioned systematically, 1-m thick sections for light microscopy at 10-m intervals, and thin sections for electron microscopy taken at 60-m intervals. The arterioles were identified as afferent or efferent, and total profiles were photographed (magnification 7500×), providing a systematic independent sample for measurements using standard stereological methods. Patients with microalbuminuria had significantly increased arteriole parameters compared with the control group: for afferent and efferent arterioles the volume fraction of matrix/media, means and (coefficient of variation, CV), was 0.47 (0.16) vs 0.33 (0.19) (p=0.0009), and 0.62 (0.14) vs 0.45 (0.23) (p=0.0004) and matrix-T, expressing amount of matrix per unit arteriolar surface, 2.38 (0.38) m vs 1.44 (0.30) m (p=0.004), and 1.62 (0.28) m vs 1.03 (0.34) (p=0.0009). Patients with normoalbuminuria showed no significant differences from the control group, and had lower values than microalbuminuric patients for all parameters except the afferent matrix-T. In the normoalbuminuric group a correlation was found between parameters for afferent arterioles and those for glomerular structure. In conclusion there is arteriolar accumulation of extracellular material in the early phase of diabetic nephropathy, concomitant with early glomerulopathy.Abbreviations IDDM Insulin-dependent diabetes mellitus - GFR glomerular filtration rate - AER albumin excretion rate - matrix-T matrix thickness - ND non-diabetic subjects - D_NA IDDM patients with normal albumin excretion rate - D_MI IDDM patients with microalbuminuria - RPF renal plasma flow - CV coefficient of variation     

Hypoxia inhibits contraction but not calcium channel currents or changes in intracellular calcium in arteriolar muscle cells

OBJECTIVE: We tested the hypothesis that hypoxia inhibits currents through L-type Ca(2+) channels and inhibits norepinephrine-induced rises in intracellular Ca(2+) in cremasteric arteriolar muscle cells, thus accounting for the inhibitory effect of hypoxia on norepinephrine-induced contraction of these cells. METHODS: Single smooth muscle cells were enzymatically isolated from second-order and third-order arterioles from hamster cremaster muscles. The effects of hypoxia (partial pressure of oxygen: 10-15 mm Hg) were examined on Ba(2+) (10 mM) currents through L-type Ca(2+) channels by use of the perforated patch clamp technique. Also, the effect of hypoxia on norepinephrine-induced calcium changes was studied using Fura 2 microfluorimetry. RESULTS: Hypoxia inhibited the norepinephrine-induced (10 microM) contraction of single arteriolar muscle cells by 32.9 +/- 5.6% (mean +/- SE, n = 4). However, hypoxia had no significant effect on whole-cell currents through L-type Ca(2+) channels: the peak current densities measured at +20 mV were -3.83 +/- 0.40 pA/pF before hypoxia and -3.97 +/- 0.36 pA/pF during hypoxia (n = 15; p > 0.05). In addition, hypoxia did not inhibit Ca(2+) transients in arteriolar muscle cells elicited by 10 microM norepinephrine. Instead, hypoxia increased basal Ca(2+) (13.8 +/- 3.2%) and augmented peak Ca(2+) levels (29.4 +/- 7.3%) and steady-state Ca(2+) levels (15.2 +/- 5.4%) elicited by 10 microM norepinephrine (n = 21; p < 0.05). CONCLUSIONS: These data indicate that hypoxia inhibits norepinephrine-induced contraction of single cremasteric arteriolar muscle cells by a mechanism that involves neither L-type Ca(2+) channels nor norepinephrine-induced Ca(2+) mobilization. Instead, our findings suggest that hypoxia must inhibit norepinephrine-induced contraction by affecting a component of the signaling pathway that lies downstream from the increases in Ca(2+) produced by this neurotransmitter.     

高血压病患者脉压差与颈动脉粥样硬化的相关性研究

目的探讨高血压病患者脉压差与颈动脉粥样硬化斑块的发生率及颈动脉内中膜厚度(IMT)的相关性。方法通过多普勒超声检查70例高血压患者颈动脉粥样硬化斑块及IMT,计算出这些患者的脉压差,观察脉压差与颈动脉粥样硬化斑块的发生率及与颈动脉内中膜厚度(IMT)的相关性。结果脉压差大的患者其颈动脉粥样硬化斑块的发生率及IMT均增高(P<0．05)。结论脉压差与颈动脉粥样硬化斑块和IMT相关,脉压差可促进动脉粥样硬化的形成和发展。     

The Effects of Diuretics on Intracellular Ca2+ Dynamics of Arteriole Smooth Muscles as Revealed by Laser Confocal Microscopy

The regulation of cytosolic Ca²⁺ homeostasis is essential for cells, including vascular smooth muscle cells. Arterial tone, which underlies the maintenance of peripheral resistance in the circulation, is a major contributor to the control of blood pressure. Diuretics may regulate intracellular Ca²⁺ concentration ([Ca²⁺]_i) and have an effect on vascular tone. In order to investigate the influence of diuretics on peripheral resistance in circulation, we investigated the alteration of [Ca²⁺]_i in testicular arterioles with respect to several categories of diuretics using real-time confocal laser scanning microscopy. In this study, hydrochlorothiazide (100 µM) and furosemide (100 µM) had no effect on the [Ca²⁺]_i dynamics. However, when spironolactone (300 µM) was applied, the [Ca²⁺]_i of smooth muscles increased. The response was considerably inhibited under either extracellular Ca²⁺-free conditions, the presence of Gd³⁺, or with a treatment of diltiazem. After the thapsigargin-induced depletion of internal Ca²⁺ store, the spironolactone-induced [Ca²⁺]_i dynamics was slightly inhibited. Therefore, the spironolactone-induced dynamics of [Ca²⁺]_i can be caused by either a Ca²⁺ influx from extracellular fluid or Ca²⁺ mobilization from internal Ca²⁺ store, with the former being dominant. As tetraethylammonium, an inhibitor of the K⁺ channel, slightly inhibited the spironolactone-induced [Ca²⁺]_i dynamics, the K⁺ channel might play a minor role in those dynamics. Tetrodotoxin, a neurotoxic Na⁺ channel blocker, had no effect, therefore the spironolactone-induced dynamics is a direct effect to smooth muscles, rather than an indirect effect via vessel nerves.     

Angiotensin II enhances the afferent arteriolar response to adenosine through increases in cytosolic calcium

Aims: Angiotensin II (Ang II) is a strong renal vasoconstrictor and modulates the tubuloglomerular feedback (TGF). We hypothesized that Ang II at low concentrations enhances the vasoconstrictor effect of adenosine (Ado), the mediator of TGF. Methods: Afferent arterioles of mice were isolated and perfused, and both isotonic contractions and cytosolic calcium transients were measured. Results: Bolus application of Ang II (10^?12 and 10^?10 m ) induced negligible vasoconstrictions, while Ang II at 10^?8 m reduced diameters by 35%. Ang II at 10^?12, 10^?10 and 10^?8 m clearly enhanced the arteriolar response to cumulative applications of Ado (10^?11 to 10^?4 m ). Ado application increased the cytosolic calcium concentrations in the vascular smooth muscle, which were higher at 10^?5 m than at 10^?8 m . Ang II (10^?11 to 10^?6 m ) also induced concentration‐dependent calcium transients, which were attenuated by AT₁ receptor inhibition. Simultaneously applied Ang II (10^?10 m ) additively enhanced the calcium transients induced by 10^?8 and 10^?5 m Ado. The transients were partly inhibited by AT₁ or A₁ receptor antagonists, but not significantly by A₂ receptor antagonists. Conclusion: A low dose of Ang II enhances Ado‐induced constrictions, partly via AT₁ receptor‐mediated calcium increase. Ado increases intracellular calcium by acting on A₁ but not A₂ receptors. The potentiating effect of Ang II on Ado‐induced arteriolar vasoconstrictions may involve calcium sensitization of the contractile machinery, as Ang II only additively increased cytosolic calcium concentrations, while its effect on the arteriolar constriction was more than additive. The potentiating effect of Ang II might contribute to the resetting of TGF.