锁骨下(动脉)窃血综合征检查的彩色多普勒超声回顾性分析

目的探讨彩色多普勒超声(CDU)在锁骨下(动脉)窃血综合征(SSS)中应用价值。方法对31例SSS的超声表现进行回顾性分析。结果31例患者中,28例为完全性SSS,3例部分性SSS。锁骨下动脉起始处闭塞18例,均为完全性SSS;狭窄13例,内径1～3.4mm,最大流速270～430cm/s。患侧上肢动脉血流频谱为单峰、低速、低阻波形。结论CDU是评价SSS的一种有价值方法。     

脾动脉盗血综合征的临床研究

目的研究门静脉高压症时是否存在脾动脉盗血及手术前后肝动脉血流动力学变化,为该类患者是否行脾切除术提供依据。方法54例正常人为对照组,69例门静脉高压症患者为试验组,门静脉高压症患者均行脾切除加贲门周围血管离断术,术前根据脾功能亢进状况分为轻度脾亢组（28例）和中重度脾亢组（41例）,采用TOSHIBAaplio50型彩色多普勒超声诊断仪,清晨空腹进行检查。常规检查肝胆脾情况,测量门静脉、脾动脉及肝动脉内径、血流参数（包括平均流速V、血流量F）。结果门静脉高压组门静脉内径明显大于对照组（P〈0.05）,血流量高于对照组（P〈0.05）,平均流速低于对照组（P〈0.05）。门静脉高压组血流量较对照组降低（P〈0.05）,中重度脾亢组肝动脉血流量较对照组有明显下降（P〈0.05）。中重度脾亢组患者脾动脉内径、平均流速及血流量较对照组均有明显升高（P〈0.01）。中重度脾亢患者脾切除后肝动脉血流量明显增加（P〈0.01）。结论门静脉高压症时门静脉血流增加,肝动脉血流量减少,脾动脉血流量明显增加,中重度脾亢时存在脾动脉盗血,脾切除后肝动脉血流量明显增加。     

不同影像学检查在锁骨下动脉盗血综合征中的诊断价值

目的评价不同影像学检查方法在锁骨下动脉盗血综合征（SSS）中的诊断价值。方法对12例SSS患者进行经颅多普勒（TCD）、颈部血管B超的检查，并与数字减影血管造影（DSA）结果相比较。结果TCD检查12例患者Ⅰ度盗血6例；Ⅱ度4例；Ⅲ度2例，9例患者经DSA检查证实。结论TCD结合颈部血管B超检查可以很好地对SSS患者进行评估，并与DSA相吻合。     

彩超对锁骨下动脉窃血综合征32例的诊断分析

目的探讨锁骨下动脉窃血综合征的彩色多普勒超声特征和诊断价值。方法回顾性分析2010年1月至2014年3月经我院超声科诊断的32例SSS患者的声像图特征及血流动力学改变,并与DSA或MRA结果对照分析。结果 32例锁骨下动脉窃血综合征主要由动脉粥样硬化及大动脉炎引起,其中左侧锁骨下动脉病变21例,右侧锁骨下动脉病变11例,Ⅰ级窃血10例,Ⅱ级窃血9例,Ⅲ级窃血8例,Ⅳ级窃血5例。结论彩色多普勒超声是检测锁骨下动脉窃血综合征一种非常有效的无创性诊断方法。     

锁骨下动脉盗血综合征椎基底动脉供血不足与盗血程度及类型的相关性分析

目的 探讨锁骨下动脉盗血综合征椎基底动脉供血不足与盗血程度及类型的关系.方法 对80例行经颅多普勒超声诊断为锁骨下动脉盗血综合征患者回顾分析,其中24例进一步行数字减影动脉血管造影（DSA）.以同侧椎动脉血流方向判定盗血程度,以基底动脉是否参与盗血为类型,对椎基底动脉供血不足与盗血程度及盗血类型进行相关性分析.结果 24例进一步行DSA检查者锁骨下动脉起始部狭窄严重程度同TCD检查同侧椎动脉盗血程度成正比（t=15.59,P＜0.05）.椎基底动脉供血不足症状与盗血程度无关（P＞0.05）.基底动脉参与盗血的患者中有21例（77.8％）存在椎基底动脉供血不足,未参与盗血的患者中有18例（33.9％）,两者比较差异有统计学意义（P＜0.05）.结论 由锁骨下动脉盗血综合征引起的椎基底动脉供血不足与同侧椎动脉盗血程度无关,与基底动脉是否参与盗血密切相关,关注基底动脉是否参与盗血有利于分析患者病情并指导临床治疗.     

Subepicardial steal and reduction of myocardial oxygen consumption by adenosine

The direct effects of adenosine on cardiac oxygen balance, hemodynamics and regional myocardial perfusion were studied in isolated canine hearts. Intracoronary infusion of adenosine produced a dose-dependent shift in the transmural distribution of coronary blood flow away from left ventricular subendocardium and a reduction in myocardial oxygen consymption (MVO₂). The data suggest that adenosine may partially decrease MVO₂ by a redistribution of flow from a high to low oxygen-extracting region of the myocardium.     

锁骨下动脉窃血综合征患者椎动脉多普勒频谱类型与动脉狭窄程度的相关性研究

目的探讨锁骨下动脉窃血综合征患者的椎动脉频谱类型与锁骨下动脉或无名动脉狭窄程度的关系。方法回顾性分析了经数字减影血管造影（DSA）证实的41例锁骨下动脉窃血综合征（SSS）患者的椎动脉多普勒超声表现,将锁骨下动脉或无名动脉的狭窄程度与椎动脉频谱类型进行对照分析。结果 41例SSS患者中,DSA诊断的轻度狭窄8例,中度狭窄16例,重度狭窄或闭塞17例,超声检查椎动脉频谱类型中窃血前期表现者11例,部分窃血表现者18例,完全窃血表现者12例,所有椎动脉窃血程度与同侧锁骨下动脉或无名动脉狭窄程度相关（r s=0.472,P〈0.05）。结论 SSS患者椎动脉的频谱表现与锁骨下动脉或无名动脉的狭窄程度密切相关,但对于多发狭窄的患者应综合分析,避免低估狭窄程度。     

Free radicals-induced changes in mesenteric microvascular dimensions in the anesthetized cat

Effect of free radicals on microvascular dimensions was studied in anesthetized cat intestinal mesentery. Generation of free radicals by xanthine oxidase, acting on endogenous substrates (e.g., xanthine, hypoxanthine), produced sustained vasodilation at pH 7.4 or at pH 6.6. These effects were reversed by superoxide dismutase (SOD), a superoxide radical (.O2-) scavenger, at pH 7.4, and by SOD plus hydroxyl radical (.OH) scavenger d-mannitol at pH 6.6. These findings suggest that the sustained vasodilation is caused by .O2- and by .OH derived from .O2- at low pH.     

多沙唑嗪对映体对麻醉猫心血管功能的选择性作用

目的研究多沙唑嗪对映体对麻醉猫心血管功能的影响。方法采用八道生理仪记录麻醉猫股动脉血压、心率以及左心室收缩压、左心室舒张末期压和左心室内压最大变化率(±dp/dtmax)。结果十二指肠给予右旋多沙唑嗪[(+)doxazosin,(+)DOX]0.03～1.0 mg.kg-1剂量依赖性降低麻醉猫收缩压、舒张压、平均动脉压和左心室收缩压(P<0.05)。十二指肠给予同等剂量的左旋多沙唑嗪[(-)doxazosin,(-)DOX]和消旋多沙唑嗪[(±)doxazosin,(±)DOX]对麻醉猫收缩压、舒张压、平均动脉压和左心室收缩压无影响(P>0.05)。3种药物对左心室舒张末期压、左心室-dp/dt、左心室+dp/dt和心率无影响(P>0.05)。结论麻醉猫十二指肠给药时,(+)DOX降低动脉血压并抑制心室收缩功能,相同剂量的(-)DOX无作用;提示DOX的手性结构对药物的心血管效应具有明显的影响。     

Effect of bulbocapnine as a peripheral dopamine receptor antagonists in the anesthetized cat

Summary We have found bulbocapnine to be an effective, apparently competitive inhibitor of dopamine depressor responses in the anesthetized, phenoxybenzamine-treated cat. The duration of action of the compound as a dopaminergic antagonist exceeded 3 hrs after an intravenous dose of 8 mg/kg. In the same preparation, however, bulbocapnine did not at all inhibit the depressor responses to acetylcholine, histamine and isoproterenol, indicating a selectivity of action. Although administration of a high dose of propranolol (2 mg/kg, i.v.) did not alter the response of the alpha-receptor blocked cat to dopamine, the subsequent infusion of bulbocapnine remained effective. These results suggest that dopamine is acting as a blood pressure depressor agent via a unique receptor mechanism.     

Do renal tubular dopamine receptors mediate dopamine-induced diuresis in the anesthetized cat?

The aim of this study was to investigate whether the pentobarbitone anesthetized cat is a suitable preparation in which to characterize renal tubular dopamine receptors. Intravenous infusion of dopamine (10-100 micrograms/kg/min) resulted in a dose-related increase in mean blood pressure (MBP), urine output, sodium excretion (UNaV), and fractional sodium excretion (FENa). This diuretic effect occurred despite little change in glomerular filtration rate, suggesting that it is a consequence of decreased tubular reabsorption. Dopamine (10-100 micrograms/kg/min, i.v.) also induced marked dose-related falls in renal vascular conductance; however, renal blood flow was not significantly reduced. The increases in MBP, urine output, UNaV, and FENa induced by dopamine (10-100 micrograms/kg/min, i.v.), were unaffected by pretreatment of cats with either the selective dopamine DA1 or DA2 receptor antagonists, SCH 23390 (30 micrograms/kg, i.v.), or domperidone (100 micrograms/kg, i.v.) respectively. In contrast, pretreatment of cats with the nonselective alpha-adrenoceptor antagonist, phentolamine (1 mg/kg, i.v.) prevented dopamine-induced increases in urine output and MBP. Infusion of the selective dopamine DA1 receptor agonist fenoldopam (0.01-10 micrograms/kg/min) into the left renal artery failed to increase left renal vascular conductance, or left kidney urine output, UNaV, or FENa. In conclusion, this study provides no evidence for the involvement of renal tubular dopamine receptors in dopamine-induced diuresis in anesthetized cats. Rather, the diuretic effect appears to be linked to stimulation of alpha-adrenoceptors.     

Effects of adenosine on neurally mediated norepinephrine release from the cat spleen.

The effects of adenosine on the release of 3H-norepinephrine (3H-NE) from the isolated, perfused cat spleen consequent to nerve stimulation were evaluated. Electrical stimulation of the splenic nerve (5 Hz/100 impulses total) caused a release of 3H-NE and a rise in perfusion pressure. Adenosine added to the perfusion fluid (final concentrations 1 X 10(-6), 1 X 10(-5), and 1 X 10(-4) M) significantly reduced the pressure response elicited by nerve stimulation. In addition, adenosine (1 X 10(-4) M) slightly increased the release of total 3H consequent to nerve stimulation. Theophylline (1 X 10(-4) M) produced both a slight increase in the release of total 3H and a diminished pressure response. The effects of adenosine were effectively antagonized by this concentration of theophylline. Neither substance had any effect on the spontaneous release of total 3H. Adenosine (1 X 10(-4) M) also antagonized the pressure response elicited by perfusion of NE.     

Effects of porcine and rat endothelin and an analog on blood pressure in the anesthetized cat

Arterial responses to a wide range of doses of porcine and rat endothelin and a monocyclic analog were compared in the anesthetized cat. Injections of the porcine peptide in doses of 0.01-0.1 nmol/kg i.v. decreased systemic arterial pressure in a dose-related manner, whereas doses of 0.3 and 1 nmol/kg i.v. elicited biphasic responses. The rat peptide, in doses of 0.03-1 nmol/kg i.v., also decreased arterial pressure in a dose-related fashion, whereas injection at 3 nmol/kg i.v. caused a biphasic response. With both peptides the biphasic response was characterized by an initial short-lived decrease followed by a secondary sustained increase in pressure. The monocyclic porcine analog in doses of 3-30 nmol/kg i.v. had no significant effect on arterial pressure. Both peptides increased cardiac output, and changes in peripheral vascular resistance in response to both peptides were not altered by sodium meclofenamate. These data suggest that arterial depressor responses to porcine and rat endothelin are similar and dose-dependent. However, the porcine peptide has 3-fold greater pressor activity in the cat. The lack of effect with the monocyclic porcine analog suggests that the two disulfide linkages are necessary for activity.     

Gallic acid attenuates pulmonary fibrosis in a mouse model of transverse aortic contraction-induced heart failure

Gallic acid, a trihydroxybenzoic acid found in tea and other plants, attenuates cardiac hypertrophy, fibrosis, and hypertension in animal models. However, the role of gallic acid in heart failure remains unknown. In this study, we show that gallic acid administration prevents heart failure-induced pulmonary fibrosis. Heart failure induced in mice, 8 weeks after transverse aortic constriction (TAC) surgery, was confirmed by echocardiography. Treatment for 2 weeks with gallic acid but not furosemide prevented cardiac dysfunction in mice. Gallic acid significantly inhibited TAC-induced pathological changes in the lungs, such as increased lung mass, pulmonary fibrosis, and damaged alveolar morphology. It also decreased the expression of fibrosis-related genes, including collagen types I and III, fibronectin, connective tissue growth factor (CTGF), and phosphorylated Smad3. Further, it inhibited the expression of epithelial-mesenchymal transition (EMT)-related genes, such as N-cadherin, vimentin, E-cadherin, SNAI1, and TWIST1. We suggest that gallic acid has therapeutic potential for the treatment of heart failure-induced pulmonary fibrosis.     

建立近红外一致性模型快速鉴别三磷酸腺苷二钠片的真伪

目的 建立近红外光谱快速鉴别三磷酸腺苷二钠片真伪的一致性模型方法.方法 在4200～12000 cm-1范围内对三磷酸腺苷二钠片分别进行隔铝塑扫描和直接接触扫描,采用近红外漫反射光谱,运用OPUS软件通过不同的预处理方法对图谱进行分析,建立一致性检验模型.结果 隔铝塑扫描和直接接触使用不同的预处理方法建立了两个一致性模型,均能很好地判定结果.结论 所建立的一致性模型能准确地对三磷酸腺苷二钠片进行初筛检验.     

Effects of adenosine and adenosine analogues on mean circulatory filling pressure and cardiac output in anesthetized rats

The effects of adenosine and adenosine analogues, 2-[p-(2-[carboxyethyl) phenethylamino]-5’-N-ethylcarboxamidoadenosine (CGS 21680) and N⁶-2-(4-aminophenyl)-ethyladenosine (APNEA), on mean arterial pressure, cardiac output, mean circulatory filling pressure, arterial resistance, venous resistance and heart rate in untreated or treated (with ganglion-blockers mecamylamine and atropine) pentobarbital-anesthetized rats were examined. Infusion of adenosine (100, 300 and 900 μg/kg/min), CGS 21680 (0.1, 0.3 and 0.9 μg/kg/ min) or APNEA (1.0, 3.0 and 9.0 μg/kg/min) reduced mean arterial pressure and arterial resistance in all groups. Adenosine and APNEA also reduced mean circulatory filling pressure, venous resistance and heart rate in untreated animals. Furthermore, APNEA but not adenosine reduced cardiac output. In contrast, CGS 21680 increased cardiac output and heart rate but did not have any effect on mean circulatory filling pressure or venous resistance. In ganglion-blocked rats, APNEA reduced cardiac output, mean circulatory filling pressure and heart rate, while adenosine did not have any effect on these parameters. In addition, APNEA and adenosine reduced arterial resistance but were unable to alter venous resistance while CGS 21680 reduced mean circulatory filling pressure and arterial resistance but did not further affect cardiac output, heart rate and venous resistance in ganglion-blocked animals. The results of the present study suggest that adenosine and APNEA dilate arterioles and vein, whereas CGS 21680 causes arterial dilatation but not venodilatation in untreated animals due to hypotension-induced sympathetic activation. A possible explanation for the present observations could be differences in the distribution of vascular A₂ versus A₃ adenosine receptors in the venous circulation. Reza Tabrizchi Received: 17 September 1996 / Accepted: 27 March 1997     

Urotensin-II: a novel systemic hypertensive factor in the cat

Urotensin-II, a potent mammalian vasoconstrictor, may play a role in the etiology of essential hypertension. However, a species suitable for assessing such a role, one where a classical systemic hypertensive response (increase in mean blood pressure and systemic vascular resistance) is observed following bolus i.v. urotensin-II administration, has yet to be identified. The present study demonstrates that the cat may represent such a species since urotensin-II potently (pEC₅₀s 9.68±0.24–8.73±0.08) and efficaciously (E_max 73±15%–205±21% KCl) constricts all feline isolated arteries studied (aortae, renal, femoral, carotid, and mesenteric conduit/resistance). Accordingly, exogenous urotensin-II (1 nmol/kg, i.v.) effectively doubles both mean blood pressure (from 99±14 to 183±15 mmHg) and systemic vascular resistance (from 0.36±0.12 to 0.86±0.20 mmHg/ml/min) in the anaesthetized cat (without altering heart rate or stroke volume). Thus, in view of these profound contractile effects, the cat could be suitable for determining the effects of urotensin-II receptor antagonism on cardiovascular homeostasis in both normal and diseased states.     

Release of radioactive purines from cat nictitating membrane labeled with 3H-adenine

Cat nictitating membranes were incubated with 1-2 x 10(-7) M 3H-adenine or 3H-adenosine for 1 h. A tissuebath ratio of about 15 was found for both compounds in intact and denervated membranes. In intact nictitating membranes sympathetic nerve stimulation (4 Hz, 5 min) caused a net release of purines (0.66 +/- 17% of the tissue content), which was reduced by alpha-blockade. Noradrenaline (1-3 microM) or tyramine 60 microM), which produced the same contractile response as did nerve stimulation, increased purine release to the same extent as did nerve stimulation. The effect of either agent was reduced or abolished by phentolamine. Purine release could also be induced by acetylcholine and ATP. This release was not altered after surgical denervation. There was an excellent correlation between the contractile response and the purine release induced by nerve stimulation, noradrenaline, tyramine and acetylcholine. However, ATP caused a larger release of 3H-purines than expected from the contractile responses, possibly indicating displacement. The results indicate that most if not all of the 3H-purines released by nerve stimulation in the cat nictitating membrane are derived from postjunctional elements.     

Establishment of an abnormal vascular patterning model in the mouse retina

Abnormalities in retinal blood vessels and neuronal function persist in eyes undergoing retinopathy of prematurity. In this study, we examined morphological and functional changes in retinal blood vessels and neurons in mice that had undergone short-term interruption of retinal vascular development through inhibition of vascular endothelial growth factor (VEGF) signaling. In mice treated with the VEGF receptor tyrosine kinase inhibitor KRN633 on postnatal day (P) 0 and 1, the vascular density in the retinal surface increased by P12, but development of deep retinal vascular plexus and choroidal vasculature was delayed until P14. Overall retinal morphology was mostly normal in KRN633-treated mice during the observation period (～P28), with the exception of P8 and P14. On P28, abnormalities in retinal vascular patterns were evident, but electroretinogram and retinal blood perfusion were within the normal range. Abnormal architecture of retinal vasculature disturbs retinal hemodynamics; therefore, mice treated postnatally with VEGF receptor inhibitors could serve as an animal model for studying the regulatory mechanism of local retinal blood flow and the effect of persistent abnormal retinal vascular patterns on the risk of onset of retinal ischemia.