Heart Rate Variability in Isolated Rabbit Hearts

The presence of heart rate variability (HRV) in patients with cardiac denervation after heart transplantation raised our interest in HRV of isolated, denervated hearts. Hearts from seven adult white ELCO rabbits were transferred to a perfusion apparatus. All hearts were perfused in the working mode and in the Langendorff mode for 20 minutes each. HRV was analyzed in the frequency domain. A computer simulated test ECG at a constant rate of 2 Hz was used for error estimation of the system. In the isolated, denervated heart, HRV was of random, broadband fluctuations, different from the well-characterized oscillations at specific frequencies in intact animals. Mean NN was 423 ± 51 ms in the Langendorff mode, 406 ± 33 ms in the working heart mode, and 500 ms in the test ECG. Total power was 663 ± 207 ms², 817 ± 318 ms², and 3.7 ms², respectively. There was no significant difference in any measure of HRV between Langendorff and working heart modes. The data provide evidence for the presence of HRV in isolated, denervated rabbit hearts. Left atrial and ventricular filling, i.e., the working heart mode, did not alter HRV, indicating that left atrial or ventricular stretch did not influence the sinus nodal discharge rate.     

Nisoldipine Cardioplegia in the Isolated Rabbit Heart

BACKGROUND: The metabolic and hemodynamic effects of nisoldipine supplementation in cardioplegia after ischemic injury were investigated in 13 isolated rabbit hearts. Group 1 consisted of 6 hearts, which received St. Thomas II cardioplegic solution. In group 2, nisoldipine was added to the cardioplegic solution at a concentration of 0.1 mg/kg in 7 hearts. METHODS: The explanted hearts were suspended from Langendorff apparatus and were perfused with Krebs-Henseleit solution. Left ventricular pressure, heart rate, malondialdehyde, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidized glutathione, creatine kinase MB, (CK-MB), aspartate transaminase, and lactate dehydrogenase (LDH) were measured before and after 60 minutes of ischemia. Peak generated pressure after ischemia was significantly higher in group 2 versus group 1 while end-diastolic pressure was significantly lower in group 2 after ischemic arrest (P <.05). RESULTS: Malondialdehyde levels were lower in group 2 (P <.05). Glutathione peroxidase and glutathione reductase levels were significantly higher in group 2 (P <.05). The only enzymatic significant difference was observed between the preischemic and postischemic levels of aspartate transaminase in group 2 (P <.05). CONCLUSIONS: These findings show beneficial effects of nisoldipine cardioplegia, although its use as a cardioplegic additive is not yet possible. We believe, however, the effects of oral nisoldipine before cardiac surgery can be studied in a clinical setting.     

急性梗阻性化脓性胆管炎肝细胞钙变化与肝细胞损害关系的实验研究

目的：探讨急性梗阻性化脓性胆管炎肝细胞钙变化及与肝细胞损害的关系。方法：采用肖氏兔化脓性胆管炎模型进行研究,对照组28只,实验组39只。各组再按术后处死时间3天、7天、14天、20天时相分组,动态观察各组肝细胞VonKossa钙染色情况及HE染色肝细胞病理改变。结果：实验组3天出现肝细胞钙增加并呈持续增加趋势,与对照组比较有差异。肝细胞病理损害呈动态加重表现。结论：兔急性梗阻性化脓性胆管炎病程中肝细胞钙存在进行性增加且肝细胞损害与肝细胞钙增加有密切关系。     

~(99)Tc~m-DTPA肾动态显像在梗阻性肾病中的应用

目的探讨99Tcm-二乙三氨五醋酸(DTPA)核素肾动态显像在梗阻性肾病中的临床价值。方法92例临床相关学科已确诊或拟诊的梗阻性肾病患者,需进一步了解双肾各自肾功能及患肾功能受损程度,术前均行核素肾动态显像和X线静脉肾盂造影(IVP)。结果受检者92例(肾脏数184只),单侧患肾92例,双侧患肾22例。除外48只正常肾脏,各种病因的136只患肾中,以结石为最多,占74.3%(101/136)。各患肾的肾功能情况为:功能正常38只(27.9%)、轻度受损32只(23.5%)、中度受损19只(14%)、重度受损25只(18.3%)、无功能肾22只(16.2%)。结论99Tcm-DTPA肾动态显像可灵敏判断肾实质功能,同时是了解总肾功能和分肾功能的无创性影像手段,为手术治疗提供重要依据。     

Obstructive Sleep Apnea and Diabetic Nephropathy: A cohort study

OBJECTIVE

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD). Obstructive sleep apnea (OSA) is common in type 2 diabetes and increases oxidative stress. Hence, OSA could promote the development and progression of DN.

RESEARCH DESIGN AND METHODS

This was a cohort study in adults with type 2 diabetes. Patients with known OSA or ESRD were excluded. DN was defined as the presence of albuminuria or an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m². DN progression was based on eGFR measurements. OSA was defined as apnea hypopnea index (AHI) ≥5 events/h. Serum nitrotyrosine abundance (a marker of nitrosative stress) was measured by ELISA.

RESULTS

A total of 224 patients were included. OSA and DN prevalence was 64.3 and 40.2, respectively. DN prevalence was higher in patients with OSA (OSA⁺) compared with those without OSA (OSA⁻) (49.3% vs. 23.8%, P < 0.001). After adjustment, OSA (odds ratio 2.64 [95% CI 1.13–6.16], P = 0.02) remained independently associated with DN. After an average follow-up of 2.5 (0.7) years, eGFR decline was greater in OSA⁺ compared with OSA⁻ patients (median −6.8% [interquartile range −16.1 to 2.2] vs. −1.6% [−7.7 to 5.3%], P = 0.002). After adjusting, both baseline OSA (B = −3.8, P = 0.044) and AHI (B = −4.6, P = 0.02) remained independent predictors of study-end eGFR. Baseline serum nitrotyrosine abundance (B = −0.24, P = 0.015) was an independent predictor of study-end eGFR after adjustment.

CONCLUSIONS

OSA is independently associated with DN in type 2 diabetes. eGFR declined faster in patients with OSA. Nitrosative stress may provide a pathogenetic link between OSA and DN. Interventional studies assessing the impact of OSA treatment on DN are needed.Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD) in many countries (1) and has significant impact on patients and health care systems (2). DN progresses slowly, starting with microalbuminuria, which progresses into overt proteinuria in 20–40% of patients, and 20% of patients will have progressed to ESRD within 20 years after onset of overt proteinuria (1). The speed of DN progression is variable and largely dependent on blood pressure (BP), obesity, metabolic control, and other factors such as male sex and ethnicity (3,4).The pathogenesis of DN is thought to be similar to other microvascular complications in which hyperglycemia and hypertension are thought to be fundamental to its development, as they promote increased oxidative and nitrosative stress (3). In addition, hemodynamic changes occur as a result of the activation of the renin-angiotensin-aldosterone (RAAS) and endothelin systems, resulting in increased systemic and intraglomerular pressure, causing hyperfiltration and albuminuria (3). Despite attempts to improve metabolic control and RAAS inhibition, DN remains very common, and many patients develop ESRD requiring renal replacement therapy. Hence, better understanding of the pathogenesis of DN is needed in order to develop more effective treatments.Several reports, including our own, have shown a high prevalence of obstructive sleep apnea (OSA) in patients with type 2 diabetes (5,6). Patients with OSA and type 2 diabetes are at increased risk of diabetic peripheral neuropathy (6). Furthermore, OSA is associated with increased oxidative and nitrosative stress as well as impaired microvascular regulation in patients with type 2 diabetes (6). Hence, it is plausible that OSA complicating type 2 diabetes could facilitate the development and progression of microvascular complications including DN.The primary aims of this study were to assess the relationship between OSA and DN and to assess the impact of OSA on the estimated glomerular filtration (eGFR) decline in patients with type 2 diabetes. Secondary aims were to assess the impact of OSA on the development of albuminuria and to explore the mechanisms by which OSA and DN could be linked.     

Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle

BACKGROUND: Lysophospholipids such as lysophosphatidylcholine (LPC) have many direct electrophysiological effects on cardiac muscle and have been implicated as a cause of lethal ventricular arrhythmias during acute myocardial ischemia. Because extracellular K(+) accumulation is also a key arrhythmogenic factor during acute ischemia, we examined the effects of LPC on cellular K(+) balance, including its interaction with adenosine triphosphate-sensitive K(+) (K(ATP)) channels. METHODS AND RESULTS: Isolated rabbit interventricular septa paced at 75 beats/min were loaded with (42)K(+) to measure unidirectional K(+) efflux rate (in (42)K(+) washout experiments) or tissue K(+) content ((42)K(+) uptake experiments) and action potential duration (APD) during exposure to 20 μM LPC for 30 minutes. LPC caused tissue K(+) content to decrease by 15 +/- 2% (n = 4) at a steady rate over 30 minutes, associated with gradual APD shortening and a delayed increase in unidirectional K(+) efflux rate. Pretreatment with 12 μM cromakalim to selectively activate K(ATP) channels shortened APD by 44 +/- 66% and had no effect on net tissue K(+) content during control aerobic perfusion. However, cromakalim increased net K(+) loss during exposure to LPC to 22 +/- 4%, a 47% increase. CONCLUSIONS: LPC induced net K(+) loss in heart, which was potentiated by the K(ATP) channel agonist cromakalim. This ATP finding suggests that if LPC accumulates to similar levels during myocardial ischemia and hypoxia, it may be an important mechanism in net K(+) loss.     

Delta Opiates Increase Ischemic Tolerance in Isolated Rabbit Jejunum

Mammalian hibernation is mediated by humoral agonists of the delta opioid receptor (DOR). Moreover, transfer of either humoral or synthetic DOR agonists to non-hibernators reportedly induces a state of improved myocardial ischemic tolerance. OBJECTIVE: To determine whether the DOR agonist D-Ala 2, D-Leu 5, enkephalin (DADLE) similarly elicits protection in noncardiac-i.e., mesenteric-tissue. METHODS: In Protocols 1 and 2, the authors developed and characterized an in vitro model of mesenteric ischemia/reperfusion in isolated rabbit jejunum by documenting the effect of increasing ischemic duration (0 to 120 minutes) and the relative importance of glucose and/or oxygen deprivation on the evolution of jejunal injury. In Protocol 3, jejunal segments were randomized to receive either no treatment (controls) or 15 minutes of pretreatment with 1 microM DADLE, followed by 60 minutes of simulated ischemia and 30 minutes of reperfusion. Jejunal injury was quantified by repeated, time-matched assessment of peak contractile force evoked by 1 microM acetylcholine (all protocols) and delineation of tissue necrosis (Protocol 1). RESULTS: Development of significant jejunal injury required combined oxygen/glucose deprivation. Moreover, there was a direct relationship between ischemic duration and tissue injury, and a significant inverse correlation between reperfusion contractile force (% of baseline) and the extent of smooth muscle necrosis (r(2) = 0.87; p < 0.01). Most notably, mesenteric ischemia/reperfusion injury was attenuated by DADLE: reperfusion contractile force was 47 +/- 5% versus 36 +/- 5% in DADLE-treated versus control segments (p < 0.01). CONCLUSIONS: Treatment with the delta opioid agonist DADLE increases ischemic tolerance of isolated rabbit jejunum.     

Bile Acid Synthesis in the Isolated, Perfused Rabbit Liver

These experiments were carried out to demonstrate the usefulness of the perfused rabbit liver for studies of bile acid metabolism, and to determine the rate-limiting enzyme of bile acid synthesis. Rabbits were fed a semisynthetic diet, with or without the addition of 1% cholestyramine, under controlled conditions. At the end of 2-5 wk, the livers were removed and perfused for 2.5 hr employing various (14)C-labeled precursors to measure de novo cholic acid synthesis. The livers were then analyzed for cholesterol, and the bile collected during the perfusion was analyzed for cholesterol and bile acids. Control bile contained, on the average, 0.34 mg of glycocholate, 7.4 mg of glycodeoxycholate, and 0.06 mg of cholesterol. After cholestyramine treatment of the donor rabbits, the bile contained 3.3 mg of glycocholate, 3.7 mg of glycodeoxycholate, and 0.05 mg of cholesterol. It was assumed that in cholestyramine-treated animals the enterohepatic circulation of the bile acids had been interrupted sufficiently to release the feedback inhibition of the rate-controlling enzyme of bile acid synthesis. Therefore, a given precursor should be incorporated into bile acids at a more rapid rate in livers of cholestyramine-treated animals, provided that the precursor was acted upon by the rate-controlling enzyme. It was found that the incorporation of acetate-(14)C, mevalonolactone-(14)C, and cholesterol-(14)C into cholate was 5-20 times greater in the livers of cholestyramine-treated animals than in the controls. In contrast, there was no difference in the incorporation of 7alpha-hydroxycholesterol-(14)C into cholate regardless of dietary pretreatment. It was concluded that given an adequate precursor pool, the 7alpha-hydroxylation of cholesterol is the rate-limiting step in bile acid formation.     

Adrenergic-dependent Effect of Adenosine-induced Ventricular Fibrillation in the Isolated Rabbit Heart

BACKGROUND: The present study examined the contributory role of endogenous catecholamines in adenosine-induced ventricular fibrillation in isolation rabbit hearts. METHODS AND RESULTS: Cardiac catecholamine depletion was induced in eleven rabbits by the administration of 6-hydroxydopamine (2 x 30 mg/kg, every 12 hours intramuscularly). Hearts were removed 24 hours later, and subjected to 12 minutes of hypoxic perfusion followed by 40 minutes of reoxygenation while heart rate was maintained with atrial pacing. One of six, and one of five hearts from 6-hydroxydopamine treated rabbits developed ventricular fibrillation during hypoxia-reoxygenation when exposed to 3,7-dimethyl-1-propargylzanthine (DMPX) (10 μM) + adenosine (ADO) (1 μM) and DMPX (10 μM) + ADO (10 μM), respectively. In hearts from a control group, not exposed to 6-hydroxydopamine, ventricular fibrillation developed in each of five (100% incidence) hearts when perfused in the presence of DMPX (10 μM) + ADO (10 μM) (P <.05). Nadolol (1 μM), a beta-adrenoceptor DMPX (10 μM) + ADO (10 μM) treated hearts (n = 6, P <.05 vs DMPX + ADO treated hearts). To ensure catecholamine depletion, spontaneously beating isolated hearts from vehicle and 6-hydroxydopamine treated rabbits were perfused under normoxic conditions while exposed to increasing concentrations of tyramine (1, 3, 10 mM) and the change in heart rate was determined. A concentration-related, positive chronotorpic response to tyramine was obtained in hearts from the vehicle treated group that was absent in hearts from 6-hydroxy-dopamine treated rabbits or hearts perfused in the presence of nadolol. CONCLUSIONS: The results demonstrate that inhibition of the cardiac adenosine A(2) receptor, unmasks an adenosine A(1) receptor profibrillatory effect that is dependent upon endogenous cardiac catecholamines and beta-adrenoreceptor activation during myocardial hypoxia-reoxygenation.     

经胸超声心动图对3种兔心力衰竭模型的检测

目的应用经胸超声心动图评价兔3种不同类型心力衰竭模型的效果。方法24只兔随机分成3组,A组急性心肌梗死组,结扎冠状动脉左前降支致前间壁心肌梗死;B组扩张型心肌病组,阿霉素经耳缘静脉给药复制扩心病模型;C组慢性压力后负荷心肌肥厚组,主动脉缩窄法制作心肌肥厚致心力衰竭模型。术后不同时间行心脏超声检查评价造模效果。结果经胸超声可获取兔心脏清晰图像。A组造模成功表现为节段性室壁运动异常和射血分数(EF)减低。B组左心扩大,心功能显著下降,并可出现心包积液。C组先出现心肌肥厚,EF增高,终末期心腔扩大,EF下降。结论应用超声心动图技术活体检测兔心力衰竭模型效果可行。     

自制心脏保存液保存离体兔心的研究

目的：初步探讨自制心脏保存液对离体兔心的保存效果。方法：取18只新西兰白兔，随机成分3组，建立非循环式Langendorff灌注模型，分别用晶体停搏液、uⅣ液和我院自制的心脏保存液在低温下保存4h；复灌后检测左心室压力、心肌酶学指标及心肌含水量。结果：自制心脏保存液组左心室压力、心肌酶学指标及心肌含水量与晶体停搏液组有显著差异，与UW液组无显著差异。结论：实验证实我院自制的心脏保存液与uⅣ液心肌保护效果相近，其配方设计基本可行。     

"Preconditioning at a Distance" in the Isolated Rabbit Heart

OBJECTIVE: Brief myocardial ischemia evokes a cardioprotective response, referred to as "ischemic preconditioning" (IP), that limits injury caused by a subsequent prolonged ischemic insult. The myocardial IP effect can be induced by ischemia of "distant" cardiac and noncardiac tissue, implicating the involvement of an as-yet-unidentified humoral trigger. If a preconditioning hormone exists, the authors hypothesize that the IP effect should be transferable, via administration of coronary effluent, from a preconditioned donor heart to a virgin non-preconditioned acceptor heart. METHODS: Isolated buffer-perfused rabbit hearts were assigned to one of four treatment groups in a donor/acceptor sequence. Donor hearts underwent either three IP cycles or a matched period of uninterrupted perfusion (control donors). Coronary perfusate collected from IP and control donor hearts was reoxygenated and transfused to virgin acceptor hearts. All hearts then underwent 30 minutes of global ischemia followed by 30 minutes of reperfusion. Left ventricular developed pressure (LVDP) (the authors' index of cardioprotection) was monitored throughout the protocol by a left ventricular (LV) balloon. RESULTS: In donor controls, LVDP assessed at 30 minutes post-reflow was restored to only 49 +/- 5% of baseline values. Recovery of LV function was significantly enhanced in both IP donor hearts (69 +/- 4%*) and IP acceptor hearts (70 +/- 6%*) vs donor controls (*p < 0.05), while, in acceptor controls, intermediate values of LVDP (62 +/- 7%) were obtained. CONCLUSION: The IP effect can be transferred between rabbit hearts, suggesting the presence of a humoral trigger signal for distant preconditioning. Isolating this hormone may have therapeutic and diagnostic implications in the management of acute myocardial ischemia.     

PAX2基因在梗阻性肾病大鼠肾小管上皮细胞重新表达的意义

【目的】探讨PAX2基因在梗阻性肾病大鼠肾小管上皮细胞的重新表达对肾间质纤维化的意义。【方法】80只大鼠随机分为：假手术组（sham组）和模型组（UUO组）各40只。于术后3d、5d、7d、14d（每组10只）处死取肾组织。光镜观察肾脏病理形态改变,免疫组化、Westernblot及realtimePCR检测肾组织PAX2蛋白和mRNA的表达。【结果】①HE和Masson染色观察到UUO组肾间质呈现明显的纤维化。②免疫组化发现sham组肾小管上皮细胞无PAX2表达;UUO组肾小管上皮细胞表达较多;③Westernblot显示PAX2蛋白水平在UU0组术后3d相比sham组明显的增加（P〈0．05）,随着梗阻时间延长PAX2蛋白表达更加明显;④realtimePCR显示,PAX2mRNA与PAX2蛋白的,矗达趋势相同。⑤相关分析：PAX2蛋白水平与肾小管损伤程度呈正相关（r=0．991,P〈0．05）,与肾间质纤维化程度呈正相关（r=0．985,P〈0．05）。【结论】胚胎发育基因PAX2在梗阻性肾病大鼠肾小管存在重新表达;并参与了梗阻性肾病肾小管损伤和肾间质纤维化的过程。     

Functional Profile of the Isolated Uremic Nephron: EVIDENCE OF PROXIMAL TUBULAR “MEMORY” IN EXPERIMENTAL RENAL DISEASE

In experimental models of glomerular and nonglomerular renal disease, single nephron filtration rate and proximal tubular reabsorption of fluid decrease or increase in parallel in the same nephron. To assess whether intrinsic adaptations in proximal tubular function, i.e., changes that are independent of the peritubular or humoral milieu, contribute to this phenomenon, segments of rabbit late superficial proximal convoluted tubules (PCT) were studied by in vitro perfusion. PCT were obtained from normal kidneys, from remnant kidneys, and from kidneys embolized with microspheres. Single nephron filtration rates are increased in the remnant and decreased in the embolized kidneys. Whereas the embolized-kidney rabbits were nonazotemic (the contralateral kidney was left in situ), the remnant-kidney animals were uremic. In order to study a nonazotemic model of increased single nephron filtration rate, PCT were also obtained from uninephrectomized rabbits.     

兔急性肺栓塞面积与血流动力学的相关性研究

[目的]制备不同梗阻面积的兔急性肺栓塞模型,探讨肺栓塞面积与血流动力学变化的相关性。[方法]通过介入方法经导管注入自体血栓选择性栓塞肺动脉,建立不同栓塞面积的兔急性肺栓塞模型;比较栓前、栓后15min,30min,1h,2h血流动力学指标变化,同时观察心脏超声影像学变化。[结果]自体血栓均按要求阻塞相应肺动脉,肺栓塞形成后心输出量下降,肺动脉压力显著增高,并在1h,2h达到峰值,各血流动力学指标随肺栓塞面积增大而变化更显著。[结论]此急性肺栓塞动物模型制作方法确切可行,具有可重复性。肺栓塞导致血流动力学及左右心室功能紊乱,栓塞面积与其损害程度呈正相关,并严重影响预后。     

超声引导下经皮射频治疗兔肾VX2瘤模型的声像图变化的动态观察

目的超声引导下经皮射频治疗兔肾VX2肿瘤模型,动态观察其声像图变化特征。方法对25只已建立VX2肾肿瘤模型的大白兔行超声引导下射频治疗,并于治疗后定期行超声检查,二维超声观察肿瘤大小和形态,彩色多普勒血流显像(CDFI)观察肿瘤内部及周边血流。结果超声成功引导所有兔肾VX2肿瘤射频治疗,治疗即刻二维声像图呈现斑片状强回声伴声影,CDFI显示毁损灶无血流信号,治疗后毁损区呈边界清楚的强回声;在肿瘤部分区域发现低回声,CDFI显示点条状血流信号,病理证实为肿瘤残存或复发。结论二维及彩色多普勒超声在兔肾VX2肿瘤射频的引导和治疗中具有特征性声像图表现,对于评价射频疗效具有重要的应用价值。     

庆大霉素影响胆红素结石形成的实验研究

本实验动态观察了庆大霉素对胆红素结石兔模型的氧自由基、前列膜素Ｅ２及胆红素结石等的影响。发现肝细胞部分氧自由基与前裂腺素Ｅ２、胆红素结石成石程度等指标在治疗组均低于非治疗组，且其动态变化相信，并呈正相关关系。提示庆大霉素可能通过其抗菌作用减少了白细胞产生氧自由基，致前列腺素Ｆ２生成减少，降低了粘（糖）蛋白的分泌，最终导致了胆红素结石生成减少。     

兔膀胱VX2肿瘤不同建模方法的超声观测

目的比较不同种植方法兔VX2膀胱肿瘤模型的生长特点,评价超声观测肿瘤生长的价值。 方法24只新西兰大白兔随机分为两组,第一组12只按瘤块包埋法制作膀胱肿瘤模型（对照组）。第二组12只采用膀胱黏膜下生理盐水充盈法进行瘤块包埋制作肿瘤模型（实验组）。于种植后第2、4周左右分别行超声检查,比较不同植瘤方式肿瘤的生长特点,超声检测肿瘤生长并与病理检查进行对照分析。 结果两组植瘤成功率均为100%。对照组第2周肿瘤结节最大直径为（1.46±0.48）cm,实验组为（0.72±0.17）cm,两组差异具有非常显著性意义（P〈0.001）;第4周对照组肿瘤结节为（2.59±0.50）cm,实验组为（2.25±0.57）cm,两组差异无显著性意义（P〉0.05）。肿瘤表现为等低回声及略高回声结节,以等低回声居多,向膀胱腔内突入,附着于膀胱壁不随体位移动。彩色多普勒和能量多普勒均可检出血流信号。频谱多普勒显示肿瘤的血供主要为动脉血流。 结论实验组肿瘤的发展过程略慢于对照组,实验组膀胱肿瘤动物模型可以更好地反映肿瘤的发生与发展过程;超声能有效检测肿瘤生长。     

Effect of Hypersensitivity on Protein Uptake Across the Air-Blood Barrier of Isolated Rabbit Lungs

In previous studies with isolated perfused rabbit lungs, we observed that human serum albumin (HSA) and ovalbumin, introduced into the isolated lungs as an aerosol, entered the pulmonary circulation antigenically intact. The "inhaled" proteins were also broken down in the lung. When lungs from animals immunized with one protein inhaled the two proteins simultaneously, absorption of intact antigen was specifically reduced, and there was a nonspecific increase in the appearance of metabolites of both proteins in the blood.In the present study, we investigated the antigen-specific and nonspecific effects of two types of hypersensitivity responses on protein absorption across the air-blood barrier of isolated rabbit lungs. In one group of lungs, an acute hypersensitivity response was induced by introducing HSA into the blood perfusing lungs from HSA-immunized rabbits. In another, the rabbits had been previously exposed to chronic HSA aerosol until their lungs exhibited a chronic immunologic inflammatory response. Lungs from both groups were insufflated simultaneously with HSA, and a nonspecific protein, ovalbumin. Lungs in which the acute anaphylactic response was induced showed no alteration in the absorption of either intact protein compared with HSA-immunized controls, but absorbed a somewhat larger quantity of breakdown products of the specific antigen. Lungs undergoing the chronic alveolar inflammation were more permeable to nonspecific protein than were noninflamed lungs. Despite the increased permeability to nonspecific protein, the absorption of antigen was blocked as effectively as in immune but noninflamed controls. In these chronically inflamed lungs, the absorption of antigen breakdown products was enhanced. The results indicate that both immunologic and inflammatory mechanisms may control the amounts of inhaled soluble proteins that reach the blood via the alveolocapillary barrier. Alterations in the absorption of inhaled proteins and their metabolites across the air-blood barrier during certain types of hypersensitivity responses may be of immunologic and pathologic significance.     

颈动脉狭窄兔模型的DSA与CTA评价

目的：探讨粥样硬化性颈动脉狭窄兔模型的DSA及CTA应用价值。材料与方法：通过植入硅橡胶圈于兔颈动脉外膜加胆固醇饲料喂养的40只颈动脉狭窄模型兔,经股动脉插管方法行DSA及CTA检查,观察模型兔颈动脉狭窄程度及影像学征像。结果：DSA技术及CTA的多平面重建（MPR）、曲面重建（CPR）、最大密度投影（M IP）和三维容积漫游（VRT）等技术均可显示兔模型的颈动脉管腔狭窄的部位、形态、范围、程度及颈动脉的血管走向。结论：DSA与CTA均能较好的反应模型兔的颈动脉狭窄部位、形态,DSA能动态观察其血液动力学的变化;CTA既可观察其形态学改变,同时也可观察血管外组织结构。