血液稀释疗法和维拉帕米对兔缺血再灌注心肌的保护作用

心肌缺血45min，再灌注180min复制兔急性心肌缺血再灌注模型。分别观察了等容血液稀释、维拉帕米以及二者联合应用对兔缺血再灌注心肌MDA含量、SOD活性及心功能的影响。实验并分四组：Ⅰ组（对照组）；Ⅱ组（稀释组）；Ⅲ组（维拉帕米组）；Ⅳ组（稀释＋维拉帕米组）。结果：①心肌组织MDA含量及SOD活性变化：与Ⅰ组缺血区心肌MDA含量相比，Ⅱ、Ⅲ、Ⅳ组均显著降低,Ⅳ组又明显低于Ⅱ、Ⅲ组；Ⅱ、Ⅲ、Ⅳ组缺血区心肌SOD活性均明显高于Ⅰ组（均P＜0．05）。②心功能变化：再灌注后，Ⅰ组心功能进行性恶化，Ⅱ组左室收缩功能（LVSP，＋dp／dt－max）和舒张功能（-dp／dt－max）有明显改善，Ⅲ组舒张功能明显改善，Ⅳ组各项心功能指标进一步好于Ⅱ、Ⅲ组（均P＜0．05）。提示：等容血液稀释和维拉帕米均能保护缺血再灌注心肌的代谢和功能，二者合用效果更加明显．表现出良好的协同效应。     

兔急性肾衰竭致心肌、胰腺损伤与中性粒细胞扣押

目的观察急性肾功能衰竭（ARF）家兔肾、心肌、胰腺髓过氧化物酶（MPO）活性的变化,探讨中性粒细胞（PMN）扣押在兔ARF致心肌、胰腺损伤的作用机制。方法42只家兔均分为对照组、HgCl2组、甘油组。其中HgCl2组以皮下注射1％HgCl2（1．3ml／kg．bw）、甘油组以肌肉注射50％甘油（10ml／kg．bw）分别复制ARF模型,均分为12、24、48h三个亚组。在不同时间点,所有动物颈总动脉插管放血,测定反映肾功能的生化指标;并制备肾、心肌、胰腺组织匀浆,检测MPO的活性。结果两个ARF模型组的血清BUN、Cre水平均显著高于对照组。两个ARF模型组的肾、心肌、胰腺组织匀浆的MPO活性在多个时间点显著高于对照组。HgCl2组BUN、Cre分别与肾、心肌、胰腺组织匀浆的MPO活性正相关;甘油组BUN、Cre分别与肾、胰腺组织匀浆的MPO活性正相关。结论PMN扣押在ARF发病学中具有重要作用,且是ARF致心肌、胰腺损伤的机制之一。     

Morphologic Alterations in Sheep After Implantation of the Akutsu Total Artificial Heart

The present report describes morphologic alterations produced in sheep after implantation of a four-chambered total artificial heart. Two groups of sheep were studied. The first group was given no special antishock therapy and had an average survival time of 25.8 hours. Major morphologic changes produced in the first group were focal infarction and massive hemorrhage of the large and small bowel, ascites, severely altered lungs and multiple infarcts in the kidneys. The second group of sheep was given antishock therapy and showed an average survival time of 35.4 hours. Severe morphologic alterations in this group were generally absent in all organs except the lungs, which showed varying degrees of congestion, hemorrhage, edema, pneumonitis and atelectasis. Death in both of the above groups was due to development of irreversible hypotension and respiratory failure.     

静脉应用bFGF对兔缺血心肌血管新生的影响

目的探讨静脉给予碱性成纤维细胞生长因子 (bFGF)对兔缺血心肌血管新生的影响。方法开胸结扎兔的冠状动脉左前降支 (LAD) ,制成急性心肌梗塞模型 ,动物被随机分为两组 :一为bFGF组 ,连续2周静脉内给予bFGF(100ug/kg) ;一为对照组 ,连续2周静脉内给予生理盐水2ml。12周时 ,处死动物 ,通过组织学观察两组兔子缺血心肌的血管新生情况。结果bFGF组缺血心肌处的血管密度与对照组比较差异无显著性 (P>0.05)。结论静脉内连续2周给予bFGF(100ug/kg)无明显促进缺血心肌血管新生的作用。     

Multidisciplinary Approach to the Treatment of Metabolic and Morphologic Alterations of HIV-Related Lipodystrophy

Abstract

Background: Treatment for metabolic and morphologic alterations in HIV-related lipodystrophy include medical therapy, physical exercise, and surgical interventions. Method: We assessed the efficacy and safety of a comprehensive multidisciplinary approach for treating morphological and metabolic alterations of the lipodystrophy syndrome in consecutive patients attending the Metabolic Clinic (MC) of the University of Modena and Reggio Emilia who had at least 2 evaluations over a 48-week period. 245 patients were evaluated: 143 (62.4%) were men, 74 (36.1%) presented with lipoatrophy, 10 (4.9%) with fat accumulation, 93 (45%) with mixed forms, 24 (11.3%) had hypercholesterolemia (LDL >160 mg/dL), 87 (38%) had hypertriglyceridemia (TG >150 mg/dL), 13 (5.7%) had diabetes (glucose >126 mg/dL), and 78 (44%) had insulin resistance (HOMA-IR >4). Results: At follow-up, a significant improvement was observed in both objective and subjective variables. Anthropometric improvement was observed in waist to hip ratio, waist circumference, and right and left cheek dermal thickness measurements. A nonsignificant improvement was observed in fat and lean regional mass by DEXA; CT showed improvement in visceral and subcutaneous adipose tissue. Glucose, HOMA-IR, total cholesterol, and APO B improved. Subjective variables improved in aesthetic satisfaction. Conclusion: We conclude that the medical and surgical interventions proposed in this multidisciplinary therapeutic approach are efficacious and safe in the management of lipodystrophy.     

rhbFGF基因及其蛋白促兔缺血心肌血管新生的对比研究

目的 探讨通过心肌内注射重组人碱性成纤维细胞生长因子(rhbFGF)基因及其蛋白促兔缺血心肌血管新生的“基因血管搭桥”的效果。方法 无菌条件下开胸结扎兔冠状动脉左前降支(LAD)，建立急性心肌梗死动物模型。将成功构建的真核表达质粒pcDNA3-bFGF、rhbFGF蛋白、生理盐水，直接四点注射人兔缺血心肌内。实验兔饲养6周、12周以后，通过病理切片光镜观察、图像分析对比研究三组间血管新生情况。结果 1)成功构建pcDNA3-bFGF真核表达质粒并制备rhbFGF蛋白；(2)pcDNA3-bFCF真核表达质粒在心肌中成功表达为rhbFGF蛋白；(3)血管新生的观察：通过对心肌内注射基因及其蛋白进行对比研究，发现心肌内注射蛋白和基因均有促兔缺血心肌血管新生的作用，而基因的促血管新生作用更强。结论 rhbFGF蛋白及基因心肌内注射均有促兔缺血心肌血管新生的作用，而基因的促血管新生效果显著。“基因治疗促血管新生”法是另一种有效的冠心病治疗方法，rhbFGF基因有重要的推广应用价值。     

Alterations in Responses to Bradykinin, Angiotensin I, and Angiotensin II During the Induction Phase of One-Kidney, One-Wrapped Hypertension and Associated Arterial Disease in Rabbits

During the induction phase of low-renin, one-kidney, one-wrapped hypertension in rabbits,serum angiotensin converting enzyme (ACE) activity is depressed and correlates inversely with the degree of necrotic arterial disease that develops. Responses to the vasoactive polypeptides, bradykinin (BK), angiotensin I (AI), angiotensin II (AII), the ACE blocker teprotide, and the AII antagonist 1-sar-8-ile AII were studied. Responses to BK, AII, and AI showed significant changes in both magnitude and duration (recovery time). Recovery time for depressor responses to BK in hypertensive rabbits was approximately three times that in the control period. One-wrapped, two-kidney control rabbits without hypertension-associated arterial disease showed no change in BK recovery time, although serum ACE activity was significantly depressed. In the experimental period BK recovery time correlated directly with the degree of arterial disease and indirectly with the final serum ACE activity. Duration of the pressor responses after AII correlated directly with the degree of arterial disease and indirectly with final serum ACE activity. In untreated hypertensive rabbits the percentage of increases in blood pressure after AI relative to control animals were decreased, and for all hypertensive rabbits' the increase in blood pressure correlated directly with the final serum ACE activity. Long-term treatment with teprotide moderated the hypertension but had little effect on serum ACE activity or the responses to BK, AII, and AI. Short-term infusions of 1-sar-8-ile AII and teprotide caused significant decreases in blood pressure in both the control and experimental periods, although no change in response to either polypeptide occurred. These studies support other evidence that pressor components of the renin-angiotensin system do not sustain the elevation of blood pressure in this form of experimental hypertension. Alterations in response patterns following AII and AI suggest that a vasodepressor system may be altered. In addition, part of the altered response to BK, and possibly AII, appears related to the development of the hypertension-associated arterial disease.     

Morphologic and clinical correlates in renal amyloidosis

Morphologic studies and clinical correlations were undertaken in 59 patients with renal amyloidosis. Spicularly arranged amyloid deposits in the glomerular capillary wall were found in all clinical groups but were more frequent and more extensive in primary amyloidosis and multiple myeloma. The severity of proteinuria correlated with the presence of spicules and podocyte destruction rather than with the amount of amyloid in the glomerulus. The spicules were associated with morphologic and clinical evidence of rapid amyloid deposition and a fulminant clinical course. The absence of spicules and the presence of extensive new basement membrane material may produce basement membrane thickening, lamination, and double capillary wall contours, which are associated with mild proteinuria and, rarely, resolution of amyloidosis. Nodular or mixed nodular-diffuse patterns of glomerular amyloid deposits were more frequent in patients with secondary amyloidosis and a longer clinical course. Renal failure generally corresponded to severe glomerular amyloidosis and tubular atrophy. However, a relatively precipitous, usually irreversible decrease in renal function frequently occurred in patients with renal amyloidosis and did not always have a morphologic explanation. The duration of life from the time of biopsy to death in patients with primary amyloidosis (nine months) was markedly shorter than in those with secondary amyloidosis (more than 50 months).     

Myocardium in acute and chronic experimental alcoholic intoxication

The myocardium of both heart ventricles in acute (AAP) and chronic (CAP) alcoholic poisoning was studied in 90 randombred rats. Functional-morphological changes typical of alcoholic cardiomyodystrophy were shown to develop in the heart in AAP and CAP. In AAP, alcoholic cardiomyodystrophy may lead to acute cardiac insufficiency and in CAP to progressive reduction of the contractile function of the heart and disturbances of conductivity in it. In AAP, however, the leading factor is the disturbance of bioenergetics as a result of toxic effect of ethanol and its metabolites on mitochondrial membranes under conditions of markedly disordered microcirculation. In CAP, along disordered microcirculation. In CAP, along with compensatory-adaptative processes in cardiomyocytes there increase the defects of the contractile apparatus, and diffuse fine-focal cardiosclerosis. This is the result of a long-term effect of ethanol and progressive hypoxia due to the affected vessels and disorders in lipid metabolism. Disorders in the function of sarcoplasmic reticulum may contribute to reduced contractile capacity of the heart.     

Morphologic diversity in malignant melanomas

A review was conducted of 335 malignant melanomas to identify variant morphologic patterns that might be confused with other tumors. In all, 27 predominantly amelanotic neoplasms with unusual histologic features were selected for additional study. These included nine with an adenoid or pseudopapillary pattern, seven small cell neoplasms, five with prominent myxoid stroma, four with a hemangiopericytoma-like appearance, and two composed of neoplastic cells with a signet-ring configuration. A diagnosis of melanoma was confirmed in all cases by Fontana-Masson strains for melanin pigment, electron microscopic examination, or the results of immunohistochemical analyses for cytokeratin, vimentin, S-100 protein, and the HMB-45 antigen. One tumor was associated with a congenital hairy melanocytic nevus, five were vulvovaginal lesions, four arose in the sinonasal tract, and one occurred in the rectum. Four of the specified microscopic patterns were observed in both primary and secondary neoplasms; the two signet-ring cell melanomas were recurrent lesions. The authors conclude that malignant melanomas may assume the histologic guise of adenocarcinomas, small cell carcinomas, and sarcomas, in a variety of tissue sites. Special studies designed to detect melanocytic differentiation are therefore appropriate in diverse differential diagnostic settings.