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Abnormal cardiac function in the streptozotocin-induced, non-insulin-dependent diabetic rat - Noninvasive assessment with Doppler echocardiography and contribution of the nitric oxide pathway

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第7期34卷 2111-2119页

作者： Joffe, II Travers, KE Perreault-Micale, CL Hampton, T Katz, SE Morgan, JP Douglas, PS Beth Israel Deaconess Med Ctr Div Cardiovasc Dept Med Harvard Thorndike Lab Boston MA 02215 USA Charles A Dana Res Inst Boston MA 02215 USA Harvard Univ Sch Med Boston MA USA

OBJECTIVES We sought to evaluate in vivo and in vitro left ventricular (LV) geometry and function in streptozotocin-induced diabetic rats and the possible role of the nitric oxide (NO) pathway. BACKGROUND Diabetes results in cardiac dysfunction;however, the specific abnormalities are unknown. Because decreased NO contributes to abnormal vascular function in diabetics, we hypothesized that NO pathway abnormalities may contribute to diabetic cardiomyopathy. METHODS Control rats and those with non-insulin-dependent diabetes mellitus (NIDDM) underwent echocardiography, hemodynamic assessment, isolated heart perfusion and measurement of exhaled NO and LV endothelial constitutive nitric oxide synthase (ecNOS). Diabetic rats had increased LV mass (3.3 +/- 0.6 vs. 2.6 +/- 0.3 g/g body weight [BW], p < 0.001) and cavity dimensions (diastolic 2.0 +/- 0.1 vs. 1.8 +/- 0.2 cm/cm tibial length [TL], p < 0.05). RESULTS Diabetic rats had prolonged isovolumic relaxation time (IVRT) (40 +/- 8 vs. 26 +/- 6 ms, p < 0.0001), increased atrial contribution to diastolic filling (0.47 +/- 0.09 vs. 0.30 +/- 0.08 m/s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 +/- 6 vs. 2 +/- 1 mm Hg, p = 0.04). Diabetic rats had increased chamber stiffness. Shortening was similar in both groups, despite reduced meridional wall stress in diabetics, suggesting impaired systolic contractility. Exhaled NO was lower in diabetic rats (1.8 +/- 0.2 vs. 3.3 +/- 0.3 parts per billion, p < 0.01) and correlated with Doppler LV filling. The ecNOS was similar between the groups. CONCLUSIONS Diabetic cardiomyopathy is characterized by LV systolic and diastolic dysfunction, the latter correlating with decreased exhaled NO. The NO pathway is intact, suggesting impaired availability of NO as contributor to cardiomyopathy. (C) 1999 by the American College of Cardiology.

关键词：血压印迹法蛋白质呼吸试验糖尿病实验性/诊断显像糖尿病实验性/代谢糖尿病实验性/病理生理学糖尿病 2型/诊断显像糖尿病 2型/代谢糖尿病 2型/病理生理学超声心动描记术多普勒心室/诊断显像心室/代谢心室/病理生理学心肌收缩一氧化氮/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅲ型大鼠 Sprague-Dawley 心室功能左动物女(雌)性大鼠

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Impaired arteriolar mechanotransduction in experimental diabetes mellitus

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JOURNAL OF DIABETES AND ITS COMPLICATIONS 1999年第5-6期13卷 235-242页

作者： Yu, GL Zou, H Prewitt, RL Hill, MA Eastern Virginia Med Sch Dept Physiol Norfolk VA 23501 USA

Decreased arteriolar distensibility in diabetes may impair signal transduction mechanisms that are required for converting a pressure stimulus into smooth muscle contraction. These studies aimed to determine if pressure-induced increases in arteriolar intracellular Ca2+ (Ca2+) are altered in diabetes and whether diabetes is associated with alterations in composition of the extracellular matrix. Studies of mechanical properties used single, isolated, and cannulated cremaster arterioles from streptozotocin (60 mg/kg) diabetic rats and age-matched controls. To measure Ca-i(2+), arterioles were loaded with Fura 2 (5 mu M) after which preparations were examined by fluorescence microscopy and image analysis. Matrix protein (type IV collagen, laminin, fibronectin) deposition was studied by immunohistochemistry. Over a range of 30-120 mm Hg control vessels showed a linear relationship (r = 0.98, p < 0.01) between intraluminal pressure and Ca-i(2+). Vessels from diabetic animals also showed a linear relationship (r = 0.99, p < 0.01), however, the mean slope was significantly (p < 0.02) less in the diabetic (0.17 +/- 0.05, n = 5) compared to controls (0.51 +/- 0.09, n = 7). Similarly, the slope of the wall tension-Ca-i(2+) relationship was significantly decreased in vessels from diabetic animals. These differences were ameliorated by treatment of diabetic animals (n = 5) with aminoguanidine. Increased content of type IV collagen, laminin and fibronectin in vessel media was evident after 2 weeks of diabetes and showed a further increase with duration of diabetes. The data suggest that for a given increase in luminal pressure arterioles from diabetic animals response with an attenuated rise in smooth muscle Ca-i(2+) This mechanotransduction defect may relate to alterations in the composition of the extracellular matrix within the arteriolar wall. (C) 2000 Elsevier Science Inc.

关键词：小动脉/药物作用小动脉/生理学小动脉/病理生理学血压钙/代谢胶原/代谢糖尿病实验性/病理生理学纤连蛋白类/代谢胍类/药理学层黏连蛋白/代谢肌平滑血管/药物作用肌平滑血管/生理学肌平滑血管/病理生理学大鼠 Sprague-Dawley 参考值信号传导/生理学动物男(雄)性大鼠

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Effects of ω-agatoxin IVA, a P-type calcium channel antagonist, on the development of spinal neuronal hyperexcitability caused by knee inflammation in rats

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JOURNAL OF NEUROPHYSIOLOGY 1999年第6期81卷 2620-2626页

作者： Nebe, J Ebersberger, A Vanegas, H Schaible, HG Univ Wurzburg Physiol Inst D-97070 Wurzburg Germany

Effects of omega-agatoxin IVA, a P-type calcium channel antagonist, on the development of spinal neuronal hyperexcitability caused by knee inflammation in rats. J. Neurophysiol. 81: 2620-2626, 1999. Both N- and P-type high-threshold calcium channels are located presynaptically in the CNS and are involved in the release of transmitters. To investigate the importance of P-type calcium channels in the generation of inflammation-evoked hyperxcitability of spinal cord neurons, electrophysiological recordings were made from wide-dynamic-range neurons with input from the knee joint in the anesthetized rat. The responses of each neuron to innocuous and noxious pressure onto the knee and the ankle were continuously assessed before and during the development of an inflammation in the knee joint induced by the injections of K/C into the joint cavity. The specific antagonist at P-type calcium channels w-agatoxin was administered into a 30-mu l trough on the spinal cord surface above the recorded neuron. In most neurons the application of omega-agatoxin before induction of inflammation slightly enhanced the responses to pressure onto the knee and ankle or left them unchanged. Two different protocols were then followed. In the control group (13 rats) only Tyrode was administered to the spinal cord during and after induction of inflammation. In these neurons the responses to mechanical stimuli applied to both the inflamed knee and to the noninflamed ankle showed a significant increase over 4 h. In the experimental group (12 rats) w-agatoxin was applied during knee injection and in five 15-min periods up to 180 min after kaolin. This prevented the increase of the neuronal responses to innocuous pressure onto the knee and to innocuous and noxious pressure onto the ankle;only the responses to noxious pressure onto the knee were significantly enhanced during development of inflammation. Thus the development of inflammation-evoked hyperexcitability was attenuated by omega-agatoxin, and

关键词：关节炎实验性/化学诱导关节炎实验性/病理学关节炎实验性/病理生理学钙通道阻滞药/药理学钙通道/药物作用钙通道 N型关节/病理学关节/病理生理学白陶土神经元/药物作用物理刺激大鼠 Wistar 蜘蛛毒液类/药理学脊髓/药物作用脊髓/病理学脊髓/病理生理学 ω蜘蛛毒素IVA 动物男(雄)性大鼠

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EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS - EFFECT OF DEXAMETHASONE ON GROWTH AND PROLIFERATION IN DRAINING LYMPH-NODE

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EXPERIMENTELLE PATHOLOGIE 1976年第6期12卷 295-300页

作者： MATOUSMALBOHAN, I HOLUB, M MARES, V LODIN, Z UNIV PRAGUE FAC MED PRAGUE 2 CZECHOSLOVAKIA CZECHOSLOVAK ACAD SCI INST CLIN & EXPTL MED PRAGUE CZECHOSLOVAKIA CZECHOSLOVAK ACAD SCI FAC PHYSIOL PRAGUE CZECHOSLOVAKIA

Dexamethasone, when administered from day 0-9 [to rats] following the sensitizing injection of encephalitogenic protein in complete Freunds adjuvant, suppressed both the characteristic enlargement of the paracortical area of the draining lymph node and the development of clinical and histopathological signs of experimental allergic encephalomyelitis. Division of cells within the node was not inhibited and therefore the effect of dexamethasone appeared to be a consequence of reduced migration of lymphocytes into the node.

关键词：地塞米松/药理学脑脊髓炎自身免疫性实验性/病理学脑脊髓炎自身免疫性实验性/病理生理学淋巴结/药物作用淋巴结/病理学淋巴结/病理生理学器官测量/药物作用大鼠近交Lew 脊髓/病理学动物女(雌)性大鼠

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Contribution of nitric oxide to the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats

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GASTROENTEROLOGY 2000年第5期118卷 937-944页

作者： Liu, HQ Ma, ZH Lee, SS Univ Calgary Gastroenterol Res Grp Liver Unit Calgary AB Canada

Background & Aims: Decreased cardiac contractility and beta-adrenergic responsiveness have been observed in cirrhosis, but the etiology remains unclear. We aimed to test the role of nitric oxide (NO), a negative inotropic agent, in the pathogenesis of cirrhotic cardiomyopathy in a rat model. Methods: Cirrhosis was induced by bile duct ligation. Four weeks after ligation or sham operation, cardiac levels of tumor necrosis factor (TNF)-alpha, guanosine 3,5'-cyclic monophosphate (cGMP), inducible NOS (NOS2), and endothelial constitutive NOS (NOS3) messenger RNA (mRNA) and protein were determined, Serum nitrite/nitrate level was measured. Cardiac contractile function was evaluated in isolated left ventricular papillary muscles in the absence and presence of the NOS inhibitor nitro-L-arginine methyl ester (L-NAME). Results: Cardiac TNF-alpha, NOS2 mRNA and protein, cGMP, and serum interleukin (IL)-1 beta and nitrite/nitrate levels were significantly higher in cirrhotic rats than sham controls. No significant differences in NOS3 mRNA or protein were found between cirrhotic and sham control rats. Baseline isoproterenol-stimulated papillary muscle contractile force was significantly lower in the cirrhotic group;with L-NAME incubation, contractile force increased significantly in cirrhotic rats but was unaffected in the controls. In normal papillary muscles, IL-1 beta attenuated the contractility, but coincubation with L-NAME again reversed this attenuation. Incubation with the exogenous NO donor S-nitroso-N-acetyl-penicillamine also blunted papillary muscle contractility. Conclusions: These results suggest that cytokine-induced stimulation of NOS2 plays a significant role in the pathogenesis of cirrhotic cardiomyopathy.

关键词：胆管印迹法蛋白质心肌疾病/病因学心肌疾病/代谢心肌疾病/病理生理学缩窄病理性环GMP/代谢细胞因子类/代谢酶抑制剂/药理学心室/代谢免疫组织化学结扎术肝硬化实验性/并发症肝硬化实验性/代谢肝硬化实验性/病理生理学心肌收缩/药物作用心肌/代谢硝酸盐类/血液一氧化氮一氧化氮供体/药理学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅱ型一氧化氮合酶Ⅲ型亚硝酸盐类/血液大鼠 Sprague-Dawley 心室功能左动物男(雄)性大鼠

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Portal flow augmentation for liver cirrhosis

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BRITISH JOURNAL OF SURGERY 2000年第8期87卷 984-991页

作者： Jiao, LR Seifalian, AM Mathie, RT Habib, N Davidson, BR UCL Royal Free & Univ Coll Med Sch Univ Dept Surg London England Hammersmith Hosp Imperial Coll Sch Med Liver Surg Unit London England

Background: Portal hypertension due to chronic liver disease is a major cause of death worldwide. Orthotopic liver transplantation offers the best therapeutic option but is available to only a minority of patients. In the past few years mechanically pumping portal venous inflow has been reported to reduce portal hypertension and improve liver function. Methods: A review of the published data on augmented portal perfusion for the treatment of portal hypertension in cirrhosis was carried out by searching Medline and other online databases. From each published study portal pressure and blood flow data before and after augmented portal perfusion were used to calculate the change in mean intrahepatic portal vascular resistance (IHPR). The standardized data were then combined to allow meta-analysis. Results: Seven papers were identified on normal and cirrhotic animal and human livers with augmented dow (50% to fourfold over baseline) for 30-180 min. Meta-analysis revealed that the increased portal venous inflow was associated with a significant rise in portal venous pressure on the hepatic side (P < 0.001), a significant reduction on the mesenteric side (P < 0.001) and a significant reduction in IHPR (P = 0.013). Limited data were available to support improved liver function, Conclusion: Detailed in vivo cirrhotic liver studies on augmented portal flow in experimental models assessing haemodynamic and functional changes are required before clinical evaluation.

关键词：人工血管血管假体植入/方法高血压门静脉/病因学高血压门静脉/病理生理学高血压门静脉/外科学肝硬化实验性/并发症肝硬化实验性/病理生理学肝硬化实验性/外科学假体和植入物猪动物人类兔大鼠

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The importance of the hypothalamo-hypophyseal-adrenal axis to the anti-inflammatory actions of the κ-opioid agonist PNU-50,488H in rats with adjuvant arthritis

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期294卷 1131-1136页

作者： Wilson, JL Carmody, JJ Walker, JS Univ New S Wales Sch Physiol & Pharmacol Sydney NSW 2052 Australia

Possible contributions of the hypothalamo-hypophyseal-adrenal axis to the development of adjuvant-induced arthritis and therapeutic actions of the prototypical kappa-opioid agonist PNU-50,488H (PNU-50) were studied in DA rats. Paw edema, nociception, histological and radiological joint damage, and tumor necrosis factor-alpha release by peritoneal macrophages were measured in adrenalectomized (ADX) and sham-operated (SHO) arthritic animals (drug-treated and untreated groups). Disease developed earlier in ADX rats (paw edema was first apparent 11 days postadjuvant compared with day 13 in SHO animals) and remained more severe in that group. Twice-daily PNU-50 treatment completely prevented the development of edema in the SHO group but was effective in the ADX animals only on day 18. PNU-50 substantially reduced the pooled severity index (combined quantitative edema, histological and radiological assessments) at day 18 in both SHO and ADX rats and to an equal extent. During disease development, the paws of SHO, but not ADX, rats became hyperalgesic;paradoxically, ADX animals were hyperalgesic during PNU-50 treatment, but the drug produced analgesia in SHO animals. Compared with cells harvested from healthy animals, macrophages from arthritic rats released about twice as much tumor necrosis factor-alpha after lipopolysaccharide stimulation. It was concluded that the hypothalamo-hypophyseal-adrenal axis influences the development of adjuvant arthritis and plays a partial role in the therapeutic action of the kappa-agonist PNU-50.

关键词：肾上腺皮质激素类/代谢肾上腺切除术镇痛药阿片类/药理学镇痛药阿片类/治疗应用关节炎实验性/药物疗法关节炎实验性/病理生理学细胞培养的水肿/药物疗法下丘脑-垂体系统巨噬细胞腹膜/代谢疼痛测定垂体肾上腺系统放射免疫测定受体阿片样 κ/激动剂肿瘤坏死因子α/生物合成动物大鼠

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CHARACTERIZATION OF L5178Y LEUKEMIC-CELLS WHICH RAPIDLY DEVELOP AND LOSE IMPLANTATION ABILITY

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1976年第1期68卷 277-283页

作者： SUTKOFF, DR BOSMANN, HB UNIV ROCHESTER SCH MED & DENTDEPT RADIAT BIOL & BIOPHYSROCHESTERNY 14642 UNIV ROCHESTER SCH MED & DENTDEPT PHARMACOL & TOXICOLROCHESTERNY 14642

Two populations of L5178Y murine leukemic cells, maintained by different methods, were studied for their implantation ability in BDF1 mice. Implantation ability was measured by number of tumor nodules formed, liver weight, and day of death of the animal. 1) Cells from a population grown for 10 years in vitro had no implantation ability; i.e., no tumor nodules were formed when injected into the tail vein. After 30 days of growth in the peritoneal cavity of BDF1 mice, these same cells were injected into the tail vein and 10 days later had produced over 200 liver tumor nodules. When cells taken from these tumors were recultured for 60 days in vitro , they lost the acquired implantation ability, but regained it after another single peritoneal passage. 2) L5178Y murine leukemic cells grown for six years in ascites tumor cells were extremely tumorigenic; over 200 tumor nodules appeared in the liver after tail vein injection. These cells were not rendered less tumorigenic and did not lose their implantation ability by in vitro culturing for 60 days. The results suggest that implantation ability is a property of the cell's growth environment; furthermore, they have strong implications for the in vivo and in vitro manipulation of this property.

关键词：细胞系培养基白血病实验性/病理生理学白血病淋巴样/病理生理学动物小鼠

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The role of polypeptide growth factors in human carcinomas: New targets for a novel pharmacological approach

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PHARMACOLOGICAL REVIEWS 2000年第2期52卷 179-206页

作者： Favoni, RE De Cupis, A Ist Nazl Ric Canc Dept Preclin Oncol Pharmacol Lab I-16132 Genoa Italy

The processes of cellular proliferation and progressive acquisition of a specialized phenotype show a high degree of coordination. In particular, these complex signaling networks mediating cell growth, differentiation, migration, and apoptosis are regulated in part by polypeptide growth factors that can act, by autocrine and/or paracrine mechanisms of action, as positive or negative modulators. Because these growth factors are unable to cross the hydrophobic cell membrane, they exert their effects via binding to cell surface receptors, most of which possess intrinsic tyrosine kinase activity. Owing to the interaction of polypeptide growth factors with their specific transmembrane receptors, a cascade of intracellular biochemical signals, resulting in the activation and repression of various subsets of genes, is triggered. One of the major incentives for studying factors that regulate processes of proliferation and differentiation is the recognition of their involvement in tumorigenesis. Genetic aberrations in growth factors signaling pathways are, in fact, inextricably linked to cancer. Malignant cells arise as a result of a stepwise progression of genetic events characterized by the unregulated expression of growth factors or components of their signaling networks. The main aim of this review is to examine the current understanding of the crucial contribution that several growth factors may have on transformation, tumorigenesis, and progression in several human tumors among the most widespread in western countries. For this purpose, we will analyze the chemistry and the molecular organization of the most important growth factors and their specific receptors. In addition, we will focus on the mechanisms of signal transduction, the complex cascade of biochemical events ensued from the growth factor/receptor binding. The present knowledge of the role of growth factor biochemical signaling networks in cancer leads to improvements not only in diagnosis and prognosis for

关键词：抗肿瘤药/药理学抗肿瘤药/治疗应用生长物质/生理学肿瘤/药物疗法肿瘤/病理生理学肿瘤实验性/药物疗法肿瘤实验性/病理生理学肽类/生理学受体生长因子/药物作用信号传导/药物作用信号传导/生理学动物人类

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Regulation of pulsatile luteinizing hormone secretion by insulin in the diabetic male lamb

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BIOLOGY OF REPRODUCTION 2000年第5期62卷 1248-1255页

作者： Bucholtz, DC Chiesa, A Pappano, WN Nagatani, S Tsukamura, H Maeda, K Foster, DL Univ Michigan Reprod Sci Program Ann Arbor MI 48109 USA Univ Michigan Dept Obstet & Gynecol Ann Arbor MI 48109 USA Univ Michigan Dept Biol Ann Arbor MI 48109 USA Univ Michigan Dept Physiol Ann Arbor MI 48109 USA Nagoya Univ Lab Anim Reprod Nagoya Aichi 46401 Japan

This study tested the hypothesis that LH secretion is modulated by insulin and that the responsiveness to hypoinsulinemia is enhanced by sex steroids. The model was the developing male lamb (12-26 wk of age) rendered diabetic by chemically induced necrosis of insulin-secreting tissue (streptozotocin). Our approach was to monitor LH secretion under diabetic conditions, with or without insulin supplementation, either in the presence or in the absence of gonadal steroids. The first experiment determined if chronic insulin supplementation could sustain LH secretion in diabetic lambs. After documentation of the induced diabetic condition, twice-daily treatment with a long-acting insulin preparation (Lente) minimized diabetes-induced hyperglycemia, sustained growth, and maintained LH pulse frequency at levels comparable to pre-diabetic conditions. A second experiment evaluated the acute regulation of LH secretion by insulin. Twenty-four hours of insulin withdrawal decreased LH pulse frequency, increased circulating glucose levels, increased the concentration of plasma non-esterified fatty acids (NEFAs), and increased urinary output of ketones. LH pulse frequency continued to decline after 96 h of insulin withdrawal. By contrast, 24 h of insulin re-supplementation increased LH pulse frequency, reduced circulating glucose and NEFA concentrations, decreased plasma cortisol, and reduced urinary output of ketones. After 96 h of insulin re-supplementation, LH pulse frequency increased further, to levels comparable with those before insulin withdrawal. A third experiment determined if the effects of insulin withdrawal on LH secretion are influenced by the presence of gonadal steroids. The same individuals were treated with a physiologic dose of estradiol (Silastic capsule, s.c.) and subsequently monitored for changes in LH secretion in the presence and in the absence of exogenous insulin. Prior to insulin withdrawal, estradiol decreased both LH pulse frequency and pulse amplitud

关键词：血糖/分析体重/药物作用糖尿病实验性/药物疗法糖尿病实验性/代谢糖尿病实验性/病理生理学雌二醇/药理学促性腺素释放激素/代谢促性腺素释放激素/分泌氢化可的松/血液胰岛素/代谢胰岛素/药理学酮类/尿促黄体激素/分泌绵羊动物男(雄)性

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