Systematic evaluation of microangiopathy in diabetic Chinese hamsters: I. Morphometric analysis of minimal glomerular basement membrane thickness in 19-23 month old Chinese hamsters

1984 ◽  
Vol 42 ◽  
pp. 190-191
Author(s):  
A.R. Diani ◽  
G.A. Sawada ◽  
T. Peterson ◽  
B.M. Wyse ◽  
M.C. Blanks ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Basement Membranes ◽  
The Body ◽  
Human Experimentation ◽  
Diabetic Microangiopathy ◽  
Diabetic Patients ◽  
Membrane Thickness ◽  
Metabolic Derangement ◽  
Basement Membrane Thickness ◽  
Chinese Hamsters

Microangiopathy has been recognized as a critical complication which afflicts the human diabetic population and magnifies the risk for permanent injury and/or mortality. One of the major manifestations of diabetic microvascular disease in man appears to be capillary basement membrane thickening (CBMT) which has been termed the “hallmark of diabetic microangiopathy”. CBMT of diabetic patients seems to be a product of vascular injury imposed by the interaction of metabolic derangement, environmental factors and genetics (1). Although the degree of thickening varies with age, duration of diabetes, severity of metabolic impairment and location in the body, capillary basement membranes from the kidney, skeletal muscle and heart are usually expanded in diabetic man. However, due to the sparsity of systematic studies and inherent problems with human experimentation, the pathogenesis of CBMT remains controversial. In an attempt to achieve a better understanding of the etiology and progression of CBMT, diabetic animal models have recently been the focal point of intensive research (2).

Systematic evaluation of microangiopathy in diabetic Chinese hamsters: II. Morphometric analysis of basement membrane thickness in the quadriceps muscle of 19-23 month old Chinese hamsters

1984 ◽  
Vol 42 ◽  
pp. 192-193
Author(s):  
G.A. Sawada ◽  
A.R. Diani ◽  
T. Peterson ◽  
B.M. Wyse ◽  
M.C. Blanks ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Quadriceps Muscle ◽  
Systematic Evaluation ◽  
Diabetic Microangiopathy ◽  
Membrane Thickness ◽  
Basement Membrane Thickness ◽  
Capillary Basement Membrane ◽  
Chinese Hamsters ◽  
Basement Membrane Thickening ◽  
Diabetic Chinese Hamsters

Capillary basement membrane thickening appears to be one of the primary manifestations of microangiopathy which affects numerous capillary beds in diabetic man. Although many diabetic animal models exhibit microangiopathy in the eyes and kidneys, few studies have demonstrated the existence of muscle capillary basement membrane thickening similar to that which occurs in human diabetics.(1) Furthermore, a limited number of investigations have been systematically designed to correlate quantification of basement membrane thickness with metabolic perturbations, age, duration, and severity of diabetes. Systematic characterization of diabetic microangiopathy may help to elucidate some of the factors underlying basement membrane thickening and serve as guidelines for therapeutic studies which are designed to prevent or inhibit basement membrane thickening. Clinically, muscle biopsies are easily obtained, and this type of characterization may also prove useful in the diagnosis of diabetic microangiopathy. Therefore, the purpose of this study was to determine if basement membrane thickening is present in the quadriceps muscle capillaries of 19-23 month old diabetic Chinese hamsters in comparison with age-matched controls.

Non-insulin-dependent diabetic microangiopathy in the inner ear

1999 ◽  
Vol 113 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Chapman T. McQueen ◽  
Andrew Baxter ◽  
Timothy L. Smith ◽  
Eileen Raynor ◽  
Sang Min Yoon ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Basement Membrane ◽  
Inner Ear ◽  
Noise Exposure ◽  
Basement Membranes ◽  
Diabetic Microangiopathy ◽  
Moderate Intensity ◽  
Membrane Thickness ◽  
Basement Membrane Thickness ◽  
Insulin Dependent

AbstractHearing loss has long been associated with diabetes mellitus. Microangiopathy, associated with thickening of the basement membranes of small vessels, has been implicated as a major source of multiple system organ disease.Objective This study was designed to evaluate changes in basement membrane thickness in the inner ear of laboratory animals suffering from non-insulin-dependent diabetes mellitus (NIDDM) with, and without, exposure to moderate intensity noise exposure in an attempt to extrapolate the same disease process in humans.Design Spontaneously hypertensive-corpulent non-insulin-dependent rats (SHR/N-cp) were selected as a genetic model for the above study. Both lean and obese rats were used in this study. A genetically similar control group of animals (LA/N-cp) were used as controls. These animals express both the lean and obese phenotypes, but they lack the NIDDM gene. Forty-eight animals in each group were sacrificed at the end of the study. The cochleas were dissected and fixed. The basement membrane of the stria vascularis was examined using transmission electron microscopy.Setting This study was a laboratory-based, standard animal study.Main outcome This study was designed to show microangiography of the inner ear as related to NIDDM with, and without, obesity and noise exposure.Results/Conclusions NIDDM alone does not cause statistically significant basement membrane thickening; however, NIDDM in combination with obesity and/or noise exposure did show significant thickening and the combination of all three showed the greatest thickening. NIDDM appeared to be the greatest contributing factor.

Microvascular Response to Tissue Injury and Capillary Ultrastructure in the Foot Skin of Type I Diabetic Patients

1995 ◽  
Vol 89 (5) ◽  
pp. 467-474 ◽  
Author(s):  
G. Rayman ◽  
R. A. Malik ◽  
A. K. Sharma ◽  
J. L. Day
Keyword(s):  
Basement Membrane ◽  
Light And Electron Microscopy ◽  
Microvascular Blood Flow ◽  
Diabetic Patients ◽  
Membrane Thickness ◽  
Type I ◽  
Basement Membrane Thickness ◽  
Doppler Flowmetry ◽  
Hyperaemic Response ◽  
Capillary Size

1. Microvascular blood flow responses to injury and capillary ultrastructure were assessed by laser Doppler flowmetry and detailed light and electron microscopy respectively in skin biopsied from 28 patients with insulin-dependent diabetes and 17 control subjects. 2. The hyperaemic response induced by biopsy (P < 0.001) and heating to 44°C (P < 0.001) was significantly lower in the diabetic patients and showed progressive impairment with the severity of complications (P < 0.001). 3. Skin capillary basement membrane thickness was significantly increased in the diabetic patients (P < 0.001) and also increased with the severity of complications (P < 0.002). Both the luminal area (P < 0.001) and the endothelial cell outer perimeter (P < 0.002), measures of luminal and capillary size, respectively, were significantly reduced in all diabetic patients. 4. Basement membrane thickness was related significantly to the impaired hyperaemic response to both biopsy (P < 0.01) and thermal injury (P < 0.01). 5. Our findings support the hypothesis that structural abnormalities, which are characterized by an early reduction in capillary size and later thickening of basement membrane, form an important mechanism for the impaired hyperaemic response in diabetic patients.

Relationships between Haemostatic Factors and Capillary Morphology in Human Diabetic Neuropathy

1992 ◽  
Vol 68 (06) ◽  
pp. 628-633 ◽  
Author(s):  
Isobel Ford ◽  
Rayaz A Malik ◽  
Paul G Newrick ◽  
F Eric Preston ◽  
John D Ward ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Peripheral Neuropathy ◽  
Basement Membrane ◽  
Diabetic Neuropathy ◽  
Fibrinolytic Activity ◽  
Diabetic Patients ◽  
Membrane Thickness ◽  
Basement Membrane Thickness ◽  
Clinical Complications ◽  
Haemostatic Factors

SummaryWe have examined haemostatic factors in 15 diabetic patients with peripheral neuropathy and 10 diabetic patients without clinical complications. Plasma and blood viscosity, fibrinogen, factor VIIIc, von Willebrand factor activity, spontaneous platelet aggregation and fibrinolytic activity were not significantly different between diabetic patients without clinical complications and diabetic patients with peripheral neuropathy. Platelet aggregation was enhanced in diabetic patients with neuropathy compared with those without complications. In the 15 patients with neuropathy and 3 without complications, who underwent biopsy of sural nerve, skin and muscle, associations were found between haemostatic variables and measures of nerve capillary pathology, notably: plasma fibrinogen and nerve capillary basement membrane thickness (r = 0.70, p <0.001); thromboxane B2 production and nerve capillary basement membrane thickness (r = –0.61, p <0.01); plasma fibrinolytic activity and endoneurial capillary lumen size (r = 0.60, p <0.01) and endothelial cell outer perimeter (r = 0.65, p <0.01). The main associations of skin and muscle capillary abnormalities were with measures of in vitro platelet aggregation, and the correlations found with nerve capillary measurements were not echoed in the overlying muscle and skin. The results are supportive of the involvement of haemostatic abnormalities in the pathogenesis of diabetic neuropathy.

HAEMOSTATIC PARAMETERS, ENDONEURIAL OXYGEN TENSION AND SURAL NERVE HISTOLOGY IN DIABETES MELLITUS

1987 ◽  
Author(s):  
I Ford ◽  
P G Newrick ◽  
R Malik ◽  
F E Preston ◽  
J D Ward ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Oxygen Tension ◽  
Sural Nerve ◽  
Clot Lysis ◽  
Diabetic Patients ◽  
Membrane Thickness ◽  
Basement Membrane Thickness ◽  
Significant Difference ◽  
Group A ◽  
Group B

We have examined coagulation parameters in 15 neuropathic (Group A) and 10 complication-free diabetic patients (Group B). Venesection and sample testing were performed under standard conditions. Group A underwent sural nerve biopsy and 14 also had measurements of endoneurial oxygen tension. Factor VIII related antigen was higher in Group A (l-617u/ml ± 0.67) compared to Group B (0.944u/ml ± 0.26); (mean ± SD; p<.0.05) perhaps suggesting endothelial cell damage, although this did not correlate with capillary basement membrane thickness or endothelial cell number nor with endoneurial oxygen levels. Platelets from Group A were more sensitive to arachidonate than those of Group B, showing aggregation thresholds in platelet rich plasma of 0.36 ± 0.17mM and 0.57 ± 0.9mM respectively compared with 0.65 ± 0.37mM in non-diabetic controls.Platelets from Group A subjects also produced more thromboxane B2 in response to arachidonate than Group B or normal controls (37.95 ± 27.5; 25.5 ± 13.0; 16.55 ± 15-5pmol/107 platelets). Blood fibrinolytic capacity measured by euglobulin clot lysis time, was diminished in NIDDs (post-occlusion ECLT 165.7 mins ± 116.0), compared to IDDs (55.5 ± 34.5) (p<0.05) due at least in part to excess of tissue plasminogen-activator inhibitor, although we found no significant difference in ECLT between Group A and Group B. Interaction between haemostatic and microvascular abnormalities in diabetes may contribute to the pathogenesis of diabetic neuropathy.

The relation between connective tissue cells and intercellular substances, including basement membranes

1975 ◽  
Vol 271 (912) ◽  
pp. 363-377 ◽  
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Immune Complexes ◽  
Hydrolytic Enzymes ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Cellular Level ◽  
Basement Membranes ◽  
The Body ◽  
Pathological Changes

Basement membranes are distributed widely in the body forming an extracellular matrix for epithelial and endothelial cells. The collagenous and glycoprotein constituents of basement membranes are synthesized by these two cell types. Disturbance of the interactions between basement membranes and their associated epithelial and endothelial cells can lead to the pathological changes seen in diseases involving basement membranes. These changes are illustrated here by reference to glomerulonephritis induced by the deposition of immune complexes in the glomerulus of the kidney, and chronic inflammatory changes occurring in the lung after inhalation of asbestos. In these diseases basement membrane changes can occur in several ways. Hydrolytic enzymes released from inflammatory cells degrade basement membranes while other factors released from these cells may stimulate synthesis of basement membrane constituents by epithelial and endothelial cells. Alternatively the physical separation of epithelial and endothelial cells from their basement membranes by space-occupying substances such as immune complexes can interfere with feedback mechanisms leading to synthesis of basement membrane constituents and cell proliferation. Studies of these pathological changes at a cellular level should shed new light on the ways in which cells interact with their pericellular environment.

The Relationship of Reticular Basement Membrane Thickness to Airway Wall Remodeling in Asthma

2002 ◽  
Vol 166 (12) ◽  
pp. 1590-1595 ◽  
Author(s):  
Alan L. James ◽  
Peta S. Maxwell ◽  
Gladys Pearce-Pinto ◽  
John G. Elliot ◽  
Neil G. Carroll
Keyword(s):  
Basement Membrane ◽  
Membrane Thickness ◽  
Airway Wall ◽  
Basement Membrane Thickness ◽  
Relationship Of ◽  
The Relationship
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