Accelerated degradation of collagen membranes in diabetic rats is associated with increased infiltration of macrophages and blood vessels

2015 ◽  
Vol 20 (7) ◽  
pp. 1589-1596 ◽  
Author(s):  
Ofer Moses ◽  
Meizi Eliezer ◽  
Carlos Nemcovsky ◽  
Haim Tal ◽  
Miron Weinreb
Keyword(s):  
Blood Vessels ◽  
Diabetic Rats ◽  
Accelerated Degradation ◽  
Collagen Membranes

scholarly journals Cross-Linked Hyaluronic Acid Slows Down Collagen Membrane Resorption in Diabetic Rats through Reducing the Number of Macrophages

2021 ◽  
Author(s):  
Meizi Eliezer ◽  
Anton Sculean ◽  
Richard J. Miron ◽  
Carlos Nemcovsky ◽  
Dieter D. Bosshardt ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Hyaluronic Acid ◽  
Diabetic Rats ◽  
Collagen Membrane ◽  
Membrane Thickness ◽  
Membrane Degradation ◽  
Healthy Group ◽  
Accelerated Degradation ◽  
Collagen Membranes ◽  
Transglutaminase Ii

Accelerated degradation of collagen membranes (CMs) in diabetic rats is associated with increased infiltration of macrophages and blood vessels. Since pre-implantation immersion of CMs in cross-linked high molecular weight hyaluronic acid (CLHA) delays membrane degradation, we evaluated its effect on the number of macrophages and endothelial cells (ECs) within the CM. Diabetes was induced with streptozotocin in 16 rats, while 16 healthy rats served as control. CM discs were labeled with biotin, soaked in CLHA or PBS and implanted under the scalp. Fourteen days later, CMs were embedded in paraffin and the number of macrophages and ECs within the CMs was determined using antibodies against CD68 and Transglutaminase II, respectively. Diabetes increased the number of macrophages and ECs within the CMs (∼2.5-fold and 4-fold, respectively). Immersion of CMs in CLHA statistically significantly reduced the number of macrophages (p<0.0001) in diabetic rats, but not that of ECs. In the healthy group, CLHA had no significant effect on the number of either cells. Higher residual collagen area and membrane thickness in CLHA-treated CMs in diabetic animals were significantly correlated with reduced number of macrophages but not ECs. Immersion of CM in CLHA inhibits macrophage infiltration and reduces CM degradation in diabetic animals.

Effect of Topical Insulin on Second-Degree Burns in Diabetic Rats

2015 ◽  
Vol 18 (2) ◽  
pp. 181-192 ◽  
Author(s):  
F. Azevedo ◽  
A. Pessoa ◽  
G. Moreira ◽  
M. Dos Santos ◽  
E. Liberti ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Smooth Muscle Actin ◽  
Healing Process ◽  
Diabetic Rats ◽  
Inflammatory Cell Infiltrate ◽  
Inflammatory Phase ◽  
General Aspects ◽  
Diabetic Wounds ◽  
Picrosirius Red ◽  
Second Degree

The healing process is complex in diabetic wounds, and the healing mechanism of burn wounds is different from that of incisional or excisional wounds. Data from our previous study indicated that topical insulin cream reduced wound closure time in diabetic rats. Our aim was to investigate the effect of topical insulin cream on wound healing following second-degree burns in control and diabetic rats. Rats were divided into four groups: control (nondiabetic) rats treated with placebo (CP), control (nondiabetic) rats treated with topical insulin cream (CI), diabetic rats treated with placebo (DP), and diabetic rats treated with topical insulin cream (DI). The wounds were assessed at 4 time points (1, 7, 14, and 26 days) post-wounding for morphometric analysis of wound sections stained with hematoxylin/eosin, α-smooth muscle actin, and Picrosirius red to evaluate general aspects of the wound, inflammatory infiltrate, blood vessels, and Types I and III collagen fibers. Histological analysis showed that topical insulin cream increased the inflammatory cell infiltrate in the DI group (at 7 and 14 days postburn, p < .05) and blood vessels (at 14 days postburn, p < .05) to levels similar to those of groups CP and CI. Wounds treated with topical insulin cream (CI and DI groups) showed significantly stronger staining for fibrillar collagen than wounds of the DP group. The use of topical insulin may reduce the duration of the inflammatory phase; improve wound reepithelialization, tissue granulation, and wound contraction; and increase collagen deposition in second-degree burns in healthy and diabetic animals.

scholarly journals Evans blue staining to detect deep blood vessels in peripheral retina for observing retinal pathology in early-stage diabetic rats

2021 ◽  
Vol 14 (10) ◽  
pp. 1501-1507
Author(s):  
Kang-Pei Shi ◽  
◽  
Chuang-Xin Huang ◽  
Chu-Sheng Cai ◽  
Yan-Jie Zhu ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Evans Blue ◽  
Early Stage ◽  
Diabetic Rats ◽  
Vascular Leakage ◽  
Blue Staining ◽  
Peripheral Retina ◽  
Pathological Changes ◽  
Retinal Blood Vessels ◽  
Leakage Area

AIM: To observe and compare the statistical significance of superficial and deep vascular leakage in the pathological changes of the diabetic rats retina after the Evans blue (EB) perfusion, and utilize the modified whole-retina spreading method to make the slides while protecting the periphery of the retina. METHODS: The Sprague-Dawley (SD) rats were randomly divided into 6 groups. Each group named as the normal groups for 4, 8, and 12wk and the diabetic groups for 4, 8, and 12wk. The EB was injected into the cardiovascular system of the rats at the different time points. The retina of each group was obtained for observation. RESULTS: The superficial vascular leakage was found in all 6 groups. The size of leakage area of superficial retinal blood vessels was (0.54±0.23)%, (0.65±0.11)%, and (0.58±0.10)% in normal group. No notable leakage was found in the deep blood vessels [(0.03±0.04)%, (0.03±0.05)%, and (0.03±0.05)%]. The deep retinal vascular leakage was found in the peripheral retina of diabetic rats. The size of leakage area of superficial retinal blood vessels in diabetic group were (0.53±0.22)%, (0.69±0.16)%, and (0.52±0.11)%. The leakage areas of deep blood vessels were (0.54±0.50)%, (1.42±0.16)%, and (1.80±0.07)% at 4, 8, and 12wk, respectively. There was a statistically difference of the leakage area between the 8th week and the 4th week of diabetes group (P=0.003). The statistically significant difference between the diabetes and the control groups was noted at 4wk and 8wk (P<0.001). CONCLUSION: The main retinal pathological changes of early-stage diabetic rats are the vascular leakage of the periphery of deep retina. Diabetic rats modeled after 8wk have semi-quantitative statistical difference compared with the normal rats, thus early intervention treatment research can start at this time point.

The influence of chronic experimental diabetes on contractile responses of rat isolated blood vessels

1985 ◽  
Vol 63 (1) ◽  
pp. 52-57 ◽  
Author(s):  
K. M. MacLeod ◽  
J. H. McNeill
Keyword(s):  
Blood Vessels ◽  
Vascular Reactivity ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Cross Sectional Area ◽  
Consistent Pattern ◽  
Sectional Area ◽  
Cross Sectional ◽  
Onset Of Diabetes ◽  
Portal Veins

The influence of experimental diabetes induced by streptozotocin on responses of rat isolated aortae and portal veins to noradrenaline, 5-hydroxytryptamine, and KCl was examined 7, 100, 180, and 360 days after the onset of diabetes. No significant changes in reactivity were seen 7 days after the onset of diabetes. After 100 days aortae from diabetic rats were supersensitive (defined as a significant increase in the pD2 value) to noradrenaline. However, 180 days after the onset of diabetes, the sensitivity of diabetic aortae to noradrenaline was not significantly different from control, while the responsiveness (defined as the maximum developed tension ÷ cross-sectional area of aorta) to 5-hydroxytryptamine was reduced. A generalized increase in both the sensitivity and responsiveness of diabetic aortae to all three agonists was observed after 360 days of diabetes. In contrast, no changes in either the sensitivity or the responsiveness of portal veins to noradrenaline, 5-hydroxytryptamine, or KCl could be detected at any time after the onset of diabetes. These results indicate that changes in vascular reactivity can be detected with increasing duration of experimental diabetes. However, these changes do not follow a consistent pattern and are not seen in all parts of the vasculature.

scholarly journals Mechanisms underlying dysfunction of retinal blood vessels in diabetic rats

2015 ◽  
Vol 145 (2) ◽  
pp. 70-73
Author(s):  
Asami Mori ◽  
Kenji Sakamoto ◽  
Tsutomu Nakahara ◽  
Kunio Ishii
Keyword(s):  
Blood Vessels ◽  
Diabetic Rats ◽  
Retinal Blood Vessels

Altered aortic and cremaster muscle prostaglandin synthesis in diabetic rats

1985 ◽  
Vol 249 (4) ◽  
pp. E374-E379 ◽  
Author(s):  
T. O. Myers ◽  
E. J. Messina ◽  
A. M. Rodrigues ◽  
M. E. Gerritsen
Keyword(s):  
Arachidonic Acid ◽  
Blood Vessels ◽  
General Feature ◽  
Vascular Reactivity ◽  
Diabetic Rats ◽  
Prostaglandin Synthesis ◽  
Cremaster Muscle ◽  
Vascular Changes ◽  
Streptozotocin Induced Diabetes ◽  
Animal Models Of Diabetes

Alterations in the synthesis and release of prostaglandins have been reported in humans and animal models of diabetes mellitus. In the present study synthesis and release of prostaglandins by thoracic aorta and cremaster muscle of rats with streptozotocin-induced diabetes of 8 wk duration was compared with age-matched controls. Prostaglandin synthesis was assessed by the measurement of immunoreactive prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) release and by quantifying metabolism of exogenous [1-14C]arachidonic acid by thoracic aortic rings and minced cremaster muscle.The cremaster muscles from diabetic rats released significantly greater quantities of PGE2 and 6-keto-PGF1 alpha and PGE2. In contrast, the aortas from diabetic rats released smaller quantities of 6-keto-PGF1 alpha and PGE2 and exhibited reduced 6-[1-14C]keto-PGF1 alpha. These studies indicate that diminished prostacyclin (PGI2) and/or PGE2 production is not a general feature of all diabetic vascular tissues, suggesting that large and small blood vessels may not be similarly affected by diabetes in regard to the metabolism of exogenous arachidonic acid and the synthesis and release of prostaglandins. Furthermore, the vascular changes often observed in conjunction with diabetes, i.e., alterations in vascular reactivity and microangiopathy in small blood vessels and atherosclerosis of large blood vessels may be related in some way to the segmental differences observed in prostaglandin synthesis.

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