Measurement of Burn-Induced Leakage of Macromolecules in Living Tissue

1978 ◽  
Vol 100 (3) ◽  
pp. 153-158 ◽  
Author(s):  
D. M. Green ◽  
K. R. Diller
Keyword(s):  
Light Microscopy ◽  
Vascular Permeability ◽  
Experimental Technique ◽  
Circulatory System ◽  
Cheek Pouch ◽  
Living Tissue ◽  
Hamster Cheek Pouch ◽  
Extravascular Space ◽  
Thermal Trauma ◽  
Preliminary Results

An experimental technique has been developed to measure changes in vascular permeability caused by thermal trauma to the microvascular bed of the hamster cheek pouch. A solution of flourescein isothiocyanate (FITC) conjugated dextran was injected directly into the circulatory system. Subsequent leakage of dye from vessels into the extravascular space was directly observed by light microscopy and recorded by sequential photography. Individual frames of the filmed record of the trauma and post-trauma process were digitized and analyzed by computer. A point-by-point densitometric evaluation of the digitized image provides a measure of extravascular accumulation of dye-tagged dextran. Preliminary results indicate that preburn treatment with large doses of heparin yields a significant reduction in burn-induced edema.

An Experimental Investigation of Burn Injury in Living Tissue

1976 ◽  
Vol 98 (2) ◽  
pp. 292-296 ◽  
Author(s):  
D. C. Ross ◽  
K. R. Diller
Keyword(s):  
Burn Injury ◽  
Thermal Control ◽  
Cellular Level ◽  
Thermal Parameters ◽  
Cheek Pouch ◽  
Maximum Temperature ◽  
Living Tissue ◽  
Burn Wound ◽  
Hamster Cheek Pouch ◽  
Experimental Apparatus

The effects of thermal insult on living tissue have been studied by direct microscopic observation of the circulatory system’s response to a controlled trauma regimen. An experimental apparatus has been developed which utilizes a unique high and low temperature stage in conjunction with a precision thermal control system to examine the injury process in the microcirculation of the golden hamster cheek pouch. Unique features of this experimental apparatus are: (1) continuous monitoring of the injury processes at the cellular level, (2) capability for quantitative assay of thermal injury, (3) precise control over the thermal parameters that govern injury, (4) versatility in isolating the effects of these individual parameters. The important thermal parameters monitored using this experimental procedure are the time rates of change of temperature during burning and cooling, the maximum temperature reached, and the length of time the tissue was held at this temperature. With this type of experimental apparatus any portion of the burn protocol, such as the maximum temperature reached during burning, may be varied while holding all other parameters constant. It is well documented that the microvascular bed is a primary site for manifestation of burn wound injury. Burn injury occurs as a consequence of rate dependent physiochemical processes, and, therefore, develops over a finite period of time subsequent to trauma. The experimental technique is designed to determine the gross response of the microvascular system to burn trauma. Initial investigations on burn injury have demonstrated a direct dependency of the extent of damage upon both the maximum temperature attained and the duration of exposure. The minimum temperature required to produce stasis within 20 s after completion of the burn in 95 ±5 percent of the microcirculation decreased exponentially with burn duration between the extremes of 85°C for 1 s exposure and 60°C for 100 s exposure.

scholarly journals Fibrin Degradation Products and Vascular Permeability

1977 ◽  
Author(s):  
Bengt Gerdin ◽  
Herman Högstorp ◽  
Olle Lindquist ◽  
Tom Saldeen ◽  
Erik Svensjö
Keyword(s):  
Molecular Weight ◽  
Vascular Permeability ◽  
High Molecular Weight ◽  
Degradation Products ◽  
Cheek Pouch ◽  
Low Molecular Weight ◽  
Hamster Cheek Pouch ◽  
Fibrin Degradation Products ◽  
Lymphatic Duct ◽  
Fibrin Clots

Increased vascular permeability plays an important role in the pathogenesis of the delayed microembolism syndrome. Fibrin degradation products (FDP) may play a role for this permeability disturbance. Fractions of lymph from the cannulated right lymphatic duct in dogs with induced microembolism syndrome and lysate from fibrin clots obtained by gel chromatography were used. The effect on vascular permeability was determined in the hamster cheek pouch and in the dorsal skin of the rat. Increased permeability was determined by leakage of fluorescein labelled dextran in the first model and by use of isotope labelled albumin in the second model. Lymph from the lymphatic duct and fractions of lysate from fibrin clots caused an increased vascular permeability of the same character in both models, the effect being partly due to high molecular weight products and partly due to low molecular weight products. The effect of high molecular weight products may possibly be due to their continous cleavage releasing low molecular weight vasoactive FDP. The effect of FDP on vascular permeability was enhanced by pretreatment with the β-adrenergic inhibitor propranolol and inhibited by the β2-adrenergie stimulator terbutaline. Bredykinin and PGE1 both increased macromolecular leakage in the hamster cheek pouch. This increase was also counteracted by terbutaline. The FDP effect on permeability might be due to contraction of the endothelial cells.

scholarly journals Five steps in leukocyte extravasation in the microcirculation by chemoattractants

1992 ◽  
Vol 1 (6) ◽  
pp. 403-409 ◽  
Author(s):  
T. Oda ◽  
M. Katori ◽  
K. Hatanaka ◽  
S. Yamashina
Keyword(s):  
Cell Layer ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Extravascular Space ◽  
Vascular Lumen ◽  
Endothelial Cell Layer ◽  
Layer 4 ◽  
Leukocyte Extravasation

For in vivo study of the phenomena observed in vitro, PMN (polymorphonuclear leukocyte) extravasation was analysed quantitatively in the microcirculation of the hamster cheek pouch using a video system. Topical application of leukotriene B4or N-formyl-methionylleucyl- phenylalanine increased dose dependently the number of PMNs adhering to the venules. Eighty to 90% of the adhering PMNs disappeared from the vascular lumen into the venular wall within 10-12 rain after the adhesion. After PMNs had passed through the endothelial cell layer, they remained in the venular wall for more than 30 min after application of the chemoattractants and appeared in the extravascular space. Thus, the process could be divided into five steps: (1) rolling and (2) adhesion to the endothelium, (3) passage through the endothelial layer (4) remaining in the venular wall, and (5) passage through the basement membrane.

The influence of oxidative stress on permeability of capillary vessels in the cheek pouch of hamsters with alloxan-induced diabetes

VASA ◽  
2004 ◽  
Vol 33 (4) ◽  
pp. 211-214
Author(s):  
Ciechanowski ◽  
Kedzierska ◽  
Golembiewska ◽  
Miklaszewicz ◽  
Domanski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Protease Inhibitor ◽  
Protective Effect ◽  
Vascular Permeability ◽  
Diamine Oxidase ◽  
Superoxide Radical ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Radical Generation

Background: The aim of the study was to assess the influence of oxidative stress on the increase of permeability of capillary vessels in animals with alloxan-induced diabetes. Material and methods: The studies were performed in microcirculation system of hamster cheek pouch. After the blockade of histamine receptors and administration of diamine oxidase (DAO) and histamine into circulation fluorescein angiography was done. In addition, the influence of superoxide dismutase, aminoguanidine (DAO inhibitor) and trascolan (protease inhibitor) on vascular permeability caused by superoxide radical generation in DAO/histamine system was assessed. Results: The number of extravasal leakages in the group receiving HA and DAO was significantly higher (p < 0.001) than in the groups receiving potential vascular "sealers", e.g. SOD, aminoguanidine or trascolan. In the group receiving aminoguanidine the number of leakages was significantly lower (p < 0.05) compared to the group receiving SOD or trascolan. Conclusions: The protective effect of aminoguanidine, superoxide dismutase or trascolan decreasing the vascular permeability, suggests that the increased vascular permeability is a result of superoxide radical generation by diamine oxidase.

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