An Experimental Investigation of Burn Injury in Living Tissue

1976 ◽  
Vol 98 (2) ◽  
pp. 292-296 ◽  
Author(s):  
D. C. Ross ◽  
K. R. Diller

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.

1978 ◽  
Vol 100 (3) ◽  
pp. 153-158 ◽  
Author(s):  
D. M. Green ◽  
K. R. Diller

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.


1998 ◽  
Vol 79 (1) ◽  
pp. 54-58 ◽  
Author(s):  
F Ghezzo ◽  
G N Berta ◽  
B Bussolati ◽  
A Bosio ◽  
G Corvetti ◽  
...  

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S113-S114
Author(s):  
Marc R Matthews ◽  
Sara Calder ◽  
Areta Kowal-Vern ◽  
Philomene Spadafore ◽  
Karen J Richey ◽  
...  

Abstract Introduction Caloric intake has been a vital component for burn wound healing and recovery. The hypothesis was that caloric requirements are based on injury severity & post-burn week as predicated by indirect calorimetry (IC)/predictive equations. Methods This was a retrospective chart review of 115 burn patients (2012–2017). Caloric requirements were determined by the Curreri equation [which includes % total body surface area (TBSA)] and IC for a 5-week period provided mainly by enteral nutrition. Patients received supplements and total parenteral nutrition as needed. Results The mean ±sd age was 43±18 years, 41±18 % TBSA, Body Mass Index of 28±7 kg/m2, and mortality of 26 (23%). The major mechanisms of injury were flame/flash/explosions. There were 59 (51%) of patients with < 40 % TBSA burns, [median Injury Severity Score (ISS) 9; Apache score 14], and 56 (49%) with ≥40 % TBSA (median ISS 25; Apache score 21), p < .0001. The Respiratory Quotient (RQ) had a median of 0.94 (range 0.79 to 1.02). The median number of surgeries for the < 40 % TBSA group was 5 versus 12 for the ≥40 % TBSA, p < .0001. The Injury Factor did not differ from weeks 1–5 (1.8 for < 40 % TBSA and 2.0 for the ≥ 40 % TBSA). The Curreri equation calculation for this study was a median 3640 (range 2161–5950) calories. The Curreri equation resulted in significantly increased caloric recommendations for the ≥ 40 %TBSA compared to the < 40 %TBSA patients, p < .0001. The < 40 %TBSA group had caloric requirements ranging between 1500- 2700 calories compared to the ≥ 40 %TBSA group, whose calories ranged between 2000–3700. The total daily caloric recommendations were also significantly increased in the ≥40 %TBSA compared to the < 40 %TBSA patients. The maximum levels of resting energy expenditure (REE) from IC, total daily calories recommended by the dietitian and average calories ranged between 3000–4500 in the < 40 %TBSA group and 3600–6700 in the ≥ 40 %TBSA group. The caloric recommendations increased for all patients from week 1 to week 3 and leveled off during weeks 4–5. Conclusions Patient caloric requirements were dependent not only on the severity of the burn injury but also the post-burn hospitalization during which surgeries, debridement/grafting, and infectious complications occurred. They increased until the third week post-burn and leveled off in the recovery period. The study caloric recommendations and requirements were consistent with the REE and Curreri equation assessments.


2000 ◽  
Vol 191 (11) ◽  
pp. 1829-1840 ◽  
Author(s):  
Narinder Gautam ◽  
Heiko Herwald ◽  
Per Hedqvist ◽  
Lennart Lindbom

Activation of polymorphonuclear leukocytes (PMNs) and adhesion to the endothelial lining is a major cause of edema formation. Although known to be dependent on the function of β2 integrins (CD11/CD18), the precise mechanisms by which adherent PMNs may impair endothelial barrier capacity remain unclear. Here, the role of transmembrane signaling by β2 integrins in PMN-induced alterations in tight junctional permeability of cultured endothelial cell (EC) monolayers was investigated. PMN activation, in the absence of proinflammatory stimuli, was accomplished through antibody cross-linking of CD11b/CD18, mimicking adhesion-dependent receptor engagement. CD18 cross-linking in PMNs added to the EC monolayer provoked a prompt increase in EC permeability that coincided with a rise in EC cytosolic free Ca2+ and rearrangement of actin filaments, events similar to those evoked by chemoattractant PMN activation. Cell-free supernatant obtained after CD18 cross-linking in suspended PMNs triggered an EC response indistinguishable from that induced by direct PMN activation, and caused clear-cut venular plasma leakage when added to the hamster cheek pouch in vivo preparation. The PMN-evoked EC response was specific to β2 integrin engagement inasmuch as antibody cross-linking of l-selectin or CD44 was without effect on EC function. Our data demonstrate a causal link between outside-in signaling by β2 integrins and the capacity of PMNs to induce alterations in vascular permeability, and suggest a paracrine mechanism that involves PMN-derived cationic protein(s) in the cellular crosstalk between PMNs and ECs.


1981 ◽  
Vol 26 (10) ◽  
pp. 761-767 ◽  
Author(s):  
A.R. Gould ◽  
C.H. Miller ◽  
A.H. Kafrawy

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