ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 14 of 41
JMBS 2017, 2(5): 69–73
Experimental Medicine and Morphology

Morphological Changes in the Rats’ Myocardium under the Conditions of Infusion Correction of the Experimental Burning Disease

Fomina L., Radoha R.

Burn shock infusion therapy is intended to compensate the loss of fluid volume, followed by support blood volume at a constant level, reducing edema syndrome, normalization of acid-base balance, electrolyte balance and blood proteins. It also increases organs’ and tissues’ perfusion. Scientific sources indicate that the problem of adequate use of infusion-transfusion solutions in condition of burn shock is unsolved yet. The main purpose of the article is to present the results of experimental research of morphological changes in myocardium of rats under the conditions of infusion correction in experimental burn disease. Infusion correction of experimental burn disease was performed using a 0.9% solution of NaCl, Lactoproteinum with Sorbitol (Lactoproteinum-C) and colloid-hyperosmolar solution HAES-LX-5%. Morphological examination of myocardial left ventricular was conducted on the 1st, 3rd and 7th days of the experiment. The analysis of the myocardial histological specifics on light-optical level illustrated that all animals had damaged cardiomyocytes after burn injuries. But the most dramatic disorders of the heart muscle circulation were on the level of hemo-microcirculation vessels, primarily, venuljarnom-capillary plethora. In the clinch, the revealed pathological changes had different degrees of severity and prevalence, depending on of the pharmacological agent that was used to improve the condition. The largest pathomorphological changes occurred in the myocardium of animals with burn injuries after infusion of the NaCl 0,9% solution, which was confirmed by morphometrical analysis. So, the expansion of peri- and endomysium constituted 39,8 ± 2,03 mkm and 13,5 ± 0,62 mkm comparing with the results taken from rats without burn injuries 29,5 ± 1,18 mkm and 4,9 ± 0,23mkm respectively, p<0.001. In this case, the areas with severe myocardial degeneration, edema and even necrosis of individual cardiomyocytes form (in response to alteration) small hearths of productive inflammation were met, containing mainly macrophages and lymphocytes. The kind of inflammation demonstrates that on the 7th day after application of NaCl 0,9% solution, the remodeling of damaged myocardium areas has not been finished. The use of combined hyperosmolar solutions reduced the extent and prevalence of structural changes in the myocardium caused by experimental burn disease. In this case, less pronounced protective effect was observed in the case of Lactoproteinum-C usage. In the myocardium signs of edema, circulatory disorders were preserved, there were also signs of productive inflammation and significant degenerative changes of cardiomyocytes. When using HAES-LX-5% during the first three days of the experiment pathologically altered isolated cardiac muscle fibers, scattered histiocytic elements in the stroma were also detected, but circulatory disorders and edema (both stromal and intracellular) were significantly lower. On the 7th day (at the end of the experiment) in animals receiving HAES-LX-5%, changes in the myocardium were minimal and mosaic, and the histological structure of the cardiac muscle was close to that in non-thermally injured animals. Signs of inflammation and severe circulatory disorders were also practically absent.

Keywords: burn disease, myocardium, morphology, rats, Lactoproteinum with Sorbitol, HAES-LX-5%

Full text: PDF (Ukr) 208K

  1. Osadchaya OI, Boyarskaya AM, Sheyman BS. Vliyanie enterosorbtsii na soderzhanie pro– i protivo–vospalitelnykh mediatorov pri tyazheloy termicheskoy travme. Vnutrishnya meditsina. 2008; 5-6: 76–8.
  2. Hoesel LM, Niederbichler AD, Schaefer J, Ipaktchi KR, Gao H, Rittirsch D, Pianko MJ, Vogt PM, J. Sarma V, Su GL, Arbabi S, Westfall MV, Wang SC, Hemmila MR, Ward PA. C5a–blockade improves burn–induced cardiac dysfunction. J Immunol. 2007; 178: 7902–10.
  3. Williams FN, Herndon DN., Suman OE, Lee JO, Norbury WB, Branski LK, Mlcak RP, Jeschke MG. Changes in cardiac physiology after severe burn injury. J Burn Care Res. 2011; 32: 269–74.
  4. Laxenaire MC, Charpentier C, Feldman L. Anaphylactoid reaction to colloid plasma substitutes: inci–dence, risk factors, mechanisme. A French multicenter prospective study. Ann Fr Anesth Reanim. 2009; 13: 301–10.
  5. Ljunstrom K. Colloid safety: fact and fiction. Ballieres Clin Anaesthesiol. 2007; 11: 163-77.
  6. Jeschke MG, Chinkes DL, Finnerty CC, Kulp G, Suman OE, Norbury WB, Branski LK, Gauglitz GG, Mlcak RP, Herndon DN. Pathophysiologic response to severe burn injury. Ann Surg. 2008; 248: 387–401.
  7. Regas FC, Ehrlich HP. Elucidating the vascular response to burns with a new rat model. J Trauma. 1992; 32 (5): 557–63.
  8. Ring J, Messmer K. Incidence and severity of anaphylactoid reactions to colloid volume substitutes. Lancet. 2007; 309 (8009): 446–69.