HISTOLOGICAL CHANGES IN MYOCARDIUM OF RATS BECAUSE OF EXPERIMENTALLY FORMED ISCHEMIA

Abstract

Introduction. In treatment practice of small animals cardiac diseases occupy a significant portion of cases among the diseases of internal organs. The total number of heart disease cases among small animals is as a whole about 10%. Unlike people, for pets myocardial infarct is rarer phenomenon, but is of the same threat to the health and quality of life

Thrombosis or embolism of the coronary arteries provoke the creation in heart of ischemia zone and necrosis of cardiomyocytes, which within the time are replaced by connective tissue scar. Due to their anatomic characteristics and, accordingly, functions, the damaged myocardium never recovers its original structure. This causes serious consequences because of abnormal heart function and the development of such complications as heart failure, arrhythmia, aneurysm, myocardium rupture etc.

Currently the search for treatment methods of myocardial ischemia and its consequences is still in process. As an important step in pathology studying is the correctly formed experimental model, so it is important to determine the optimal method of myocardial ischemia formation with changes typical for the given pathology.

Objective. To determine the best method of experimental myocardial ischemia formation and to examine the dynamics of microstructural changes in it for further study of treatment modes of this pathology.

Methods. Female of laboratory rats weighing 210-250gr, aged 3 months were used for research. Animals were divided into three groups: 1st included animals with ligated left coronary artery, 2^nd  - with coagulated left coronary artery, 3rd was the control one. All manipulations with animals were performed under general anesthesia for what 2% solution of sodium thiopental with the dose of 4 mg per 100 g of live weight was injected once intraperitoneally.

To determine the optimal method of modeling myocardial two ways were used. In the first experimental group myocardial was modeled by imposing ligatures. The needlewas approached to the front descending branch of the left coronary artery at approximately 3mm from the apex of the heart and then the ligature was tightening. In the second group myocardial was modeled by artery coagulation in the abovementioned place by hot needle, cessation of blood circulation occurred due to stenosis of the artery under high temperature.

Sampling of tissue for histological studies while examining of myocardial ischemic was performed at 7, 12, 17 and 25 day. In order to investigate histostructure of infarction, sections were stained with hematoxylin and eosin for detecting connective tissue, according to the method of Van Gieson.

Results. To determine the optimal method of myocardial ischemia formation with subsequent development of ischemic necrosis of infarction area such as heart attack, two methods of forming this disease were learned.

We found that full changes, typical for myocardial ischemia with subsequent necrosis of myocardial areas, can be achieved by vessel ligation, so in further studies of ischemia course this method was used.

The basis for further histological studies was the presence of the following macroscopic changes: an increase in heart size relative to the norm, the presence of aneurysms, ischemia visible area (slightly lighter and denser texture than normal) drily surface section.

7 days after myocardial infarction modeling there were inflammation, infiltration of  tissuearea damaged by macrophages, white blood cells and the formation of granulation tissue as barrier around the site of injury. In the area of ischemia there were observed miotsytoliz of cardiomyocytes and coagulation necrosis. Simultaneously the increased activity of stromal component was observed.

12 days after the formation of myocardial infarctionintensification, the formation of scar tissue and collagen adjournment without formation of collagen fibers were observed. Outside infarction area the swelling cardiomyocytes and sludge formation of red blood cells in the capillaries were observed. In some parts of the infarct zone some islands of necrotic cardiomyocytes were observed.

After 17 days the initial stages of connective tissueformation in the area of pathological process was observed. The presence of  collagen fibers was observed in the central areas of infarction. Intracellular swelling of cardiomyocytes was observed outside the area of damage.

25 days after the myocardial infarction formation the activeformation and structuring of connective tissue was observed in the area of damage. Pathological process captured not only the infarction zone but also adjacent areas, which also were showing signs of progressive peripheral myocardial infarction. Scar tissue is heterogeneous (Figure 12), indicating non-momentary development.

During the course of myocardial infarction its area was increasing, that presumably may occur due to compression of blood vessels by swollen damaged cardiomyocytes.

Conclusions

1. The best method of myocardial ischemia formation in rats is left coronary artery ligation.

2. Myocardial ischemia, modeled by ligation imposing on coronary artery, is followed by the development of classical picturing of coronary heart disease.

3. The process of myocardial infarction course is complicated with the expansion of ischemiczone, apparently due to swelling of damaged cardiomyocytes and squeezing  by them the vascular of zone, outside the infarction.

4.Studying of microstructural changes in myocardial on the background of ischemic infarct allows to determine the stages of the process.