Histological Changes

As result of the adrenergic storm, tissue injury has been observed in the experimental animal and in organs procured from brain-dead organ donors. The injury pattern is widely distributed through the examined organs and follows the pattern observed in conditions in which ischemia and reperfusion play an important role. Thus, the role of calcium overload and oxygen free radicals are interrelated to the Autonomic storm.3

In the heart, under light microscopy, approximately 75% of the experimental animals exhibited various degrees of focal myocyte necrosis (Fig. 3.4). This has

Fig. 3.4. Light microscopy of the heart following induction of brain death in the baboon. The subendocardium (Left) has the histological appearance of an acute myocardial infarct. There is myocyte necrosis, edema and interstitial hemorrhages. H & E X 100.

been observed mainly in the sub-endocardial area but does occur in both the atria and ventricles.7,8 The myocyte necrosis assumes the form of contraction bands, coagulative and myocytolysis. There is also mononuclear cell infiltrate and edema surrounding the necrotic myocyte, on occasion, resembling the appearance of acute rejection.11,12

Contraction band necrosis has also been observed in the conduction tissues such as in the AV node and the bundle of His. Histological examination of the lamina media of the coronary arteries has shown the presence of smooth muscle contraction bands and intracellular calcium deposits.

Examination by electron microscopy of the donor heart has shown sarcom-eres in a hypercontractile state as well as disrupted organelles (Fig. 3.5). The mitochondrial injury consists of various degrees of integrity disruption affecting the membranes, matrix, cristae and deposition of electron dense material evolving towards a secondary lysosome.13

In the lungs, approximately 30% of examined animals subjected to experimental brain death had pulmonary edema rich in protein (Fig. 3.6). Hemorrhages were also present in the alveolar wall and in the alveolar spaces. Endothelial capillary disruption was also observed.10

Possibly the most striking findings were detected by electron microscopy in the kidney (Fig. 3.7). The glomerular structure remained preserved. However, examination of the glomerulus from kidneys procured from brain-dead animals had significant engorgement and the capillary spaces were filled with red blood

Fig. 3.5. Electron microscopy of a rabbit heart following induction of brain death. The sarcomeres are in a hyper-contractile state. Some are stretched and disrupted. There is scalloping of the sarcolemma and electron dense deposits in the mitochondria. Uranyl acetate and lead citrate x 11.000.
Fig. 3.6. Light microscopy of a baboon lung following induction of brain death. There is disruption and thickening of the alveolar septa as well as interstitial hemorrhages. Protein rich deposits within the alveolar spaces are observed. H & E x 100.

Fig. 3.7. Electron microscopy of the renal cortex from (A) alive and following brain death (BD) induction (B) in the rabbit. Significant glomerular abnormalities are observed: Following BD, there is significant red blood cells entrapment in the glomerular capillaries and marked reduction of the capillary diameter. This may result from a hyper-contractile response of the afferent and efferent glomerular arterioles to the catecholamine storm. Uranyl acetate X 5.500.

Fig. 3.7. Electron microscopy of the renal cortex from (A) alive and following brain death (BD) induction (B) in the rabbit. Significant glomerular abnormalities are observed: Following BD, there is significant red blood cells entrapment in the glomerular capillaries and marked reduction of the capillary diameter. This may result from a hyper-contractile response of the afferent and efferent glomerular arterioles to the catecholamine storm. Uranyl acetate X 5.500.

cells. These changes are possibly directly related to arteriolar capillary spasms which occurred during the sympathetic storm. Other changes were observed at the mitochondrial level, but in lesser degree than in the heart.14

The liver under light microscopy shows frequent fatty deposits and loss of glycogen. Electron microscopy again shows preserved nuclear and membrane structure. However, scattered mitochondrial injury was noted, similar to that observed in the kidneys.

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