The Role of Cardiac Ganglia in the Prevention of Coronary Atherosclerosis: An Analytical Examination of Cholesterol-fed Rabbits

Background: The heart is innervated by the autonomic nervous system, which contributes to the control of the heart's rhythm and coronary circulation. It has been suggested that the cardiac fibers of the vagus nerve play important roles in controlling circulatory functions and in protecting against atherosclerotic pathologies in coronary arteries. Aims: To investigate the presence of atherosclerotic differences in the coronary arteries of cholesterol-fed rabbits by measuring the density of cardiac ganglia neurons. Study Design: Animal experiment. Methods: This study was conducted using 45 male rabbits. Over a period of 16 weeks, they were kept on an atherogenic diet of water ad libitum and high fat (8.6%) containing saturated fatty acids with 205 mg/kg of cholesterol (1%) per day. Then, their hearts were removed and examined by histopathological methods. Atherosclerotic plaques of the main coronary arteries were examined using the Cavalieri method. Atherosclerosis index values (AIVs) were estimated as the wall surface area/plaque surface area, and the results were analyzed with the Kruskal-Wallis and Mann-Whitney U tests. Results: While the average atherosclerosis index value was estimated to be ≤8% in 21 animals, the atherosclerosis index value was 9-20% in animals with minor plaque detection (n=11) and ≥20% in animals with major plaque detection (n=10). Increased atherosclerosis index values were more common in animals with low neuron densities than in animals with high neuron densities (p<0.017). Conclusion: The low neuron density of the cardiac ganglia in cholesterol-fed rabbits is associated with an increased atherosclerotic plaque incidence and volume.

Neurogenic Stress Cardiomyopathy Following Subarachnoid Hemorrhage Is Associated with Vagal Complex Degeneration: First Experimental Study.

BACKGROUND: Neurogenic stunned myocardium (NSM) is a devastating complication of subarachnoid hemorrhage (SAH). The most widely accepted mechanism in the pathogenesis of NSM and takotsubo cardiomyopathy is catecholamine-mediated direct myocardial injury. The aim of this study is to examine if there is any effect of sympathetic overactivity of the stellate ganglions on myocardial tissues, secondary to vagal complex degeneration in SAH-induced NSM. MATERIALS AND METHODS: This study was conducted on 25 New Zealand female rabbits. After the examination, all animals were assigned into 3 groups randomly: a control group (n = 5), a sham group (n = 5), and a study group (n = 15) that was subjected to experimental SAH with double injection of blood into the cisterna magna. After 7 animals exhibited NSM, all animals were killed. Their brains, vagal complexes, stellate ganglions, and hearts were extracted and examined by histopathologic methods. Degenerated nodose ganglion neurons and stellate ganglion neuron densities were compared with degenerated myocardial tissue/normal myocardial tissue ratios, and the results were analyzed with the Mann-Whitney U test. RESULTS: Three rabbits in the study group died immediately after the second injection of blood. NSM developed in 7 animals after 1 to 5 days, which was diagnosed with transthoracic echocardiography. Interestingly, the animals that developed NSM had more stellate ganglia neurons and more degenerated neuron densities of nodose ganglia (P < 0.001). CONCLUSIONS: NSM and takotsubo cardiomyopathy may be induced by vagal complex degeneration and sympathetic overactivity, which originated from more neurons, including stellate ganglia and more degenerated neuron densities of nodose ganglia.

Coronary fat embolism following subarachnoid hemorrhage: an experimental study.

BACKGROUND: Subarachnoid hemorrhage (SAH) can lead to neurogenic pulmonary edema (NPE), and chylomicron metabolism may be altered unfavorably in acute lung injury. This study aimed to investigate the possible effect of NPE on the development of coronary fat embolism. METHODS: This study was conducted on 27 rabbits, 5 of which were used as the control (n=5). Experimental SAH was induced in 15 of the animals by injecting homologous blood into the cisterna magna, and the remaining 7 animals were administered only isotonic saline solution (Sham, n=7) in the same manner under general anesthesia. After 21 days, all the animals were euthanized, and their hearts, lungs, and brains underwent histopathological examination. RESULTS: Six animals died of SAH during the experiment, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. The histopathologic findings revealed minimal changes in the lungs, heart, and brains of the surviving animals; however, an abundant amount of fat globules was found in the coronary arteries of the six nonsurviving animals. There was a meaningful difference between the number of occluded coronary arteries with fatty globules in the surviving and nonsurviving animals (P<.001). However, the difference between the survivors and the isotonic-saline-injected group was not meaningful (P>.05). Coronary fat embolism was an important mortality factor following SAH (P<.005). CONCLUSIONS: In SAH-induced NPE, the leakage of chylomicrons into the systemic circulation may lead to coronary fat embolism, which has not yet been reported in the literature.

Unraveling of the Effect of Nodose Ganglion Degeneration on the Coronary Artery Vasospasm After Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: Cardiac arrest is a major life-threatening complication of subarachnoid hemorrhage (SAH). Although medullary cardiocirculatuar center injury and central sympathetic overactivity have been suspected of initiating coronary artery spasm-induced cardiac arrest, we aimed to elucidate the effects of vagal ischemia at the brainstem on coronary vasospasm and sudden death in SAH. METHODS: Twenty-six rabbits were randomly divided into 3 groups. Control (n = 5); SHAM (n = 8), and SAH group (n = 13). Experimental SAH was applied by injecting homologous blood into the cisterna magna, and the SHAM group was injected with isotonic saline solution also in the cisterna magna., Twenty-one days after the injection, histopathologic changes of the neuron density of nodose ganglia, the vasospasm index values of the coronary arteries, and the electrocardiographic events were analyzed. RESULTS: Increased vasospasm index of the coronary arteries and degenerated neuron density of nodose ganglion were significantly different between animals with SAH, control, and SHAM groups (P < 0.005). If neurons of the nodose ganglia are lesioned due to ischemic insult during SAH, the heart rhythm regulation by vagus afferent reflexes is disturbed. CONCLUSIONS: We found that there is causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with SAH. Vagal pathway paralysis induced by indirect sympathetic overactivity may trigger coronary vasospasm and heart rhythm disturbances. Our findings will aid in the planning of future experimental studies and in determining the clinical relevance of such studies.

Preventive Role of Hilar Parasympathetic Ganglia on Pulmonary Artery Vasospasm in Subarachnoid Hemorrhage: An Experimental Study.

AIM: Pulmonary arteries are mainly innervated by sympathetic vasoconstrictor and parasympathetic vasodilatory fibers. We examined whether there is a relationship between the neuron densities of hilar parasympathetic ganglia and pulmonary vasospasm in subarachnoid hemorrhage (SAH). MATERIAL AND METHODS: Twenty-four rabbits were divided into two groups: control (n=8) and SAH (n=16). The animals were observed for 20 days following experimental SAH. The number of hilar parasympathetic ganglia and their neuron densities were determined. Proportion of pulmonary artery ring surface to lumen surface values was accepted as vasospasm index (VSI). Neuron densities of the hilar ganglia and VSI values were compared statistically. RESULTS: Animals in the SAH group experienced either mild (n=6) or severe (n=10) pulmonary artery vasospasm. In the control group, the mean VSI of pulmonary arteries was 0.777±0.048 and the hilar ganglion neuron density was estimated as 12.100±2.010/mm < sup > 3 < /sup > . In SAH animals with mild vasospasm, VSI=1.148±0.090 and neuron density was estimated as 10.110±1.430/mm < sup > 3 < /sup > ; in animals with severe vasospasm, VSI=1.500±0.120 and neuron density was estimated as 7.340±990/mm < sup > 3 < /sup > . CONCLUSION: There was an inverse correlation between quantity and neuron density of hilar ganglia and vasospasm index value. The low numbers and low density of hilar parasympathetic ganglia may be responsible for the more severe artery vasospasm in SAH.