The pathogenesis and progression of hypertensive heart disease are unclear; however, both involve a genetic predisposition and environmental influences. To test the role of exogenous factors, we examined the hearts of spontaneously hypertensive rats (SHR) exposed to noise stress and ethanol intake. Twenty-two SHR and nine normotensive Wistar rats (NWR) were continuously exposed to a 65 db, 4 and 250 Hz tone for 52 weeks. Twelve of these SHR aged 20-22 weeks were concomitantly given 20% ethanol in their drinking water up to week 52. Eight SHR and 12 NWR served as controls. We examined hemodynamic parameters, the cardiac configuration, the cardiac microvasculature, interstitial tissue, and ischemic myocardial lesions. We found that noise stress significantly increased the microvessel wall area, the number of microvessels with an outer diameter > 19 microns, the degree of cardiac fibrosis, and the extent of ischemic myocardial lesions in SHR, but not in NWR. These effects were all ameliorated and the diastolic blood pressure was lowered by the ingestion of ethanol. Cardiac weights and dimensions, heart rate and dp/dtmax were not influenced by either noise or ethanol intake. These results suggest that hypertensive heart disease in SHR can be aggravated by noise stress. Ethanol ameliorates these changes by mechanisms which remain to be explored.

Animals↗

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Causative role of coronary microvessels for the development and progression of chronic myocardial lesions in spontaneously hypertensive rats (SHR).

The pathomechanisms responsible for the development and progression of myocardial alterations in hypertensive heart disease are largely unknown. Using newly developed preparation and measuring procedures in 78 SHR and 82 controls aged 3-78 weeks, topological relations were detected between focal morphological appearances of chronic myocardial ischemia (fml.) and pathological microvessel (mv.) reactions characterized by morphometric signs of chronic contractions. The smallest ramifications are of particular pathogenic importance. A generalized peak of pathological mv. reactions between the 16th and 24th weeks is responsible for the development of first fml. The further progression of the area density of fml. from 1.26 +/- 0.85% (24th week) to 31.82 +/- 8.60% (78th week) is attributable to the further increase in pathological mv. reactions caused by organ-specific influences. The histological and morphometric findings suggest that the pathological mv. reactions are aggravated by their own effects at the local level.

Adenosine Triphosphatases↗

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Observations on the significance of the thyroid gland to the dentist.

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Dental Care↗

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Gift ethics.

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Conflict of Interest↗