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Question: The experiments aim to answer the question whether early changes in the lamina elastica interna of peripheral arteries causing consecutive plasmatic insudation of the vascular wall ("plasmatic vasculosis" according to GOLDBLATT) can be visualized by electron microscopy. Demonstration of early lesions in the elastica interna would facilitate the interpretation of structural changes in the arterial periphery during acute hypertension and its consecutive symptoms.

In 55 rats, not accustomed to the process of blood pressure measurement and given daily doses from 1.25 - 10.0 mg angiotensin in depot form for up to 3 days, as much as 70% of the animals died of circulatory failure. Blood pressure increase was either absent or was very low after low doses. Histologically, the myocardium revealed focal destruction of muscle fibres with mesenchymal cell proliferation in many places; the epithelium of numerous renal tubuli was changed hydropically; the liver showed focal necroses of the parenchyma; the adrenal cortex showed stress reactions, and the arterioles of the splanchnic area -- changes of the plasmatic vasculose from the 3rd day of experiment. By contrast, in 51 rats accustomed to the measuring process prior to the experiment and given high doses of angiotensin, only moderate blood pressure rise and scattered cases of death (4%) occurred, low doses caused a strong blood pressure elevation. With otherwise equal histologic organ diagnoses, liver necroses were absent, except for two cases. This differential response of the two animal groups to varying angiotensin doses and the pathogenesis of the changes observed are discussed.

The experiments aim to answer the question whether early changes in the lamine elastica interna of peripheral arteries causing consecutive plasmatic insudation of the vascular wall ("plasmatic vasculosis" according to GOLDBLATT) can be visualized by electron microscopy. Demonstration of early lesions in the elastica interna would facilitate the interpretation of structural changes in the arterial periphery during acute hypertension and its consecutive symptoms.37 male albino rats, 3 to 4 1/2 months of age, body weight: 250 to 350 g. Controls 19 rats of similar age and body weight, 6 of which were injected the carrier substance of depot angiotensin PVP (VEB Berlin-Chemie). The test arrangement is represented in table 1. 3 hours to 10 weeks after starting the treatment different groups of experimental animals were sacrificed. Several animals were administered tracer substances for demonstration of early disturbances in permeability (ferritin: 20 to 40 mg per 100 g body weight, 3 to 60 min ante mortem; charcoal: 10 to 20 mg per 100 g body weight diluted in 1.5 to 3.0 ml of distilled water 15 to 30 min ante mortem). Electron microscopic investigations were carried out in arterioles of 15 mum to 100 mum in diameter which had been removed from the stomach, colon, jejunum, pancreas, mesenterium, partially from the brain and heart, in cases also from the lungs. For comparable specimens with respect to early ultrastructural changes only such tissue sections were selected that were light microscopically free from lesions. Preparation for electron microscopy was done in the common way.in light microscopically intact arterioles of all 3 groups (see table 1) the well-known disturbances of intimal permeability were electron microscopically observed already after 3 hours of experimentation. These changes occur always in the splanchnic organs and in the heart. Contrarily they do not regularly occur in the brain. In rats impaired by experimental neurosis (group III) the disturbances in perfusion of the intima recede, the consequences of enhanced metabolix activity in the media predominate in the sence of a "non-specific mesenchymal reaction" (HAUSS et al. 1964). However, it should be taken into consideration that this enhanced metabolic activity and cell proliferation may actually warrant the relative stability of the elastic barrier observed in this experimental group. In rats with nephrogenic and angiotensin-induced hypertension the experiments result in principally similar lesions of the lamina elastica interna originating from the vascular lumen. The diverging results in rats impaired by neurotically conditioned disturbed regulation of the blood pressure speak in favor of a prevailing reaction of the media at well preserved structures of the lamina elastica interna.