PubMed Health⌕ Search

Biomedical subjects

M Rutczyński

Publications and source records attributed to M Rutczyński.

5 recordsLinked to original sources
PubMed1981

Cerebral blood flow and ultrastructural studies of the brain capillaries in the early state of hypertension in SHR+.

The 133Xe single bolus injection technique was used for measuring the cerebral blood flow (CBF) in spontaneously hypertensive (SHR) and normotensive rats. Their age was from 5 to 25 weeks and corresponded to the time before the initiation of the arterial blood pressure (BP) increase to the constant phase of hypertension. CBF in SHR 5 and 10 weeks of age was significantly higher than in all other groups being 155 +/- 7.2 and 151 +/- 9.3 ml/min/100 g, respectively. At 15 weeks of age the localization of the reactive products of ATP and CTP became scanty and spread over the endothelial cytoplasm. Further, at 25 weeks an enlarged number of empty pinocytic vesicles and astrocytic foot processes filled with flocculent electron dense material was found. These data suggest that the initial high CBF preceding the increase of BP can initiate the irreversible disorder of endothelial cells in brain capillaries.

Animals↗
PubMedDate not supplied

Tissue catecholamine concentrations in spontaneously hypertensive rats.

Tissue concentrations of noradrenaline (NA), dopamine (DA) and adrenaline (A) were compared in spontaneously hypertensive (SHR) and normotensive (NCR) rats, aged 1, 3, 8, 14 and 24 weeks The organs analyzed included the brain, subdivided into prosencephalon and rhombencephalon, heart, adrenal glands and kidney. Brain catecholamines were significantly lower in SHR than in NCR, and the difference appeared already at the age of 3 weeks. Concomitant increase was found in the adrenal NA and A concentrations of the SHR. Concentration of NA in the heart decreased in the SHR following onset of hypertension. It is concluded that the diminished NA, DA and A concentrations in the brain as well as the augmented adrenal NA and A levels in the SHR may be causally related to the development of hypertension, while the heart NA level reflects the secondary, hypertension -- related changes.

Adrenal Glands↗
PubMedDate not supplied

Metabolism of 3H-catecholamines in the heart and adrenals of spontaneously hypertensive rats (SHR) after running stress.

The metabolism of 3H-catecholamines after i.p. injection of 3H-tyrosine was studied in the heart and adrenals of spontaneously hypertensive (SHR) and normotensive Wistar (NCR) rats at rest and following running stress. In the heart of 8-week-old NCR a sharp stress-induced increase of the levels of 3H-A and 3H-DA with an elevation of the levels of their metabolites was observed. In contrast, there was no stress-related change in the levels of 3H-NA, 3H-A and 3H-VMA in the hearts of young SHR, while the 3H-DA level, though increased after stress, remained still lower than in the age-matched NCR. In the phase of established hypertension (24 weeks) lower levels of 3H-NA and 3H-A in the heart already present at rest, as compared with NCR, remained lower after stress but the elevation of the level of their metabolites 3H-VMA and 3H-MA, was similar in both strains. In the adrenals of 8-week-old SHR the basal 3H-A level was already higher than in NCR. Stress provoked a marked decrease of adrenal 3H-A accompanied by increased formation of 3H-MA and an increase in the levels of 3H-NA and 3H-DA, more pronounced in SHR than NCR. In the phase of advanced hypertension a further elevation of 3H-A and 3H-MA and an increase of basal 3H-DA level in the adrenals were found at rest. The decreased levels of 3H-catecholamines in the heart of stressed young and non-stressed older SHR may indicate an increase in their rate of release and/or their impaired synthesis. An increased basal level of 3H-A in the adrenals of SHR concomitant with the development of hypertension, may reflect an increased synthesis and/or decreased release, as evidenced by the proportionally lower increase of its extraneuronal metabolite 3H-MA. The adrenal response to stress, more intense in SHR than in NCR, may be considered as due to enhanced release of 3H-A from the gland.

Adrenal Glands↗