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Biomedical subjects

A Gruszka

Publications and source records attributed to A Gruszka.

At least 19 recordsLinked to original sources

The effect of selective sst1, sst2, sst5 somatostatin receptors agonists, a somatostatin/dopamine (SST/DA) chimera and bromocriptine on the "clinically non-functioning" pituitary adenomas in vitro.

The aim of the work was to investigate the effects of somatostatin analogs acting selectively on sst1 (BIM-23926), sst2 (BIM-23120) and sst5 (BIM-23206) receptor subtypes on the viability of "clinically non-functioning" pituitary adenomas in vitro. The effects of native SST (SST-14), a SST/DA chimera (BIM-23A387) and a D(2)-dopamine receptor agonist bromocriptine (BC) were also examined. The study was performed on 10 surgically removed pituitary macroadenomas, diagnosed before surgery as "non-functioning". A part of each tumor was mechanically dispersed and digested with collagenase to isolate the tumoral cells. Another part of each tumor was fixed, embedded in paraffin and immunostained to reveal the pituitary hormones and SST receptor subtypes (sst1, sst2A, sst2B, sst3, sst4, sst5). The tumoral cell suspensions were incubated for 24 h with the substances mentioned above. The quantity of viable cells was estimated using the EZ4U system. The results were compared with the immunohistochemical evaluation of the hormonal profile of adenoma and the sst receptor subtype immunoreactivities present. The findings indicate that selective sst1, sst2 and sst5 receptors agonists, SST/DA chimera and D(2)-dopamine receptor agonist bromocriptine affect the viability of some, but not all, "clinically non-functioning" pituitary adenomas in vitro. The most effective was bromocriptine. The investigated somatostatin analogs including SST/DA chimera exerted roughly similar inhibitory effects. Further studies are needed to fully evaluate the potential usefulness of these compounds in the pharmacological treatment of "non-functioning" pituitary tumors.

Adenoma↗

Anti-tumoral action of octreotide and bromocriptine on the experimental rat prolactinoma: anti-proliferative and pro-apoptotic effects.

OBJECTIVES: The purpose of the study was to compare the effects of bromocriptine (BC) - D-2 receptor agonist and octreotide (OCT) - somatostatin analog on the tumor weight, prolactin (PRL) secretion, cell proliferation and apoptosis in the diethylstilboestrol (DES)-induced rat prolactinoma. MATERIAL AND METHODS: Male four-week Fisher 344 rats were used in the experiment. The animals were implanted subcutaneously (s.c.) with capsules containing DES. Six weeks after the implantation the rats were given OCT (2 x 25 microg/animal/24 h s.c.) or BC (3 mg/kg b.w./24 h s.c.) for 10 days. The incorporation of bromodeoxyuridine (BrDU) into the tumor cell nuclei was used as an index of cell proliferation (labeling index - LI). The labeling of nuclear DNA fragmentation according to the TUNEL method was considered as an index of apoptosis (AI). PRL was measured by radioimmunoassay (RIA). RESULTS: It has been found that OCT and BC significantly decreased the tumor weight and LI of tumor cells to the same extent. Both OCT and BC suppressed the PRL levels, but the inhibitory effect of BC was stronger than that of OCT. BC and OCT significantly enhanced the number of apoptotic cells in the tumor, but the pro-apoptotic effect of BC was more pronounced. The joint treatment exerted additive effects on tumor mass reduction, PRL secretion and cell proliferation, but OCT attenuated the pro-apoptotic effect of BC. CONCLUSIONS: Summing up, both OCT and BC inhibit PRL secretion and cell proliferation. The anti-tumoral action of BC, and to some extent the action of OCT, is also connected with induction of apoptosis.

Animals↗

Angiotensins II and IV stimulate the rat adrenocortical cell proliferation acting via different receptors.

OBJECTIVE: The effects of angiotensins II (Ang II) and IV (Ang IV,3-8 fragment of angiotensin II) on the adrenocortical cell proliferation have been investigated in the rat. METHODS: The male adult Wistar rats were injected subcutaneously with saline, captopril or captopril together with either Ang II or Ang IV. A part of animals received additionally losartan - an antagonist of AT1 subtype of angiotensin receptors. Bromodeoxyuridine (BrDU) incorporation into cell nuclei was used as the index of cell proliferation. RESULTS: It was found that both Ang II and Ang IV increased the BrDU labeling in the adrenal cortex of captopril-pretreated rats. This effect involved mainly the zona glomerulosa cells. The proliferogenic effect of Ang II was blocked by AT1 receptor antagonist losartan. In contrast, losartan did not block the effect of Ang IV. CONCLUSION: Both Ang II and Ang IV stimulate the adrenocortical cell proliferation in the rat, but they act via different receptors - AT1 in the case of Ang II and non-AT1 (probably AT4) in the case of Ang IV.

Adrenal Cortex↗

[Transient ST segment elevation after electrical cardioversion of atrial fibrillation].

In 50 patients (30F, 20M), aged 47 +/- 8 who underwent artificial heart valve implantation, the transient ST segment elevation (uST) of at least 0.1 mV on ECG immediately after electrical cardioversion (KE) of atrial fibrillation (MP) was evaluated. uST of 2 +/- 0.7 mV, lasting for 1.5 +/- 0.8 minutes was observed in 52% of cases (15F, 9M). Occurrence of uST correlated significantly with the following parameters: enlarged left atrium, high values of energy delivered during KE, history of more than cardiosurgical operation. Inversely, uST did not depend on duration of MP, efficacy of KE, BMI and the time span between the operation and KE.

Adult↗