[Serious neurological sequelae of a myocarditis]. / Eine Myokarditis mit gravierenden neurologischen Folgen.

HISTORY AND ADMISSION FINDINGS: A 39-year-old woman developed severe dyspnea subsequent to a respiratory tract infection. Furthermore an acute loss of vision occurred two days prior to admission. DIAGNOSES AND TREATMENT: Left ventricular dilatation due to myocarditis had led to decompensated cardiac insufficiency. The loss of vision (cortical blindness) had been caused by multiple brain infarctions in the posterior cerebral circulation due to basilary artery occlusion subsequent to cardiogenic embolism. During anticoagulation with heparin and antiplatelet drugs a large, space-occupying intracranial hemorrhage occurred in a posterior cerebral artery infarction. Emergency decompressive craniectomy was necessary. Heart insufficiency and left ventricular dilatation resolved later on. Hydrocephalus became obvious after cranioplasty, thus leading to shunt procedure. COURSE: After long-term neurorehabilitation, accompanied by several complications and two neurosurgical procedures, the patient gained more independence in her activities of daily living and quality of life. In the light of the initial burden of symptoms this course was rather favorable. CONCLUSION: Myocarditis as a cause for acute heart insufficiency has to be taken into account in young patients without any history of cardiac abnormalities and preceding infections. Cardioembolic stroke may be a consequence. Decisions in secondary stroke prevention should be made on an individual base with regard to medical guidelines as well as risk factors. Neurorehabilitation of sufficient length and quality can lead to functional recovery, improvement of independence in activities of daily living and quality of life, even if the initial situation seems worse and medical complications accompany the course.

Relaxin triggers calcium transients in human granulosa-lutein cells.

Although the peptide hormone relaxin is synthesized by the human corpus luteum in vivo, its potential to serve as a local factor in the regulation of luteal function is not clear. Using an enzyme-linked immunosorbent assay for human relaxin, we detected relaxin in the culture medium of human granulosa-lutein cells as early as after 6 days in culture. Moreover, 1 x 10(5) IU/l human chorionic gonadotropin stimulated relaxin release about fourfold during a 48-h incubation on culture days 6-8 (and 7-9), but not earlier (on days 1, 3 and 4). The stimulatory action of human chorionic gonadotropin on progesterone release was not influenced by relaxin, and relaxin alone was without stimulatory effect. However, human recombinant relaxin (between 0.1 and 12.5 micrograms/l) increased intracellular free Ca2+ basal levels to maximal peak levels exceeding 1000 nmol/l in about 64% of all tested cells (N = 168) with no obvious dependency on the culture day. The relaxin-induced Ca2+ signal was not affected by removal of extracellular Ca2+. As depletion of intracellular Ca2+ stores by ionomycin rendered the cells unresponsive to relaxin or diminished their ability to respond, these results point to an intracellular source of the Ca2+ signal. In summary, our data indicate the presence of a functional relaxin receptor on human granulosa-lutein cells, which is linked to Ca2+ release from intracellular stores.

Decavanadate displaces inositol 1,4,5-trisphosphate (IP3) from its receptor and inhibits IP3 induced Ca2+ release in permeabilized pancreatic acinar cells.

Inositol 1,4,5-trisphosphate (IP3) induced Ca2+ release in digitonin permeabilized rat pancreatic acinar cells is specifically inhibited by decavanadate. The Ca2+ release induced with 0.18 microM IP3 is half maximally inhibited with approximately 5 microM decavanadate. Complete inhibition is achieved with around 20 microM decavanadate. Removal of decavanadate from the permeabilized cells fully restores sensitivity towards IP3, indicating the reversibility of the inhibition. Oligovanadate, which inhibits ATP dependent Ca2+ uptake into intracellular stores, does not influence IP3 induced Ca2+ release. In order to reveal the mechanism underlying the effects of the different vanadate species, binding of IP3 to the same cellular preparations was investigated. We found that binding of IP3 to a high affinity receptor site (Kd approx. 1.2 nM) could be abolished by decavanadate but not by oligovanadate. With 0.5 microM decavanadate, IP3 binding was half maximally inhibited. A similar potency of decavanadate was also found with adrenal cortex microsomes which bind IP3 with the same affinity (Kd approx. 1.4 nM) as permeabilized pancreatic acinar cells. Labelled IP3 was displaced from these subcellular membranes with similar kinetics by unlabelled IP3 and decavanadate. The data suggest that the inhibitory action of decavanadate on IP3 induced Ca2+ release is a consequence of its effect on binding of IP3 to its receptor.

Effect of GTP and Ca2+ on inositol 1,4,5-trisphosphate induced Ca2+ release from permeabilized rat exocrine pancreatic acinar cells.

The effects of Ca2+ and GTP on the release of Ca2+ from the inositol 1,4,5-trisphosphate (IP3) sensitive Ca2+ compartment were investigated with digitonin permeabilized rat pancreatic acinar cells. The amount of Ca2+ released due to IP3 directly correlated with the amount of stored Ca2+ and was found to be inversely proportional to the medium free Ca2+ concentration. Ca2+ release induced by 0.18 microM IP3 was half maximally inhibited at 0.5 microM free Ca2+, i.e. at concentrations observed in the cytosol of pancreatic acinar cells. GTP did not cause Ca2+ release on its own, but a single addition of GTP (20 microM) abolished the apparent desensitization of the Ca2+ release which was observed during repeated IP3 applications. This effect of GTP was reversible. GTP gamma S could not replace GTP. Desensitization still occurred when GTP gamma S was added prior to GTP. The reported data indicate that GTP, stored Ca2+ and cytosolic free Ca2+ modulate the IP3 induced Ca2+ release.