Biomedical subjects

A Aida

Publications and source records attributed to A Aida.

27 records · Page 2Linked to original sources

PubMed1992

[A case of hypereosinophilic syndrome exhibiting left ventricular systolic dysfunction].

A 16-year-old woman suffering from bronchial asthma since 2 years previously was admitted to the hospital because of high grade fever, dyspnea, skin eruption and arthralgia. Laboratory data revealed pronounced eosinophilia with elevated immunoglobulin E value. A chest X-ray film showed cardiomegaly with pulmonary congestion. Left ventriculograms showed diffusely reduced motion of the left ventricle (LV). Various clinical symptoms and laboratory data were resolved shortly after the administration of corticosteroids, but the LV dysfunction persisted for at least three months. Left ventriculograms 2 years later disclosed a marked improvement of the LV wall motion. In both the acute and the chronic phase, endomyocardial biopsy of both ventricles revealed non-specific histological findings comprising disarrangement of myocytes and interstitial fibrosis, suggesting post-myocarditis. This case was characterized by LV dysfunction possibly due to eosinophilic myocarditis associated with hypereosinophilic syndrome, and by its functional improvement with long-term corticosteroid therapy.

Adolescent↗

PubMed1991

[Effects of differently composed liposomes on pulmonary arterial pressure in sheep--involvement of pulmonary intravascular macrophages].

The authors previously reported that liposomes, when injected intravenously, produce transitory pulmonary hypertension with increased secretions of thromboxane A2 from activated intravascular macrophages that phagocytize liposomes in sheep. In the present study, we attempted to determine whether such responses were modified by the lipid compositions of the liposomes. Five different types of liposomes were prepared by reverse-phase evaporation. The liposomes used were composed of phosphatidylcholine (PC), cholesterol (CHOL), and either phosphatidylglycerol (PG-liposomes), phosphatidylserine (PS-liposomes), phosphatidylethanolamine (PE-liposomes), stearlyamine (SA-liposomes) or none (PC-liposomes). The net charges of PG and PS-liposomes were negative, SA-liposomes were positive, PE- and PC-liposomes were neutral. Each liposome was injected intravenously to obtain a pulmonary arterial pressure response. Arterial blood was sampled before and after liposome injections to measure thromboxane B2 concentrations. All liposomes, but not PC-liposomes, produced pulmonary arterial hypertension associated with increased arterial thromboxane B2 concentrations, irrespective of the net surface charge of the liposome. PG and PS-liposomes, both of which were negatively charged, showed different dose-response curves, the two different types of neutral liposomes showed different responses, and PC-liposomes produced a small increase in pulmonary arterial pressure. PE-liposomes produced marked increases in the pulmonary arterial pressure. From these results, the authors concluded that pulmonary arterial pressure responses to the liposomes are modified by the lipid compositions of the liposomes, and that this is not caused by the difference in the net charge of each liposome.

Animals↗

PubMed1991

[Effects of antiplatelet serum on the pulmonary intravascular macrophage].

Antiplatelet serum (APS) has been used to investigate the role of platelets in lung injury. However, the effect of APS on pulmonary intravascular macrophages (PIMs) is unknown. Therefore we investigated the effects of APS on PIMs. A bolus injection of APS raised pulmonary arterial pressure with the production of thromboxane. Fluorescence- and electronmicroscopy revealed that PIMs engulfed APS-platelets complexes after the APS injection. Repeated injections of APS increased the ratio of PIMs which engulfed platelets and the number of platelets in a PIM, but attenuated phagocytosis of liposomes by PIMs to decrease liposome-induced pulmonary hypertension and production of thromboxane. From the above data it was concluded that APS injection causes PIMs to engulf APS-platelets complexes, and that APS injection attenuates the phagocytosis of liposomes by PIMs, and thereby diminishes liposome-induced pulmonary hypertension and production of thromboxane.

Animals↗

PubMed1988