Ultrastructure and histochemistry of rat myocardial capillary endothelial cells in response to diabetes and hypertension

Insufficient growth and rarefaction of capillaries, followed by endothelial dysfunction may represent one of the mostcritical mechanisms involved in heart damage. In this study we examined histochemical and ultrastructural changes inmyocardial capillary endothelium in two models of heart failure streptozotocin-induced diabetes mellitus (STZ) and NO-deficient hypertension in male Wistar rats. Diabetes was induced by a single i.v. dose of STZ (45 mg/kg) and chronic 9-week stage was analysed. To induce NO-deficient hypertension, animals were treated with inhibitor of NO synthase L-nitroarginine methylester (L-NAME) (40 mg/kg) for 4 weeks. Left ventricular tissue was processed for enzyme cata-lytic histochemistry of capillary alkaline phosphatase (AlPh), dipeptidyl peptidase IV (DPP IV), and endothelial NOsynthase/NADPH-diaphorase (NOS) and for ultrastructural analysis. In diabetic and hypertensive rats, lower/absentAlPh and DPP IV activities were found in focal micro-areas. NOS activity was significantly reduced and persisted onlylocally. Quantitative evaluation demonstrated reduction of reaction product intensity of AlPh, DPP and NOS by 49.50%,74.36%, 20.05% in diabetic and 62.93%, 82.71%, 37.65% in hypertensive rats. Subcellular alterations of endothelialcells were found in heart of both groups suggesting injury of capillary function as well as compensatory processes.Endothelial injury was more significant in diabetic animals, in contrast the adaptation was more evident in hypertensiveones. Concluding: both STZ-induced diabetes- and NO-deficient hypertension-related cardiomyopathy were accompa-nied by similar features of structural remodelling of cardiac capillary network manifested as angiogenesis and angiopathy.The latter was however, predominant and may accelerate disappearance of capillary endothelium contributing to myo-cardial dysfunction.

Brief report: Plasma oxytocin is lower in children with Asperger syndrome and associated with autistic trait attention to detail

Aim: Autism spectrum disorders (ASD) are described as a continuum of severity gradient of autistic symptoms diffusing through particular ASD diagnoses, however the biological correlates among individuals with the different ASD diagnoses slightly or considerably differ. Oxytocin (OT) has been implicated to play an important role in autism etiology. Lower OT levels have been previously found in children with infantile autism, however in a group of high-functioning autistic subjects, no differences have been shown compared to controls. Moreover, whereas the opposite patterns of OT associations with social measures have been found in children with infantile autism compared to healthy children, no associations have been found in individuals with high-functioning autism. We aimed to find out the plasma OT differences between separate group of children with Asperger syndrome (AS) and healthy children and the associations of OT with particular autistic traits in a group of children with AS. Methods: We included 9 children (m = 6, f = 3) with AS at the age 9 to 12 years and 9 age- and gender-matched controls. OT levels were analyzed by ELISA method. Autistic traits in children with AS were evaluated by Autism Spectrum Quotient (AQ), child and adolescent versions. Results: Children with AS had significantly lower plasma OT levels compared to healthy children. We found the significant negative correlation of OT level and AQ Attention to detail area score. Conclusion: In spite of the lower OT level in children with AS, which is also previously found in children with infantile autism, the pattern of OT associations with autistic traits more resembles the pattern in non-autistic population. Our preliminary results support the hypothesis of continuum within the ASD particular diagnoses in the terms of biological correlates.

Autoantibodies against G-Protein-Coupled Receptors Modulate Heart Mast Cells

Mast cells are believed to be involved in myocardial tissue remodelling under pathophysiological conditions. We examined the effects of autoantibodies against G-protein-coupled receptors in sera of patients with heart diseases on myocardial mast cells in the cultured neonatal Sprague-Dawley rat heart cells. Cells collected at day 3 and 10 of the culture were preincubated with autoantibodies against α-adrenoceptor and angiotensin Ⅱ ATl-receptor, agonist phenylephrine and angiotensin Ⅱ, and control IgG. The pretreated cultured cells were stained for selected mast cell markers tryptase, chymase and TNF-α The cultured cells were also processed for observation with electron microscopy. The autoantibodies-treatment of the 3-day cultured cells caused both increased intensity of immunofluorescence （p 〈 0.05） and their enlarged diameters of the mast cells when compared to age-matched ones. In contrast, the fluorescence of preincubated 10-day-old mast cells was decreased compared with controls （p 〈 0.01）. In control samples, the fluorescence of 10-day-old mast cells was significantly higher than that of 3-day-old ones （p 〈 0.001）. Results of electron microscopy examination demonstrated there was an increased granulation of treated 3-day-old mast cells, while a degranulation of mast cells at day 10 of application. The results suggest the modulation effect of the autoantibodies against G-protein-coupled receptors on mast cells, indicating a potential functional link between the autoantibodies against G-protein-coupled receptors and the mast cells in progression of heart disease.