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Purpose: To investigate whether leptin acts directly on the anterior hypophysis by influencing gonadotropin secretion in vivo., Materials and Methods: Cycling female rats were catheterised for frequent blood sampling and were either fasted or allowed free access to food. Stereotactic lesion of the medial preoptic area (MPOA) of the hypothalamus was performed in order to eliminate gonadotropin releasing hormone (GnRH) production. Leptin was administered at a dose of one mg/kg i.v. and blood samples were taken just before leptin administration and then after 30, 60, 90, 120, and 180 minutes. Plasma gonadotropin levels were determined. With completion of sampling, the brains were removed and the localisation of the lesions was verified histologically., Results: Leptin at one mg/kg induced an increase in luteinizing hormone (LH) secretion in fasting rats, both in those with a lesion and those with intact medial preoptic area with a peak occurring 90 minutes after infusion. The augmenting effect was more prominent when the hypothalamus was intact. There was no effect in fed animals with or without lesion. Similarly, no effect was observed on follicle stimulating hormone (FSH) levels in any of the experimental groups., Conclusions: Leptin acts directly on the hypophysis enhancing LH but not FSH secretion. Nutritional state influences leptin's effect on the hypothalamus and the hypophysis.

Our study aims to investigate the effect of a low-dose pioglitazone regimen on bone mineral density and bone formation-resorption markers in control and diabetic rats. Wistar rats were divided into 4 groups: non-diabetic controls, control rats receiving pioglitazone (3 mg/kg), streptozocin-treated diabetic rats (50 mg/kg), diabetic rats treated with pioglitazone (3 mg/kg). The duration of the experiment was 8 weeks. Diabetes in our rats was associated with weight loss, increased urinary calcium excretion and reduced plasma osteocalcin levels. Diabetes mellitus did not affect bone mineral density. Pioglitazone administration had no impact on bone formation and resorption markers levels and did not modify bone mineral density in the four studied groups. Pioglitazone at the 3 mg/kg dose was not associated with significant skeletal complications in our experimental model.

Both the forward and inverse problems of electrocardiography rely on the precise modelling of the anatomic and electrical properties of the thoracic tissues. This, in turn, requires good knowledge of the electrical anisotropy as well as conductivity inhomogeneity of the heart, lungs and the rest of the thorax. Cardiac electrical anisotropy is related to its microstructure (fibre length, density and orientation). We hereby present detailed three-dimensional (3D) meshes of the thorax and heart, using image data from contiguous 2D magnetic resonance (MR) imaging slices as well as a realistic 3D cardiac fibre orientation model that derives its data from high-resolution ex vivo human heart MR images and from histology specimens of heart tissue. Using specific software, we integrated the 3D thorax and heart meshes in one that addresses the related modelling requirements for the solution of the forward and inverse problems of electrocardiography.

Sepsis and septic shock are great challenges for the doctors who treat critically ill patients. A big part of the scientific community is performing researches about the pathophysiology and treatment of this clinical problem. The endothelium has a very significant role in the alterations that sepsis causes especially to the circulatory system. The disorders of the normal function of the endothelium include derangement of the vascular tone, increase of endothelium permeability, activation of the endothelial cells, production of various regulators and disorders of coagulation. Nitric oxide is the modulator that mediates the action of most vasodilators. The overproduction of nitric oxide during sepsis is possibly the most important cause of the vasopressor-resistant hypotension which characterizes septic shock. The levels of natriuretic peptides are also increased. These peptides act through several ways on the circulatory system both peripherally and directly on the myocardium. Endothelin, vasopressin, adrenomedullin and prostacyclin are vasoactive substances that have their own role in the regulation of the circulatory system during sepsis.

Background/aims: We studied the effect of the combined treatment with an angiotensin-converting enzyme (ACE) inhibitor (ramipril) and eplerenone compared with ramipril alone in streptozocin-induced diabetic rats., Methods: Wistar rats were divided into 4 groups: nondiabetic controls, streptozocin-treated diabetic rats (50 mg/kg), diabetic rats receiving ramipril (1 mg/kg) and diabetic rats treated with the combination of ramipril (1 mg/kg) and eplerenone (100 mg/kg) for 8 weeks. Our model produced early-stage diabetic nephropathy., Results: The diabetic rats developed polyuria, proteinuria, hyperfiltration (assessed by creatinine clearance) and histopathological evidence of renal injury including glomerular hypertrophy and mesangial expansion. Ramipril reduced proteinuria but its combination with eplerenone did not produce any greater benefit. Both treatment approaches prevented glomerular hypertrophy. Addition of eplerenone to ramipril prevented glomerular hyperfiltration., Conclusion: Whether eplerenone should be used in addition to an ACE inhibitor or an angiotensin receptor blocker at an early stage of diabetic nephropathy remains questionable., (Copyright 2010 S. Karger AG, Basel.)

Aortas from Watanabe heritable hyperlipidemic rabbits show in vitro impaired vasodilatory response to atrial natriuretic peptide (ANP) during atherosclerosis progression. To test a similar reaction in vivo, the effect of ANP administration on pulse wave velocity (PWV, index of aorta stiffness) was investigated in 10 normal and 10 cholesterol-fed (2% cholesterol-loaded feeding for 4 weeks) anesthetized male New Zealand White (NZW) rabbits. Invasively taken carotid and femoral blood pressures (BP) were recorded, simultaneously with ECG, and blood samples for ANP measurement (by RIA) were taken at 0 min and 20, 40, 60 min following an intravenous 20-min administration of either 0.2 microg kg(-1)min(-1) hANP in 5 ml normal saline or only 5 ml saline. Mild to moderate atherosclerosis was found in ascending aorta. BP decreased by ANP only at 20 min in both groups, whereas only in cholesterol-fed rabbits the borderline (p=0.09) increased at 0 min PWV was lowered (p=0.008) in all recording times. With any degree of increase of systolic BP (SBP) PWV increased less in ANP receivers. Atherosclerosis and SBP were the most important determinants of PWV and the effect of ANP was independent of confounding factors. It is concluded that short-term ANP administration in doses to achieve levels approximately threefold the pretreatment ones in normal and mildly to moderately atherosclerotic anesthetized NZW rabbits, causes an improvement of aorta stiffness only in atherosclerotic rabbits.

Objective: The aim of this study was to evaluate the changes in the levels of vasoactive eicosanoid hormone-like substances PGE2, PGI2 and TXA2 in hemodialysis (HD)patients who were following a long-term physical training program during the hemodialysis session., Design: A total of 50 patients with Chronic Kidney Disease (CKD) (stage 5)on hemodialysis and 35 healthy individuals who served as controls (C) were evaluated. The 50 CKD patients were divided into two groups: the HD group consisted of 31 patients who received usual care without any physical activity during the hemodialysis sessions, while group HD/Exer included 19 patients who followed a program of physical exercise for six months. Plasma levels of PGE2, 6-Keto-PGF1alpha (the stable derivative of PGI2) and TXB2 (the stable derivative of TXA2) were measured by reliable enzymo-immunoassay methods (EIA) in HD and HD/Exer patients before and after the hemodialysis sessions as well as in the group of C., Results: The plasma levels of PGE2 and 6-keto-PGF1alpha in group HD Exer/before patients were higher than those in group HDbefore (20.39+/-5.82 and 1449.19+/-553.41 vs 17.68+/-5.36 and 1295.10+/-384.43 pg/ml, p=0.044 and p=0.067, respectively), while the plasma levels of TXB2 were lower in HD Exer/before patients compared to HDbefore(499.76+/-67.51 vs 608.01+/-80.23 pg/ml, p=0.041). The plasma levels of PGE2 and 6-keto-PGF1alpha in group HD Exer/after patients were significantly higher compared to those in HDafter patients (23.01+/-5.70 and 1618.19+/-435.07 vs 16.57+/-4.97 and 1005.44+/-317.16 pg/ml, p<0.001 and p<0.040, respectively). However, significantly lower values in the plasma levels of TXB2 in HD Exer/after compared to HDafter patients (363.10+/-51.91 vs 439.75+/-62.34 pg/ml, p=0.030) were detected. As expected, PGE2 and 6-keto-PGF1alpha values were lower in C than in the groups of patients with CKD., Conclusions: The data indicate that exercise training during HD exerts a beneficial effect on the levels of the vasoactive eicosanoid hormone-like substances in patients on HD.

In cardiac transplantation has been recognized some "abnormalities" in recipient ECG. We investigated the influence of heart geometrical position within the chest cavity as well as somatometric parameters on body surface torso potentials. Two control patients with different Body Mass Index (BMI) were undergone a chest MRI scan. Using specific software we created two tetrahedral meshes that could be applied in our study. A post-mortem human heart was undergone a MRI scan and we also created its tetrahedral mesh. Using second software we extracted the heart mesh of control's torsos and we replaced them with the mesh of the post-mortem heart. The last program also assessed the influence of heart (re)positioning within the thorax, on the body surface potentials. The Finite Elements Method (FEM) was used to solve the forward electrocardiographic problem for both torsos, under the assumption that all the ventricular myocardium of the one post-mortem heart was excited. FEM was also applied in simulating Body Surface Potential Mapping (BSPM) on the first thorax torso for nine different heart positions. For BSPM, FEM has been applied on Poison equation. The results show higher BSPM in patient with lower BMI and significant changes in BSPM when heart was rotated round its long axis. Conversely, the heart shifts (long x- or y- axis) didn't cause significant changes on simulated BSPM.

Hypoxic-ischaemic (HI) encephalopathy is a severe complication of perinatal asphyxia and remains a frequent cause of a variety of brain disorders with long-term effects on the patients' life. The associated brain damage is strongly related to the toxic action of excitatory amino acids, especially glutamate and aspartate. Lamotrigine is an anti-epileptic drug that blocks the voltage-gated sodium channels of the presynaptic neuron and inhibits the release of glutamate. In the present study a well-established model of perinatal asphyxia in 7-d-old rats was used to investigate the effect of lamotrigine on HI-induced damage to different hippocampal brain structures, since disruption of this brain area is thought to play a key role in schizophrenia and epilepsy. Therefore, a combination of ischaemia, induced by unilateral occlusion of the left common carotid artery, followed by exposure to a 1-h period of hypoxia, was carried out in neonatal 7-d-old rats. Immediately after the insult, lamotrigine was given i.p. The histological outcome in the hippocampus was conducted and the tissue levels of glutamate, aspartate, GABA, and glutamine in the same area were determined. A remarkable reduction of HI-evoked damaged neurons in most of the investigated hippocampal regions was noted after lamotrigine administration. Furthermore, lamotrigine decreased the asphyxia-induced hippocampal tissue levels of glutamate and aspartate. Immediately after perinatal asphyxia GABA levels were enhanced, while levels of glutamine were decreased. Lamotrigine administration did not affect either GABA or glutamine levels. These results suggest a neuroprotective effect of lamotrigine in this particular animal model of neonatal HI encephalopathy.

Background: Previous studies have shown that elastic properties of the aorta decrease, while left atrial dimensions, the contribution of left atrial systole to left ventricular filling, and left ventricular mass increase with age. In most studies, however, aortic function, and ventricular and atrial parameters were performed in different populations, and thus, the earliest manifestation of aging in the cardiovascular system is not known. The present study was undertaken to define the earliest cardiovascular abnormality(ies) occurring in the cardiovascular system with age., Patients and Method: In 181 normotensive subjects (147 females and 34 males) age 22-64 years, left ventricular mass, volumes, function and work (echocardiography and blood pressure), left atrial volumes and stroke volume (biplane area-length method by echo), pulse wave velocity (PWV) (carotid to femoral artery, Doppler), and left atrial kinetic energy were measured simultaneously: left atrial kinetic energy = 1/2 mv2, where m = left atrial stroke volume x 1.06 (blood specific gravity), v = transmitral A wave velocity. Regression analyses were performed to correlate all measured cardiovascular parameters with age., Results: Pulse wave velocity (r = 0.51), left atrial kinetic energy (r = 0.42), and A wave velocity (r = 0.38) were correlated to age, while left ventricular mass, function and work were not. Multiple regression analysis among ten clinical and echocardiographic parameters demonstrated that only age contributed independently to pulse wave velocity; only age and pulse wave velocity were contributed independently to left atrial kinetic energy; and only age contributed independently to A wave velocity., Conclusions: The data demonstrate that age-related alterations in aortic function and left atrial work (left atrial kinetic energy) can be defined prior to changes in left ventricular structure and systolic function. Simultaneous studies of left atrial, left ventricular, and aortic function are required to better understand the effect of aging on the cardiovascular system.