Chronic heart failure has become a significant health problem. Cardiac surgery has an important role in the treatment of patients with heart failure. There are traditional surgical techniques in cardiac surgery – coronary revascularization, valve surgery, ventricular reconstructive surgery as well as new surgical techniques – cardiac support device (CorCap), mechanical circulatory support and resynchronization therapy. Cardiac surgery has a definitive role in the treatment algorithm for chronic heart failure., J. Pirk., and Obsahuje seznam literatury
To evaluate the role of chloride in the pathogenesis of salt-dependent deoxycorticosterone (DOC) hypertension, we studied young Wistar rats chronically loaded with sodium bicarbonate (NaHCO3) or sodium chloride (NaCl) which were administered either in the diet or in the drinking fluid. Selective sodium loading (without chloride) increased blood pressure (BP) in DOC-treated animals only if NaHCO3 was provided in the diet. In contrast, no significant blood pressure changes were induced by DOC treatment in rats drinking NaHCO3 solution. Hypernatremia and high plasma osmolality occurred only in rats drinking NaCl or NaHCO3 solutions. Compared to great volume expansion in NaCl-loaded DOC-treated rats, the degree of extracellular fluid volume expansion (namely of its interstitial fraction) was substantially lower in both NaHCO3-loaded groups in which significant hypokalemia was observed. NaHCO3-drinking rats without significant blood pressure response to DOC treatment represented the only experimental group in which blood volume was not expanded. In conclusion, our data confirm previous observations that NaHCO3 loading is less potent in eliciting DOC hypertension than NaCl loading, but blood pressure rise in rats fed NaHCO3 diet clearly demonstrated that selective sodium loading could potentiate the development of DOC hypertension if NaHCO3 is offered within the appropriate dietary regimen. The reasons for the failure of NaHCO3-drinking rats to elevate blood pressure in response to chronic mineralocorticoid treatment are not obvious. However, the absence of a significant plasma volume expansion together with hypernatremia and increased plasma osmolality suggest a considerable degree of dehydration in these animals which fail to increase their fluid consumption compared to water drinking rats.
Traditionally, the dorsal column-medial lemniscus system has been viewed as a pathway not involved in pain perception. However, recent clinical and experimental studies have provided compelling evidence that implicates an important role of the dorsal column pathway in relaying visceral nociceptive information. Several clinical studies have shown that a small lesion that interrupts fibers of the dorsal columns (DC) that ascend close
to the midline of the spinal cord significantly relieves pain and decreases analgesic requirements in patients suffering from cancer originating in
visceral organs. Behavioral, electrophysiological and immunohistochemical methods used under experimental situations in animals showed that DC lesion lead to decreased activation of thalamic and gracile neurons by visceral stimuli, suppressed inhibition of exploratory activity induced by visceral noxious stimulation and prevented potentiation of visceromotor reflex evoked by colorectal distention under inflammatory conditions. Whereas the surgical lesion of the DC tract has proven to be clinically successful, a pharmacological approach would be a better strategy to block this pathway and thus to improve visceral pain conditions under less dramatic circumstances than cancer pain. Our finding that PSDC neurons start to express receptors for substance P after colon inflammation suggests new targets for the development of pharmacological strategies for the control of visceral pain.
a1_Vascular resistance in the mammalian pulmonary circulation is affected by many endogenous agents that influence vascular smooth muscle, right ventricular myocardium, endothelial function, collagen and elastin deposition, and fluid balance. When the balance of these agents is disturbed, e.g. by airway hypoxia from high altitude or pulmonary obstructive disorders, pulmonary hypertension ensues, as characterized by elevated pulmonary artery pressure (PPA). Among neuropeptides with local pulmonary artery pressor effects are endothelin-1 (ET-1), angiotensin II (AII), and substance P, and among mitigating peptides are calcitonin gene-related peptide (CGRP), adrenomedullin (ADM), atrial natriuretic peptide (ANP), vasoactive intestinal peptide (VIP) and ET-3. Moreover, somatostatin28 (SOM28) exacerbates, whereas SOM14 decreases PPA in hypoxic rats, with lowering and increasing of lung CGRP levels, respectively. Pressure can also be modulated by increasing or decreasing plasma volume (VIP and ANP, respectively), or by induction or suppression of vascular tissue remodeling (ET-1 and CGRP, respectively). Peptide bioavailability and potency can be regulated through hypoxic up- and down- regulation of synthesis or release, activation by converting enzymes (ACE for AII and ECE for ET-1), inactivation by neutral endopeptidase and proteases, or by interaction with nitric oxide (NO). Moreover, altered receptor density and affinity can account for changed peptide efficacy. For example, upregulation of ETA receptors and ET-1 synthesis occurs in the hypoxic lung concomitantly with reduced CGRP release. Also, receptor activity modifying protein 2 (RAMP2) has been shown to confer ADM affinity to the pulmonary calcitonin-receptor-like receptor (CRLR). We recently detected the mRNA encoding for RAMP2, CRLR, and the CGRP receptor RDC-1 in rat lung., a2_The search for an effective, lung selective treatment of pulmonary hypertension will likely benefit from exploring the imbalance and restoring the balance between these native modulators of intrapulmonary pressure. For example, blocking of the ET-1 receptor ETA and vasodilation by supplemental CGRP delivered i. v. or via airway gene transfer, have proven to be useful experimentally., I. M. Keith., and Obsahuje bibliografii
Gastrointestinal hormones play an important role in the neuroendocrine regulation of food intake and postprandial satiety. Ghrelin is a 28-amino acid orexigenic peptide produced mainly by the stomach that is involved in both the long-term regulation of body weight and the short-term regulation of postprandial satiety. Impairments in ghrelin secretion may in concert with other factors play an important role in the development of both obesity and anorexia nervosa. Despite an intensive research the critical factors regulating physiological postprandial ghrelin response in healthy individuals and its modification by the presence of obesity and anorexia nervosa are only partially understood. The potential contribution of ghrelin to the differences of diet- vs. surgical-induced weight losses in morbidly obese patients is now also being recognized. The aim of this review is to summarize the current knowledge about the physiology and pathophysiology of ghrelin and to discuss its potential in the prevention and/or treatment of obesity and anorexia nervosa., I. Dostálová, M. Haluzík., and Obsahuje seznam literatury
This paper looks at housing strategy in a wider social and economic context and argues that a household’s (class) position in society depends on important life decisions, one of the most important of which is a person’s employment strategy and preparation for the period of retirement (pensions), which is related to housing decisions. The main context of these decisions is the welfare regime, but also a country’s economic structure (varieties of capitalism) and housing system (tax and subsidy elements of programmes). However, as the paper argues, these systems are also changing in relation to the macro effect of individual decisions.
Ferritin and increased iron stores first appea red on the list of cardiovascular risk factors more than 30 years ago and their causal role in the pathogenesis of atherosclerosis has been heavily discussed since the early 1990s. It seems that besides traditional factors such as hyperlipoprotein emia, hyp ertension, diabetes mellitus, obesity, physical inactivity, smoking and family history, high iron stores represent an additional parameter that could modify individual cardiovascular risk. The role of iron in the pathogenesis of atherosclerosis was origina lly primarily associated with its ability to cataly ze the formation of highly reactive free oxygen radicals and the oxidation of atherogenic lipoproteins. Later, it became clear that the mechanism is more complex. Atherosclerosis is a chronic fibroprolife rative inflammatory process and iron, through increased oxidation stress as well as directly, can control both native and adaptive immune responses. Within the arterial wall, iron affects all of the cell types that participate in the atherosclerotic proces s (monocytes/macrophages, endothelial cells, vascular smooth muscle cells and platelets). Most intracellular iron is bound in ferritin, whereas redox-active iron forms labile iron pool. Pro-inflammatory and anti-inflammatory macrophages within arterial plaque differ with regard to the amount of intracellular iron and most probably with regard to their labile iron pool. Yet, the relation between plasma ferritin and intracellular labile iro n pool has not been fully clarified. Data from population studies document that the consumption of meat and lack of physical activity contribute to increased iron stores. Patients with hereditary h emochromatosis, despite extreme iron storage, do not show i ncreased manifestation of atherosclerosis probably due to the low expression of hepcidin in macrophages., P. Kraml., and Obsahuje bibliografii
We assessed IgG antibody to Toxoplasma gondii in 300 inpatients with schizophrenia (SG), 150 outpatients with anxiety and depressive disorders (PCG), and 150 healthy blood donors (HCG). Seropositivity rates were 60.7% for SG, 36.7% for PCG, and 45.3% for HCG (p<0.001). The seropositivity rate for anti-Toxoplasma IgG antibodies in SG was significantly higher that in PCG (X2=23.11, OR=2.66, p=0.001) and HCG (X2=9.52, OR=1.86, p=0.002). Among SG, 85% of those who reported close cat contact had IgG antibodies to T. gondii. Close cat contacts were reported by 59% of SG, 6% of PCG, and 9% of HCG (p<0.001). There was a nonsignificant positive association between toxoplasmosis and schizophrenia for people with a contact with a cat (OR=2.221, p=0.127, CI95=0.796-6.192), and significant negative association between toxoplasmosis and schizophrenia for people without contact with a cat (OR=0.532, p=0.009, CI95=0.332-0.854). Close cat contact (OR=2.679, p<0.001), 51-65-year age group (OR=1.703, p<0.001) and education [illiterate+primary (OR=6.146, p<0.001) and high school (OR=1.974, p=0.023)] were detected as independent risk factors in multivariate logistic regression. The effect of toxoplasmosis on risk of schizophrenia disappeared in the complex model analyzed with multivariate logistic regression. In conclusion, our data suggest that the toxoplasmosis has no direct effect on the risk of schizophrenia in Turkey but is just an indication of previous contacts with a cat.
This review focuses on current knowledge of leptin biology and the role of leptin in various physiological and pathophysiological states. Leptin is involved in the regulation of body weight. Serum leptin can probably be considered as one of the best biological markers reflecting total body fat in both animals and humans. Obesity in man is accompanied by increased circulating leptin concentrations. Gender differences clearly exist. Leptin is not only correlated to a series of endocrine parameters such as insulin, glucocorticoids, thyroid hormones, testosterone, but it also seems to be involved in mediating some endocrine mechanisms (onset of puberty, insulin secretion) and diseases (obesity, polycystic ovary syndrome). It has also been suggested that leptin can act as a growth factor in the fetus and the neonate., R. Janečková., and Obsahuje bibliografii