We will review the main animal models for the major neuropsychiatric disorders, focusing on schizophrenia, Alzheimer?s disease, Parkinson?s disease, depression, anxiety and autism. Although these mental disorders are specifically human pathologies and therefore impossible to perfectly replicate in animals, the use of experimental animals is based on the physiological and anatomical similarities between humans and animals such as the rat, and mouse, and on the fact that 99% of human and murine genomes are shared. Pathological conditions in animals can be assessed by manipulating the metabolism of neurotransmitters, through various behavioral tests, and by determining biochemical parameters that can serve as important markers of disorders.
Adrenomedullin (ADM), a ubiquitous vasoactive peptide, has been the target of a multitude of studies concerning its effect on the vascular tone. The present work aims at clarifying a series of its interactions with the renin-angiotensin system.The study uses the rat aorta ring as a model of conductance vessels, with or without vascular endothelium, and the second order branch of rat mesenteric arteries as a model of resistance arteries.Interactions between various concentrations of ADM and angiotensin II (Ang II) were studied, in the presence of L-NAME (a nitric oxide [NO] synthase inhibitor) and methylene blue (MB; a soluble guanylate cyclase inhibitor).Results point out differences in the mechanism of the inhibitory action of ADM upon Ang II effects in the two vessel types studied. Inhibition of Ang II contraction by ADM involves guanylate cyclase in both cases. However, NO is involved in ADMinduced inhibition of angiotensinergic vasoconstriction only in the conductance arteries, not in the resistance ones.
Despite the improvements in the treatment of coronary artery disease (CAD) and acute myocardial infarction (MI) over the past 20 years, ischemic heart disease (IHD) continues to be the most common cause of heart failure (HF). In clinical trials, over 70% of patients diagnosed with HF had IHD as the underlying cause. Furthermore, IHD predicts a worse outcome for patients with HF, leading to a substantial increase in late morbidity, mortality, and healthcare costs. In recent years, new pharmacological therapies have emerged for the treatment of HF, such as sodium-glucose cotransporter-2 inhibitors, angiotensin receptor-neprilysin inhibitors, selective cardiac myosin activators, and oral soluble guanylate cyclase stimulators, demonstrating clear or potential benefits in patients with HF with reduced ejection fraction. Interventional strategies such as cardiac resynchronization therapy, cardiac contractility modulation, or baroreflex activation therapy might provide additional therapeutic benefits by improving symptoms and promoting reverse remodeling. Furthermore, cardiac regenerative therapies such as stem cell transplantation could become a new therapeutic resource in the management of HF. By analyzing the existing data from the literature, this review aims to evaluate the impact of new HF therapies in patients with IHD in order to gain further insight into the best form of therapeutic management for this large proportion of HF patients.
Free radicals and reactive oxygen species are produced in the human body as a part of metabolic processes. Reactive species in low levels are important for cellular activities. Excessive amounts of reactive species can be harmful because they can produce lipid peroxidation, proteins and ADN oxidation. For reduce these harmful effects the organism requires an antioxidant defence. Oxidative stress is involve in atherosclerosis, coronary heart disease, metabolic syndrome, type 2 diabetes mellitus. The aerobic and anaerobic exercises have different effects on the muscles, but both influence positively the biomarkers of oxidative stress. Studies prove that aerobics increase endogenous antioxidant status. Regular moderate exercises produce an increase in antioxidant activity, due to the changes in redox homeostasis. The aim of this review is to discuss the importance of a constant physical activity for increase the body's antioxidant system and to protect against oxidative stress.
Cardiovascular diseases (CVDs) represent the most important epidemic of our century, with more than 37 million patients globally. Furthermore, CVDs are associated with high morbidity and mortality, and also increased hospitalization rates and poor quality of life. Out of the plethora of conditions that can lead to CVDs, atherosclerosis and ischemic heart disease are responsible for more than 2/3 of the cases that end in severe heart failure and finally death. Current therapy strategies for CVDs focus mostly on symptomatic benefits and have a moderate impact on the underlying physiopathological mechanisms. Modern therapies try to approach different physiopathological pathways such as reduction of inflammation, macrophage regulation, inhibition of apoptosis, stem-cell differentiation and cellular regeneration. Recent technological advances make possible the development of several nanoparticles used not only for the diagnosis of cardiovascular diseases, but also for targeted drug delivery. Due to their high specificity, nanocarriers can deliver molecules with poor pharmacokinetics and dynamics such as: peptides, proteins, polynucleotides, genes and even stem cells. In this review we focused on the applications of nanoparticles in the diagnosis and treatment of ischemic heart failure and atherosclerosis.
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