984 resultados para VASCULAR RESISTANCE
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
Septic shock remains one of the most common challenges for the small animal practicing, presenting high mortality rates frequently associated with late identification of this syndrome, as well as an inappropriate treatment. In general, disruption of homeostasis occurs with an intense activation of inflammatory cascade, which leads to a damage to endothelial cells and an exposure to these cytokines, which will result in vasodilation and increased capillary permeability. Thus, there is a drop in blood pressure, even after aggressive fluid resuscitation. Therefore, drugs such as vasopressors, which act by increasing systemic vascular resistance, and inotropes, which have an effect on heart pump, should be administered in order to raise blood pressure, ensuring adequate tissue perfusion. The objective of this review was to gather information about the various drugs used in vasopressors/inotropes therapy, trying to explain the role of each one in different situations, in order to increase the survival rate in dogs affected with septic shock
Resumo:
Pós-graduação em Fisiopatologia em Clínica Médica - FMB
Resumo:
Pós-graduação em Fisiopatologia em Clínica Médica - FMB
Resumo:
Nitric oxide (NO) is a free radical gas, inorganic, which has seven electrons of nitrogen and oxygen eight, possessing an unpaired electron. This radical is produced from L-arginine by a reaction mediated by the enzyme NO synthase. NO it is about a radical of who acts abundant on a variety of biological processes, particularly when produced by endothelial cells plays a significant role in cardiovascular control, as a modulator of peripheral vascular resistance and platelet aggregation. This free radical has also a neurotransmitter and mediator of the immune system. NO kidney function has been considered in many physiological functions such as: (a) regulation of hemodynamics and glomerular function tubuloglomerular, (b) participation in pressure natriuresis (c) maintaining medullar perfusion (d) inhibiting sodium reabsorption tubular, and (e) acting as a modulator of the activity of the sympathetic nervous system. Given these functions, the occurrence of its deficiency is associated with chronic kidney disease (CKD) in vasoconstriction and consequently glomerular hypertension, high blood pressure (HBP), proteinuria and progression of renal dysfunction. This work has the scope to describe the role of NO in renal physiology and pathophysiology of CKD.
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
Coordenadação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Resumo:
Pós-graduação em Anestesiologia - FMB
Resumo:
Pós-graduação em Medicina Veterinária - FCAV
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
Pós-graduação em Doenças Tropicais - FMB
Resumo:
Pós-graduação em Doenças Tropicais - FMB
Resumo:
Increased reactive oxygen species (ROS) promote matrix metalloproteinase (MMP) activities and may underlie cardiomyocyte injury and the degradation of cardiac troponin I (cTI) during acute pulmonary thromboembolism (APT). We examined whether pretreatment or therapy with tempol (a ROS scavenger) prevents MMP activation and cardiomyocyte injury of APT. Anesthetized sheep received tempol infusion (1.0 mg kg(-1) min(-1), i.v.) or saline starting 30 min before or 30 min after APT (autologous blood clots). Control animals received saline. Hemodynamic measurements were performed. MMPs were studied in the right ventricle (RV) by gelatin zymography, fluorimetric activity assay, and in situ zymography. The ROS levels were determined in the RV and cTI were measured in serum samples. APT increased the pulmonary arterial pressure and pulmonary vascular resistance by 146 and 164 %, respectively. Pretreatment or therapy with tempol attenuated these increases. While APT increased RV + dP/dt (max), tempol infusions had no effects. APT increased RV MMP-9 (but not MMP-2) levels. In line with these findings, APT increased RV MMP activities, and this finding was confirmed by in situ zymography. APT increased the RV ROS levels and tempol infusion, before or after APT, and blunted APT-induced increases in MMP-9 levels, MMP activities, in situ MMP activities, and ROS levels in the RV. cTI concentrations increased after APT, and tempol attenuated these increases. RV oxidative stress after APT increases the RV MMP activities, leading to the degradation of sarcomeric proteins, including cTI. Antioxidant treatment may prevent MMP activation and protect against cardiomyocyte injury after APT.