Navegando por Palavras-chave "hypotension"

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    ACE activity during the hypotension produced by standardized aqueous extract of Cecropia glaziovii Sneth: A comparative study to captopril effects in rats
    (Elsevier B.V., 2007-05-01) Ninahuaman, M. F. M. L.; Souccar, C.; Lapa, A. J.; Lima-Landman, M. T. R.; Universidade Federal de São Paulo (UNIFESP)
    To evaluate the effect of the standardized aqueous extract (AE) of Cecropia glaziovii Sneth on the plasma angiotensin I converting enzyme (ACE-EC 3.4.15. 1) activity, rats were treated with a single dose of AE (1 g/kg, p.o.) or repeatedly (0.5 g/kg/bid, p.o.) for 60 days. Captopril (50 mg/kg, p.o.) was used as positive control on the same animals. the effects on the blood pressure were recorded directly from the femoral artery (single dose), or indirectly by the tail cuff method (repeated doses) in conscious rats. the plasma ACE activity was determined spectrofluorimetrically using Hypuril-Hystidine-Leucine as substrate. the arterial blood pressure, heart rate and plasma ACE activity were not significantly modified within 24 h after a single dose administration of AE. Comparatively, blood pressure in captopril treated rats was reduced by 7-16% and heart rate was increased by 10-20% from 30 min to 24 h after drug administration. ACE activity after captopril presented a dual response: an immediate inhibition peaking at 30 min and a slow reversal to 32% up-regulation after 24 h. To correlate the drug effects upon repeated administration of either compound, normotensive rats were separated in three groups: animals with high ACE (48.8 +/- 2.6 nmol/min/ml), intermediate ACE (39.4 +/- 1.4 nmol/min/ml) and low ACE (23.5 +/- 0.6 nmol/min/ml) activity, significantly different among them. Repeated treatment with AE reduced the mean systolic blood pressure (121.7 +/- 0.5 min Hg) by 20 min Hg after 14 days. the hypotension was reversed upon washout 60 days afterwards. Likely, repeated captopril administration decreased blood pressure by 20mm Hg throughout treatment in all groups. After 30 days treatment with AE (0.5 g/kg/bid, p.o.) the plasma ACE activity was unchanged in any experimental group. After captopril (50 mg/ kg/bid, p.o.) administration the plasma ACE activity was inhibited by 50% within I h treatment but it was up-regulated by 120% after 12 h in all groups. It is concluded that the hypotension produced by prolonged treatment with AE of C. glaziovii is unrelated to ACE inhibition. (C) 2006 Elsevier GmbH. All rights reserved.
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    Hemodynamic and thermoregulatory effects of xylazine-ketamine mixture persist even after the anesthetic stage in rats
    (Universidade Federal de Minas Gerais, Escola de Veterinária, 2012-08-01) Picollo, Camila [UNIFESP]; Serra, Andrey Jorge [UNIFESP]; Levy, Rozeli Ferreira [UNIFESP]; Antonio, Ednei Luiz [UNIFESP]; Santos, Leonardo dos [UNIFESP]; Tucci, Paulo José Ferreira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Nove de Julho; Universidade Federal do Espírito Santo
    The xylazine-ketamine mixture (KX) is an anesthetic approach commonly administered to assess cardiovascular function in rodents. This study aimed to examine if the cardiovascular and thermoregulatory effects of KX could persist after the anesthetic state ceased in rats. Male Wistar rats were anesthetized with K (50mg/kg) X (10mg/kg) through the intra-peritoneal route. Hemodynamic and thermoregulatory repercussions were evaluated in animals in awake state, during an anesthetic depth and after complete recovery of anesthetized state. KX was efficient to significantly induce deep anesthesia in all rats after 10min. A complete recovery of anesthetized state was observed only after 210min. Compared with preanesthetic state and control animals that received no drug, KX induced a significant reduction of systolic and diastolic blood pressure at 10min. Hypotension was more prominent at 150min. The heart rate was also significantly reduced after 10 min of KX and the highest magnitude of bradycardia was observed at 30min. In addition, rectal temperature was markedly decreased at 30min of KX and the higher reduction occurred at 150min. The hemodynamic and thermoregulatory effects of KX were maintained even after complete anesthetic recovery.
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    Immediate and 24-h blood pressure-lowering effects of arm crank exercise in patients with traumatic lower-limb amputation: a randomized cross-over study
    (Lippincott Williams & Wilkins, 2018) Paula-Ribeiro, Marcelle [UNIFESP]; Martinez, Daniel G.; Lima, Jorge R. P.; Laterza, Mateus C.
    Aim: This study aimed to investigate the clinic and 24-h postexercise hypotension (PEH) after a moderate-intensity arm crank exercise session in individuals with traumatic lower-limb amputation.Participants and methodsNine men (4617 years) with unilateral traumatic lower-limb amputation participated in two experimental sessions conducted randomly: an aerobic exercise (EXE: arm crank ergometer, 30min) or a control session (CON: participants remained seated on the cycle ergometer, 30min). Clinic and 24-h systolic, diastolic, and mean blood pressure (BP) response were measured after both sessions. The clinical measurements of blood flow and forearm vascular resistance (FVR) were also performed.ResultsCompared with the preintervention period, the BP levels did not change in the CON session. However, EXE resulted in a significant hypotensive effect in systolic (-10 +/- 0.9mmHg, P0.05), diastolic (-11 +/- 1.5mmHg, P0.05), and mean BP (-11 +/- 1.2mmHg, P0.05) during the entire postexercise period. The PEH was accompanied by a decreased FVR over the entire postintervention period (P0.05). Significant reductions were found for 24-h average systolic, diastolic, and mean BP levels (P=0.03, 0.01, and 0.02, respectively) following EXE compared with the CON session.ConclusionThese results showed, for the first time, that individuals with traumatic lower-limb amputation presented immediate and 24-h PEH after a single bout of arm crank exercise testing. The PEH at the clinic condition was justified, at least in part, by the reduction in peripheral FVR.
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    Increased susceptibility to endotoxic shock in transgenic rats with endothelial overexpression of kinin B(1) receptors
    (Springer, 2008-07-01) Merino, Vanessa F. [UNIFESP]; Todiras, Mihail; Campos, Luciana A.; Saul, Vera; Popova, Elena; Baltatu, Ovidiu C.; Pesquero, Joao B. [UNIFESP]; Bader, Michael; Max Delbruck Ctr Mol Med; Universidade Federal de São Paulo (UNIFESP)
    Two kinin receptors have been described, the inducible B(1) and the constitutive B(2). B(1) receptors are important in cardiovascular homeostasis and inflammation. To further clarify their vascular function, we have generated transgenic rats (TGR(Tie2B(1))) overexpressing the B(1) receptor exclusively in the endothelium. Endothelial cell-specific expression was confirmed by B(1)-agonist-induced relaxation of isolated aorta, which was abolished by endothelial denudation of the vessel. This vasodilatation was mediated by nitric oxide (NO) and K(+) channels. TGR(Tie2B(1)) rats were normotensive but, in contrast to controls, reacted with a marked fall in blood pressure and increased vascular permeability after intravenous injection of a B(1) agonist. After lipopolysaccharide treatment, they present a more pronounced hypotensive response and marked bradycardia associated with increased mortality when compared to non-transgenic control animals. Thus, the transgenic rats overexpressing kinin B(1) receptors exclusively in the endothelium generated in this study support an important role of this receptor in the vasculature during the pathogenesis of endotoxic shock.
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    Involvement of central alpha(1)- and mu(2)-adrenoceptors on cardiovascular responses to moxonidine
    (Elsevier B.V., 2007-06-01) Moreira, Thiago S.; Takakura, Ana C.; Menani, Jose V.; Colombari, Eduardo; Universidade Federal de São Paulo (UNIFESP); Univ Estadual Paulista
    In the present study we compared the effects produced by moxonidine (alpha(2)-adrenoceptor/imidazoline agonist) injected into the 4th cerebral ventricle and into the lateral cerebral ventricle on mean arterial pressure, heart rate and on renal, mesenteric and hindquarter vascular resistances, as well as the possible action of moxonidine on central alpha(1)- or alpha(2)-adrenoceptors to produce cardiovascular responses. Male Holtzman rats (n = 7-8) anesthetized with urethane (0.5 g/kg, intravenously - i.v.) and alpha-chloralose (60 mg/kg, i.v.) were used. Moxonidine (5, 10 and 20 nmol) injected into the 4th ventricle reduced arterial pressure (-19 +/- 5, -30 +/- 7 and -43 +/- 8 mmHg vs. vehicle: 2 +/- 4 mmHg), heart rate (-10 +/- 6, - 16 +/- 7 and -27 +/- 9 beats per minute - bpm, vs. vehicle: 4 +/- 5 bpm), and renal, mesenteric and hindquarter vascular resistances. Moxonidine (5, 10 and 20 nmol) into the lateral ventricle only reduced renal vascular resistance (-77 +/- 17%, - 85 +/- 13%, -89 +/- 10% vs. vehicle: 3 +/- 4%), without changes on arterial pressure, heart rate and mesenteric and hindquarter vascular resistances. Pre-treatment with the selective alpha(2)-adrenoceptor antagonist yohimbine (80, 160 and 320 nmol) injected into the 4th ventricle attenuated the hypotension (-32 +/- 5, -25 +/- 4 and -12 +/- 6 mmHg), bradycardia (-26 +/- 11, -23 +/- 5 and -11 +/- 6 bpm) and the reduction in renal, mesenteric and hindquarter vascular resistances produced by moxonidine (20 nmol) into the 4th ventricle. Pretreatment with yohimbine (320 nmol) into the lateral ventricle did not change the renal vasodilation produced by moxonidine (20 nmol) into the lateral ventricle. the alpha(1)-adrenoceptor antagonist prazosin (320 nmol) injected into the 4th ventricle did not affect the cardiovascular effects of moxonidine. However, prazosin (80, 160 and 320 nmol) into the lateral ventricle abolished the renal vasodilation (-17 +/- 4, -6 +/- 9 and 2 +/- 11%) produced by moxonidine. the results indicate that the decrease in renal vascular resistance due to moxonidine action in the forebrain is mediated by alpha(1)-adrenoceptors, while the cardiovascular effects produced by moxonidine acting in the brainstern depend at least partially on the activation of coadrenoceptors. (c) 2007 Elsevier B.V. All rights reserved.