Navegando por Palavras-chave "arterial pressure"
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- ItemSomente MetadadadosAFFERENT PATHWAYS INVOLVED in CARDIOVASCULAR ADJUSTMENTS INDUCED BY HYPERTONIC SALINE RESUSCITATION in RATS SUBMITTED TO HEMORRHAGIC SHOCK(Lippincott Williams & Wilkins, 2009-08-01) Costa, Eloisa Ferreira de Almeida; Pedrino, Gustavo Rodrigues [UNIFESP]; Lopes, Oswaldo Ubriaco [UNIFESP]; Cravo, Sergio Luiz [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Oeste Paulista Presidente PrudenteThe peripheral hyperosmolarity elicited by intravenous infusion of hypertonic saline (HS) can be beneficial in treating hemorrhagic shock. However, the neural mechanisms involved in this resuscitation remain unknown. the present study sought to determine the effects of selective baroreceptor denervation on arterial blood pressure response during HS resuscitation in rats submitted to hemorrhagic shock. Male Wistar rats (280-320 g) were anesthetized with thiopental sodium (40 mg/kg, i.v.), and the femoral artery and jugular vein were cannulated for MAP and heart rate recording and HS infusion (3 mol/L NaCl; 0.18 mL/100 g body weight, >2 min). Hemorrhagic shock was obtained by withdrawing blood over 30 min until a MAP of 60 mmHg was obtained. This level of MAP was maintained for a further 30 min through subsequent blood withdrawal or reinfusion. Next, animals were divided into selective aortic and/or carotid denervation or sham groups before infusing HS. Results showed that in the sham group (n = 12), HS infusion increased MAP to levels close to baseline (from 65 +/- 3 to 112 +/- 5 mmHg, 10 min after HS). in the aortic denervated group (n = 10), HS infusion also increased MAP (from 54 +/- 3 to 112 +/- 5 mmHg, 10 min after HS). in contrast, in the carotid denervation group (n = 8), the increase in MAP induced by HS infusion was abolished (from 53 +/- 3 to 73 +/- 12 mmHg, 10 min after HS). These results indicate that in hemorrhaged rats, HS infusion produces a pressor effect that is likely to be mediated through carotid rather than aortic baroreceptors.
- ItemAcesso aberto (Open Access)Blood flow measurements in rats using four color microspheres during blockade of different vasopressor systems(Assoc Bras Divulg Cientifica, 2005-01-01) De Angelis, Katia; Gama, V. M. [UNIFESP]; Farah, VAM; Irigoyen, Maria Claudia [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Univ Santo Amaro; Univ Sao Judas TadeuThe use of colored microspheres to adequately evaluate blood flow chancres under different circumstances in the same rat has been validated with a maximum of three different colors due to methodological limitations. the aim of the present study was to validate the use of four different colors measuring four repeated blood flow. changes in the same rat to assess the role of vasopressor systems in. controlling arterial pressure (AP). Red (150,000), white (200,000)), yellow (150,000), and blue (200,000) colored microspheres were infused into the left ventricle of 6 male Wistar rats 1) at rest and 2) after vasopressin (aAVP, 10 mug/kg, iv), 3) renin-angiotensin (losartan, 10 ms/kg iv), and 4) sympathetic system blockade (hexamethonium., 20 mg/kg, iv) to determine blood flow changes. AP was recorded and processed with a data acquisition system (1-kHz sampling frequency). Blood flow changes were quantified by spectrophotometry absorption peaks for colored microsphere components in the tissues evaluated. Administration of aAVP and losartan slightly reduced the AP (-5.7 +/- 0.5 and -7.8 +/- 1.2 mmHg, respectively), while hexamethonium induced a 52 +/- 3 mmHg fall in AP. the aAVP injection increased blood flow in lungs (78%), liver (117%) and skeletal muscle (>150%), while losartan administration enhanced blood flow in heart (126%), lungs (100%), kidneys (80%), and gastrocnemius (75%) and soleus (94%) muscles. Hexamethonium administration reduced only kidney blood flow (50%). in conclusion, four types of colored microspheres can be used to perform four repeated blood flow measurements in the same rat detecting small alterations such as changes in tissues with low blood flow.
- ItemSomente MetadadadosEffects of AV3V lesion on pilocarpine-induced pressor response and salivary gland vasodilation(Elsevier B.V., 2005-09-07) Takakura, ACT; Moreira, T. S.; De Luca, L. A.; Renzi, A.; Menani, J. V.; Colombari, E.; Universidade Federal de São Paulo (UNIFESP); Univ Estadual PaulistaThe cholinergic agonist pilocarpine injected intraperitoneally (ip) increases mean arterial pressure (MAP) and superior mesenteric (SM) vascular resistance and reduces submandibular/sublingual gland (SSG) vascular resistance. in the present study, we investigated the effects of electrolytic lesions of the anteroventral third ventricle (AV3V) region on the changes in MAP, SM, and SSG vascular resistances induced by ip pilocarpine. Male Holtzman rats anesthetized with urethane (1.0 g/kg) and chloralose (60 mg/kg) were submitted to sham or electrolytic AV3V lesions and bad pulsed Doppler flow probes implanted around the arteries. Contrary to sham rats, in 1-h and 2-day AV3V-lesioned rats, pilocarpine (4 mu mol/kg) ip decreased MAP (-41 +/- 4 and -26 4 mm Hg, respectively, vs. sham: 19 +/- 4 mm Hg) and SM (-48 +/- 11 and -45 +/- 10%, respectively, vs. sham: 41 +/- 10%) and hindlimb vascular resistances (-65 +/- 32 and -113 +/- 29%, respectively, vs. sham: 19 +/- 29%). in 7-day AV3V-lesioned rats, pilocarpine produced no changes on MAP and SM and hindlimb vascular resistances. Similar to sham rats, pilocarpine reduced SSG vascular resistance 1 h after AV3V lesions (-46 +/- 6%, vs. sham: -40 +/- 6%), but it produced no effect 2 days after AV3V lesions and increased SSG vascular resistance (37 6%) in 7-day AV3V-lesioned rats. the responses to ip pilocarpine were similar in 15-day sham and AV3V-lesioned rats. the cholinergic antagonist atropine methyl bromide (10 nmol) iv slightly increased the pressor response to ip pilocarpine in sham rats and abolished for 40 min the fall in MAP induced by ip pilocarpine in 1-h AV3V-lesioned rats. the results suggest that central mechanisms dependent on the AV3V region are involved in the pressor responses to ip pilocarpine. Although it was impaired 2 and 7 days after AV3V lesions, pilocarpine-induced salivary gland vasodilation was not altered 1 h after AV3V lesions which suggests that this vasodilation is not directly dependent on the AV3V region. (c) 2005 Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosEnhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanisms(Amer Physiological Soc, 2000-05-01) Sato, Monica Akemi [UNIFESP]; Menani, Jose Vanderlei; Lopes, Oswaldo Ubriaco [UNIFESP]; Colombari, Eduardo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Estadual PaulistaBilateral common carotid occlusion (BCO) over a period of 60 s in conscious rats produces a biphasic presser response, consisting of an early (peak) and late (plateau) phase. In this study we investigated 1) the effects of lesions of the commissural nucleus of the solitary tract (commNTS) on the cardiovascular responses produced by BCO in conscious rats and 2) the autonomic and humoral mechanisms activated to produce the presser response to BCO in sham- and commNTS-lesioned rats. Both the peak and plateau of the presser response produced by BCO increased in commNTS-lesioned rats despite the impairment of chemoreflex responses induced by intravenous potassium cyanide. In sham rats sympathetic blockade with intravenous prazosin and metoprolol, but not vasopressin receptor blockade with the Manning compound, reduced both components of BCO. In commNTS-lesioned rats the sympathetic blockade or vasopressin receptor blockade reduced both components of BCO. The results showed 1) the sympathetic nervous system, but not vasopressin, is important for the presser response to BCO during 60 s in conscious sham rats; 2) in commNTS-lesioned rats, despite chemoreflex impairment, BCO produces an increased presser response dependent on sympathetic activity associated with vasopressin release; and 3) the increment in the presser response to BCO in commNTS-lesioned rats seems to depend only on vasopressin secretion.
- ItemSomente MetadadadosHemodynamic effects elicited by microinjection of glutamatergic agonists into NTS of conscious rats(Amer Physiological Soc, 2001-09-01) Dias, Ana Carolina Rodrigues [UNIFESP]; Talman, William T.; Colombari, Eduardo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Iowa; Vet Affairs Med CtrIn this study, we characterized the arterial pressure, heart rate, and regional vascular conductance responses elicited by unilateral microinjection of ionotropic glutamatergic agonists N-methyl-D-aspartic acid (NMDA and non-NMDA) into the nucleus of tractus solitarius (NTS) of conscious rats. Microinjections of NMDA and S-alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) caused changes in mean arterial pressure (MAP). Lower doses elicited decreases in MAP, whereas higher doses elicited biphasic responses (decreases followed by increases). Both agonists induced bradycardia and elicited dose-dependent vasoconstriction in the renal, mesenteric, and hindquarter beds. AMPA elicited delayed vasodilation in the hindquarter bed but NMDA did not. Bradycardia and initial hypotension produced by each agonist were abolished by systemic administration of the muscarinic antagonist methylatropine. However, methylatropine did not affect either the vasoconstriction or the vasodilatation. The contrasting hemodynamic effects produced by NMDA and AMPA could be caused by activation of differential subsets of NTS neurons. Preferential activation of one subset could produce the NMDA-related responses, whereas activation of another subset would elicit AMPA-related responses.
- ItemSomente MetadadadosInvolvement 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 PaulistaIn 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.
- ItemRestritoLesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake(Assoc Bras Divulg Cientifica, 2007-08-01) Blanch, Graziela Torres; Freiria-Oliveira, Andre Henrique; Colombari, Eduardo [UNIFESP]; Menani, Jose Vanderlei; Colombari, Debora Simões de Almeida [UNIFESP]; UNESP; Universidade Federal de São Paulo (UNIFESP)The nucleus of the solitary tract (NTS) is the primary site of the cardiovascular afferent information about arterial blood pressure and volume. the NTS projects to areas in the central nervous system involved in cardiovascular regulation and hydroelectrolyte balance, such as the anteroventral third ventricle region and the lateral parabrachial nucleus. the aim of the present study was to investigate the effects of electrolytic lesion of the commissural NTS on water and 0.3 M NaCl intake and the cardiovascular responses to subcutaneous injection of isoproterenol. Male Holtzman rats weighing 280 to 320 g were submitted to sham lesion or electrolytic lesion of the commissural NTS (N = 6-15/group). the sham-lesioned rats had the electrode placed along the same coordinates, except that no current was passed. Water intake induced by subcutaneous isoproterenol (30 mu g/kg body weight) significantly increased in chronic (15 days) commissural NTS-lesioned rats (to 2.4 +/- 0.2 vs sham: 1.9 +/- 0.2 mL 100 g body weight(-1) 60 min(-1)). Isoproterenol did not induce any sodium intake in sham or in commissural NTS-lesioned rats. the isoproterenol-induced hypotension (sham: -27 +/- 4 vs commissural NTS-lesioned rats: -22 +/- 4 mmHg/20 min) and tachycardia (sham: 168 +/- 10 vs commissural NTS: 144 +/- 24 bpm/20 min) were not different between groups. the present results suggest that the commissural NTS is part of an inhibitory neural pathway involved in the control of water intake induced by subcutaneous isoproterenol, and that the overdrinking observed in lesioned rats is not the result of a cardiovascular imbalance in these animals.
- ItemAcesso aberto (Open Access)Role of the medulla oblongata in normal and high arterial blood pressure regulation: the contribution of Escola Paulista de Medicina - UNIFESP(Academia Brasileira de Ciências, 2009-09-01) Cravo, Sergio Luiz [UNIFESP]; Campos, Ruy Ribeiro [UNIFESP]; Colombari, Eduardo [UNIFESP]; Sato, Mônica A.; Bergamaschi, Cassia Toledo [UNIFESP]; Pedrino, Gustavo Rodrigues [UNIFESP]; Ferreira-Neto, Marcos L.; Lopes, Oswaldo Ubriaco [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Faculdade de Medicina do ABC Departamento de Morfologia e Fisiologia; Federal de Uberlândia Faculdade de Educação FísicaSeveral forms of experimental evidence gathered in the last 37 years have unequivocally established that the medulla oblongata harbors the main neural circuits responsible for generating the vasomotor tone and regulating arterial blood pressure. Our current understanding of this circuitry derives mainly from the studies of Pedro Guertzenstein, a former student who became Professor of Physiology at UNIFESP later, and his colleagues. In this review, we have summarized the main findings as well as our collaboration to a further understanding of the ventrolateral medulla and the control of arterial blood pressure under normal and pathological conditions.