RESUMO
Despite being involved in homeostatic control and hydro-electrolyte balance, the contribution of medullary (A1 and A2) noradrenergic neurons to the hypertonic saline infusion (HSI)-induced cardiovascular response after hypotensive hemorrhage (HH) remains to be clarified. Hence, the present study sought to determine the role of noradrenergic neurons in HSI-induced hemodynamic recovery in male Wistar rats (290-320 g) with HH. Medullary catecholaminergic neurons were lesioned by nanoinjection of antidopamine-ß-hydroxylase-saporin (0.105 ng·nl-1) into A1, A2, or both (LES A1; LES A2; or LES A1+A2, respectively). Sham rats received nanoinjections of free saporin in the same regions (SHAM A1; SHAM A2; or SHAM A1+A2, respectively). After 15 days, rats were anesthetized and instrumented for cardiovascular recordings. Following 10 min of stabilization, HH was performed by withdrawing arterial blood until mean arterial pressure (MAP) reaches 60 mmHg. Subsequently, HSI was performed (NaCl 3 M; 1.8 ml·kg-1, i.v.). The HH procedure caused hypotension and bradycardia and reduced renal, aortic, and hind limb blood flows (RBF, ABF, and HBF). The HSI restored MAP, heart rate (HR), and RBF to baseline values in the SHAM, LES A1, and LES A2 groups. However, concomitant A1 and A2 lesions impaired this recovery, as demonstrated by the abolishment of MAP, RBF, and ABF responses. Although lesioning of only a group of neurons (A1 or A2) was unable to prevent HSI-induced recovery of cardiovascular parameters after hemorrhage, lesions of both A1 and A2 made this response unfeasible. These findings show that together the A1 and A2 neurons are essential to HSI-induced cardiovascular recovery in hypovolemia. By implication, simultaneous A1 and A2 dysfunctions could impair the efficacy of HSI-induced recovery during hemorrhage.
RESUMO
Injeções no núcleo parabraquial lateral (NPBL) de muscimol, agonista de receptores GABAA, promove aumento de pressão arterial e induz ingestão de NaCl 0.3 M e água em ratos normovolêmicos, saciados e depletados de sódio. A doença periodontal é uma condição inflamatória que promove a liberação de citocinas pró-inflamatórias, tais como IL-6 e TNF-α e a destruição das estruturas de suporte do dente. As citocinas pró-inflamatórias podem modular a neurotransmissão GABAérgica e ativar neurônios do NPBL. Neste estudo, investigamos o efeito da ativação GABAérgica no NPBL com muscimol na ingestão de NaCl hipertônico e água e parâmetros cardiovasculares em ratos normovolêmicos, saciados e depletados pelo modelo FURO+CAP com doença periodontal. Foram utilizados ratos Wistar divididos em dois grupos: com doença periodontal induzida por ligadura (DP) e sem doença periodontal (grupo controle). Quinze (15) dias após a indução da doença periodontal em ambos os grupos foram implantadas cânulas bilaterais no NPBL. Ratos saciados controles que receberam injeções bilaterais no NPBL de muscimol tiveram aumento na ingestão de NaCl 0.3 M (15.8 ± 2.4 vs. salina: 0.2 ± 0.1 ml/180 min) e água (14.2 ± 1.2 vs. salina: 0.6 ± 0.3 ml/180 min). Em ratos saciados com doença periodontal houve aumento significativo da ingestão de NaCl 0.3 M e água, porém a ingestão de água em ratos com doença periodontal foi significamente menor (6.0 ± 1.4 vs. controle: 14.2 ± 1.2 ml/210 min). Injeções de muscimol no NPBL de ratos tratados com FURO+CAP (grupo controle), promoveu aumento significativo na ingestão de NaCl 0.3 M (25.9 ± 5.8 e vs. salina: 5.7 ± 1.0 ml/180 min) e água (19.9 ± 1.2 vs. salina: 11.2 ± 1.0 ml/180 min). Em ratos com doença periodontal e tratados com FURO+CAP, injeções de muscimol não promoveu aumento significativo na ingestão de NaCl 0.3 M (10.9± 2.92 vs. salina: 5.6 1.3 ml/210 min) e água (13.4 2.3 vs. salina: 8.2 1.5 ml/210 min). Em ratos saciados e tratados com FURO+CAP, a doença...
GABAA receptor activation with muscimol in the lateral parabrachial nucleus (LPBN) induces water and hypertonic sodium chloride (NaCl) intake in rats. The purpose of this study was to investigate whether local inflammatory event, such as periodontal disease, is able to alter the effects of injections of muscimol (GABAA receptor agonist) into the LPBN on water and 0.3 M NaCl intake in fluid replete rats and in rats treated with diuretic furosemide (FURO) combined with a low dose of the angiotensin-converting enzyme inhibitor captopril (CAP) injected subcutaneously. Male Wistar rats were divided into two groups: with experimental ligature- induced periodontal disease (PD) and those without PD (control conditions). Fifteen days after application of the ligature, both groups had cannulas implanted bilaterally into the LPBN, and were given simultaneous access to water and 0.3 M NaCl intake.In fluid replete rats without PD, injections of muscimol (0.5 nmol/0.2 μl) into the LPBN induced 0.3 M NaCl intake (15.8 ± 2.4 vs. saline: 0.2 ± 0.05 ml/210 min), water intake (14.2 ± 1.2 vs. saline: 0.6 ± 0.3 ml/210 min) and pressor response (15 ± 3.3 mmHg, vs. saline: 0.6 ± 1.3 mmHg). In fluid replete rats (PD group), a decrease was observed in water intake (6.0 ± 1.4 ml/210 min), pressor response (7.5 ± 3.1 mmHg), but not in 0.3 M NaCl intake induced by muscimol. In rats with FURO + CAP- treatment (control group), injections of muscimol into the LPBN increased 0.3 M NaCl (25.9 ± 5.8 vs. saline: 5.7 1.0 ml/210 min) and water intake (19.9 1.2 vs. saline: 11.2 1.0 ml/210 min). In rats with FURO + CAP-treatment (PD group), a decrease was observed in 0.3 M NaCl intake (10.9 ± 2.9 ml/210 min) and water intake (13.4 2.3 ml/210 min) after muscimol injection into the LPBN. IL-6 (40.41 ± 0.25 vs. control: 38.87 ± 0.23 pg/ml) and TNF- (14.58 ± 1.73 vs. control: 3.39 ±0.33 pg/ml) plasmatic concentrations and alveolar bone loss (1.29 ± 0.04 mm vs. control: 0.50 ± 0.02 mm), was higher...