Role of the medial septal area on the cardiovascular, fluid and electrolytic responses to angiotensin II and cholinergic activation into the subfornical organ in rats

In the present study we investigated the effect of electrolytic lesion of the medial septal area (MSA) on the pressor and dipsogenic response to cholinergic activation and angiotensin II (ANGII) injection into the subfornical organ (SFO) in rats. In addition the effect of MSA lesion on the natriuresis, kaliuresis and diuresis after cholinergic activation of the SFO was also investigated. Sham- and MSA-lesioned rats with a stainless steel cannula implanted into the SFO was used. The injection of ANGII (12 ng) into the SFO in sham rats produced pressor (24 ± 2 mmHg) and dipsogenic (9.6 ± 1.1 ml/h) responses. MSA lesion, both acute (2-6 days) and chronic (15-19 days), reduced the pressor (14 ± 2 mmHg) and dipsogenic (2.7 ± 1 ml/h) responses to ANGII into SFO. The injection of the cholinergic agonist carbachol (2 nmol) into the SFO in sham rats produced pressor (48 ± 4 mmHg), dipsogenic (10 ± 1.2 ml/h), natriuretic (457 ± 58 μEq/2 h) and kaliuretic (249 ± 16 μEq/2 h) responses. Acute, but not chronic MSA lesion reduced the pressor (27 ± 3 mmHg), natriuretic (198 ± 55 μEq/2 h) and kaliuretic (128 ± 16 μEq/2 h) responses to carbachol into SFO. No change in the dipsogenic response to carbachol into the SFO was observed in MSA-lesioned rats. Antidiuresis after carbachol was observed only in MSA-lesioned rats. The present results show that the MSA plays a role on the pressor, natriuretic and kaliuretic responses to cholinergic activation of the SFO in rats and on the pressor and dipsogenic responses to ANGII into the same area. In addition, they provide circumstancial evidence for separate circuits subserving the dipsogenic response to central cholinergic and angiotensinergic activation. A facilited diuresis after MSA lesion is also suggested.

Cardiopulmonary and acid-base effects of desflurane and sevoflurane in spontaneously breathing cats

The cardiopulmonary effects of desflurane and sevoflurane anesthesia were compared in cats breathing spontaneously. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressures; partial pressure of end tidal carbon dioxide (PETCO(2)), arterial blood pH (pH), arterial partial pressure of oxygen (PaO(2)) and carbon dioxide (PaCO(2)); base deficit (BD), arterial oxygen saturation (SaO(2)) and bicarbonate ion concentration (HCO(3)) were measured. Anesthesia was induced with propofol (8 +/- 2.3 mg/kg IV) and maintained with desflurane (GD) or sevoflurane (GS), both at 1.3 MAC. Data were analyzed by analysis of variance (ANOVA), followed by the Tukey test (P < 0.05). Both anesthetics showed similar effects. HR and RR decreased when compared to the basal values, but remained constant during inhalant anesthesia and PETCO(2) increased with time. Both anesthetics caused acidemia and hypercapnia, but BD stayed within normal limits. Therefore, despite reducing HR and SAP (GD) when compared to the basal values, desflurane and sevoflurane provide good stability of the cardiovascular parameters during a short period of inhalant anesthesia (T20-T60). However, both volatile anesthetics cause acute respiratory acidosis in cats breathing spontaneously. (c) 2004 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.

Hypothalamic disconnection caudal to paraventricular nucleus affects cardiovascular and drinking responses to central angiotensin II and carbachol

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Evaluation of cardiorespiratory effects of combinations of dexmedetomidine and atropine in cats

The cardiovascular effects of dexmedetomidine alone or in combination with atropine were studied in six cats. Cats underwent four treatments in a randomized crossover design as follows: DEX15, saline + dexmedetomidine 15 mu g/kg; DEX30, saline + dexmedetomidine 30 mu g/kg; ADEX15, atropine + dexmedetomidine 15 mu g/kg; ADEX30, atropine + dexmedetomidine 30 mu g/kg. Pulse rate (PR) and systolic arterial pressure (SAP) decreased in DEX15 and DEX30. Premedication with atropine was effective in preventing bradycardia (PR < 100 beats/min) and resulted in a biphasic effect in blood pressure. Hypertension was followed by a gradual decrease in SAP. Rate pressure product decreased in DEX15 and DEX30 whereas in ADEX15 and ADEX30 it remained within baseline values for at least 60 min. Although premedication with atropine in cats sedated with dexmedetomidine prevents bradycardia, it induces hypertension and increases myocardial oxygen consumption. The magnitude of cardiovascular effects produced by dexmedetomidine in cats does not seem to be dose-related. (C) 2009 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.

Comparison of medetomidine-ketamine and dexmedetomidine-ketamine anesthesia in golden-headed lion tamarins

The cardiovascular, respiratory, and anesthetic effects of medetomidine-ketamine (20 μg/kg bodyweight [BW] and 10 mg/kg BW) (MK group) or dexmedetomidine-ketamine (10 μg/kg BW and 10 mg/kg BW) (DK group) were studied in golden-headed lion tamarins. Heart rate decreased after administration of both combinations; this reduction was statistically greater in the DK group than in the MK group after 15 and 45 minutes. Systolic arterial pressure decreased in a similar way in both groups, except at 15 minutes, when systolic arterial pressure was significantly lower in the DK group. Diastolic arterial pressure, mean arterial pressure, respiratory rate, and rectal temperature were progressively reduced in all groups. Sedation time was significantly shorter and anesthesia time was significantly longer in the DK group compared with MK group. Anesthetic quality and analgesia scores were significantly greater at 5 and 15 minutes in the DK group compared with the MK group. The administration of dexmedetomidine-ketamine is as safe and effective as the administration of medetomidine-ketamine in tamarins.

Role of the bed nucleus of the stria terminalis in cardiovascular changes following chronic treatment with cocaine and testosterone: A role beyond drug seeking in addiction?

Neural plasticity has been observed in the bed nucleus of the stria terminalis (BNST) following exposure to both cocaine and androgenic-anabolic steroids. Here we investigated the involvement of the BNST on changes in cardiovascular function and baroreflex activity following either single or combined administration of cocaine and testosterone for 10 consecutive days in rats. Single administration of testosterone increased values of arterial pressure, evoked rest bradycardia and reduced baroreflex-mediated bradycardia. These effects of testosterone were not affected by BNST inactivation caused by local bilateral microinjections of the nonselective synaptic blocker CoCl2. The single administration of cocaine as well as the combined treatment with testosterone and cocaine increased both bradycardiac and tachycardiac responses of the baroreflex. Cocaine-evoked baroreflex changes were totally reversed after BNST inactivation. However, BNST inhibition in animals subjected to combined treatment with cocaine and testosterone reversed only the increase in reflex tachycardia, whereas facilitation of reflex bradycardia was not affected by local BNST treatment with CoCl2. In conclusion, the present study provides the first direct evidence that the BNST play a role in cardiovascular changes associated with drug abuse. Our findings suggest that alterations in cardiovascular function following subchronic exposure to cocaine are mediated by neural plasticity in the BNST. The single treatment with cocaine and the combined administration of testosterone and cocaine had similar effects on baroreflex activity, however the association with testosterone inhibited cocaine-induced changes in the BNST control of reflex bradycardia. Testosterone-induced cardiovascular changes seem to be independent of the BNST. © 2013 IBRO.

Type-2 diabetes mellitus and the frequency of the G22A polymorphism of the adenosine deaminase gene in a mixed population in Brazil

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Stress vulnerability during adolescence: comparison of chronic stressors in adolescent and adult rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Adolescent vulnerability to cardiovascular consequences of chronic social stress: Immediate and long-term effects of social isolation during adolescence

It has been demonstrated that disruption of social bonds and perceived isolation (loneliness) are associated with an increased risk of cardiovascular morbidity and mortality. Adolescence is proposed as a period of vulnerability to stress. Nevertheless, the impact of chronic social stress during this ontogenic period in cardiovascular function is poorly understood. Therefore, the purpose of this study was to compare the impact in cardiovascular function of social isolation for 3 weeks in adolescent and adult male rats. Also, the long-term effects of social isolation during adolescence were investigated longitudinally. Social isolation reduced body weight in adolescent, but not in adult animals. Disruption of social bonds during adolescence increased arterial pressure without affecting heart rate and pulse pressure (PP). Nevertheless, social isolation in adulthood reduced systolic arterial pressure and increased diastolic arterial pressure, which in turn decreased PP without affecting mean arterial pressure. Cardiovascular changes in adolescents, but not adults, were followed by facilitation of both baroreflex sensitivity and vascular reactivity to the vasodilator agent acetylcholine. Vascular responsiveness to either the vasodilator agent sodium nitroprusside or the vasoconstrictor agent phenylephrine was not affected by social isolation. Except for the changes in body weight and baroreflex sensitivity, all alterations evoked by social isolation during adolescence were reversed in adulthood after moving animals from isolated to collective housing. These findings suggest a vulnerability of adolescents to the effects of chronic social isolation in cardiovascular function. However, results indicate minimal cardiovascular consequences in adulthood of disruption of social bonds during adolescence. © 2015 Wiley Periodicals, Inc. Develop Neurobiol, 2015.

Indeterminate form of chagas disease and metabolic syndrome: a dangerous combination

Chagas’ disease (CD) has been a major concern in public health in Latin America countries and in Brazil there are about 3 million people suffering from this disease. With the social and economic changes which have been occurring in the last 6 decades in the country, there have been a lot of changes in the population life style with severe metabolic consequences, especially for those with Chagas' disease. The objective of this study was to evaluate the prevalence of metabolic syndrome in individuals with the indeterminate form of CD. A total of 74 individuals, mean age of 55.6 years, participated in the study. Anthropometric and biochemical evaluations were performed. Overweight/obesity was found in 86.5 % of individuals, increased waist circumference in 72.5%, and 67% had more than 30% of fat mass. Hyperglycemia and dyslipidemia were observed in 24.3% and 75.7% of patients, respectively. Metabolic syndrome was diagnosed in 48.2% of patients. The family history revealed high prevalence of cardiovascular diseases (80.3%), systemic arterial hypertension (57.1%) and diabetes mellitus (42.8%). A total of 90% of patients were overweight/obese, and it is well known that increased adipose tissue, specially visceral adipose tissue is highly associated with dyslipidemia and cardiovascular diseases, as well as imbalance in production of proinflammatory and antiinflammatory cytokines produced by that tissue. Adipocytes are also known as a reservoir for Trypanosoma cruzi, favoring an increase in parasite load and a possible reacutization of the disease. Therefore, the study individuals are at high risk of developing cardiovascular diseases as well as further symptomatic form of the Chagas' disease, mainlychagastic cardiopathy.