Publications by authors named "João Blanco"

6 Publications

  • Page 1 of 1

Derivation and validation of a national multicenter mortality risk stratification model - the ExCare model: a study protocol.

Braz J Anesthesiol 2021 Jul 26. Epub 2021 Jul 26.

Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.

Introduction: Surgical care is essential for proper management of various diseases. However, it can result in unfavorable outcomes. In order to identify patients at higher risk of complications, several risk stratification models have been developed. Ideally, these tools should be simple, reproducible, accurate, and externally validated. Unfortunately, none of the best-known risk stratification instruments have been validated in Brazil. In this sense, the Ex-Care model was developed by retrospective data analysis of surgical patients in a major Brazilian university hospital. It consists of four independent predictors easily collected in the preoperative evaluation, showing high accuracy in predicting death within 30 days after surgery.

Objectives: To update and validate a Brazilian national-based model of postoperative death probability within 30 days based on the Ex-Care model. Also, to develop an application for smartphones that allows preoperative risk stratification by Ex-Care model.

Methods: Ten participating centers will collect retrospective data from digital databases. Variables age, American Society of Anesthesiologists (ASA) physical status, surgical severity (major or non-major) and nature (elective or urgent) will be evaluated as predictors for in-hospital mortality within 30 postoperative days, considered the primary outcome.

Expected Results: We believe that the Ex-Care model will present discriminative capacity similar to other classically used scores validated for surgical mortality prediction. Furthermore, the mobile application to be developed will provide a practical and easy-to-use tool to the professionals enrolled in perioperative care.
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http://dx.doi.org/10.1016/j.bjane.2021.07.003DOI Listing
July 2021

Chronic cholinergic stimulation promotes changes in cardiovascular autonomic control in spontaneously hypertensive rats.

Auton Neurosci 2015 Dec 21;193:97-103. Epub 2015 Oct 21.

Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil. Electronic address:

Hypertension is often accompanied by autonomic dysfunction, which is detrimental to cardiac regulation. On the other hand, cholinergic stimulation through inhibition of acetylcholinesterase appears to have beneficial effects on cardiac autonomic control. Thus, our objective was to investigate the effects of chronic cholinergic stimulation on hemodynamic and cardiovascular autonomic control parameters in spontaneously hypertensive rats (SHR). For this, 26-week-old SHR (N = 32) and Wistar Kyoto rats (WK; N = 32) were divided into two groups: one treated with vehicle (H2O; N = 16) and the other treated with pyridostigmine bromide (PYR; N = 16) in drinking water (25 mg/kg/day) for 2 weeks. All groups were subjected to recording of arterial pressure (AP) and heart rate (HR), quantification of ejection fraction (EF), evaluation of cardiac tonic autonomic balance by means of double autonomic blockade with methylatropine and propranolol, analysis of systolic AP (SAP) and HR variability (HRV), and evaluation of baroreflex sensitivity (BRS). AP, HR, and EF were reduced in the SHR-PYR group compared with the SHR-H2O group. Evaluation of autonomic parameters revealed an increase in vagal tone participation in cardiac tonic autonomic balance and reduced SAP variability; however, no changes were observed in HRV or BRS. These results suggest that chronic cholinergic stimulation with pyridostigmine bromide promotes reduction in the hemodynamic parameters AP, HR, and EF. Additionally, tonic autonomic balance was improved and a reduction in LF oscillations of SAP variability was observed that could not be attributed to BRS, as the latter did not change. Further studies should be conducted to identify the mechanisms involved in the observed responses.
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http://dx.doi.org/10.1016/j.autneu.2015.09.002DOI Listing
December 2015

Physical exercise attenuates the cardiac autonomic deficit induced by nitric oxide synthesis blockade.

Arq Bras Cardiol 2009 Jan;92(1):31-8

Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Rua Luís Basso 130, Jardim Recreio, Ribeirão Preto, SP, Brazil.

Background: The nitric oxide (NO) synthesis blockade is characterized by an increase in the cardiac sympathetic activity and the physical training promotes the decrease in the sympathetic activity.

Objective: We investigated the effect of the NO synthesis blockade on the autonomic cardiovascular control in rats submitted to aerobic exercises during a 10-week period.

Methods: Male Wistar rats were divided in four groups: control rats, treated with chow food and water ad libitum for 10 weeks (CR); control rats, treated with N G-nitro-L-arginine methyl ester (L-NAME) during the last week (CRL); rats trained during 10 weeks on an electrical treadmill (TR); rats trained for 10 weeks and treated with L-NAME during the last week (TRL). The autonomic cardiovascular control was investigated in all groups with the use of a double blockade with methylatropine and propranolol and analysis of variability.

Results: The CRL and TRL groups presented hypertension. The CRL group presented tachycardia and predominance of the sympathetic tonus in heat rate (HR) measurement after the pharmacological autonomic blockade. The TR group presented bradycardia and lower intrinsic HR when compared to the others. The evaluation of the HR variability showed lower absolute and normalized values in the low frequency (LF) band in the CRL group. On the other hand, the TRL presented an increase in the LF band in absolute values. The analysis of variability of the systemic arterial pressure (SAP) showed that the CRL and TRL groups presented higher values in the LF band.

Conclusion: The previous physical exercise prevented the deficit in the autonomic cardiac control induced by the treatment with L-NAME, but did not prevent the increase in the SAP variability.
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http://dx.doi.org/10.1590/s0066-782x2009000100006DOI Listing
January 2009

The effect of ovariectomy on cardiac autonomic control in rats submitted to aerobic physical training.

Auton Neurosci 2008 Dec 3;143(1-2):5-11. Epub 2008 Jul 3.

Department of Biomechanics, Medicine and Rehabilitation of School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900, Ribeirão Preto, SP, Brazil.

We have investigated the ovariectomy effects on the cardiovascular autonomic adaptations induced by aerobic physical training and the role played by nitric oxide (NO). Female Wistar rats (n=70) were divided into five groups: Sedentary Sham (SS); Trained Sham (TS); Trained Hypertensive Sham treated with N(G)-nitro-L-arginine methyl ester (L-NAME) (THS); Trained Ovariectomized (TO); and Trained Hypertensive Ovariectomized treated with L-NAME (THO). Trained groups were submitted to a physical training during 10 weeks. The cardiovascular autonomic control was investigated in all groups using different approaches: 1) pharmacological evaluation of autonomic tonus with methylatropine and propranolol; 2) analysis of heart rate (HR) and systolic arterial pressure (AP) variability; 3) spontaneous baroreflex sensitivity (BRS) evaluation. Hypertension was observed in THS and THO groups. Pharmacological analysis showed that TS group had increased predominance of autonomic vagal tonus compared to SS group. HR and intrinsic HR were found to be reduced in all trained animals. TS group, compared to other groups, showed a reduction in LF oscillations (LF=0.2-0.75 Hz) of pulse interval in both absolute and normalized units as well as an increase in HF oscillations (HF=0.75-2.50 Hz) in normalized unit. BRS analysis showed that alpha-index was different between all groups. TS group presented the greatest value, followed by the TO, SS, THO and THS groups. Ovariectomy has negative effects on cardiac autonomic modulation in trained rats, which is characterized by an increase in the sympathetic autonomic modulation. These negative effects suggest NO deficiency. In contrast, the ovariectomy seems to have no effect on AP variability.
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http://dx.doi.org/10.1016/j.autneu.2008.05.003DOI Listing
December 2008

Heart rate and arterial pressure variability in the experimental renovascular hypertension model in rats.

Auton Neurosci 2008 May 13;139(1-2):38-45. Epub 2008 Feb 13.

Department of Biomechanics, Medicine and Rehabilitation, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.

This study was conducted in one kidney, one clip (1K1C) Goldblatt hypertensive rats to evaluate vascular and cardiac autonomic control using different approaches: 1) evaluation of the autonomic modulation of heart rate (HR) and systolic arterial pressure (SAP) by means of autoregressive power spectral analysis 2) assessment of the cardiac baroreflex sensitivity; and 3) double blockade with methylatropine and propranolol. The 1K1C group developed hypertension and tachycardia. The 1K1C group also presented reduction in variance as well as in LF (0.23+/-0.1 vs. 1.32+/-0.2 ms2) and HF (6.6+/-0.49 vs. 15.1+/-0.61 ms2) oscillations of pulse interval. Autoregressive spectral analysis of SAP showed that 1K1C rats had an increase in variance and LF band (13.3+/-2.7 vs. 7.4+/-1.01 mmHg2) in comparison with the sham group. The baroreflex gain was attenuated in the hypertensive 1K1C (-1.83+/-0.05 bpm/mmHg) rats in comparison with normotensive sham (-3.23+/-0.06 bpm/mmHg) rats. The autonomic blockade caused an increase in the intrinsic HR and sympathetic predominance on the basal HR of 1K1C rats. Overall, these data indicate that the tachycardia observed in the 1K1C group may be attributed to intrinsic cardiac mechanisms (increased intrinsic heart rate) and to a shift in the sympathovagal balance towards cardiac sympathetic over-activity and vagal suppression associated to depressed baroreflex sensitivity. Finally, the increase in the LF components of SAP also suggests an increase in sympathetic activity to peripheral vessels.
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http://dx.doi.org/10.1016/j.autneu.2008.01.001DOI Listing
May 2008

Nitric oxide synthesis blockade increases hypertrophy and cardiac fibrosis in rats submitted to aerobic training.

Arq Bras Cardiol 2007 Aug;89(2):88-93, 99-104

Faculdade de Medicina de Ribeirão Preto, Universidade Estadual de Londrina, Uberaba, MG, Brazil.

Objective: The objective of the present study was to evaluate cardiac tissue adaptations in rats submitted to aerobic training after nitric oxide (NO) synthesis blockade.

Methods: The animals (n=48) were divided into four groups: sedentary (CONTROL group); hypertensive after administration of NG-nitro-L-arginine methyl ester for 7 days (L-NAME Group); trained for 8 weeks through swimming exercises (TRAINED Group);trained and treated with L-NAME during the last week (L-NAME TRAINED Group). All the animals were submitted to the experiment procedures for blood pressure (BP) readings and cardiac morphometric evaluation.

Results: In comparison to the other groups, the L-NAME and L-NAME TRAINED groups were hypertensive (p<0.05); however, BP elevation in the L-NAME TRAINED group was significantly lower than the L-NAME group (p<0.05). The heart weight indexes for the TRAINED and L-NAME TRAINED groups were higher than the CONTROL and L-NAME groups (p<0.05). Also they had presented higher rates of macroscopic cardiac area and cardiac fibrosis in relation to the rest (p<0.05); comparisons revealed that the values for the L-NAME TRAINED group were significantly higher (p<0.05) than the others.

Conclusion: Short term NO synthesis blockade in sedentary animals induced hypertension but did not cause cardiac hypertrophy. In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays an important role in cardiac tissue adaptations caused by aerobic exercise.
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http://dx.doi.org/10.1590/s0066-782x2007001400005DOI Listing
August 2007
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