RESUMO
This manuscript aims to provide a simple and concise discussion on heart rate variability (HRV) for small animal veterinarians. Despite the fact that heart rate variability analysis techniques have been used for quite a long time in medical sciences, it seems to be not completely understood by a large fraction of veterinarian professionals, thereby, reducing the possible benefits to patients that could arise from such information. The analysis of the R-R intervals enables the veterinarian to evaluate autonomic sympathetic and parasympathetic modulation of the heart, composing the so-called cardiac autonomic balance. Several pathophysiological states lead to profound changes in autonomic balance, especially in the cardiovascular system. Therefore, heart rate variability methods remain a valuable and powerful tool for the diagnosis and prognosis of cardiovascular diseases.
Esta revisão tem como objetivo fornecer uma discussão breve e simples acerca da variabilidade da frequência cardíaca (VFC) para veterinários de pequenos animais. Apesar de as técnicas de análise da variabilidade da frequência cardíaca já serem utilizadas há bastante tempo nas ciências médicas, aparentemente não são totalmente compreendidas por grande parte dos profissionais veterinários, reduzindo, assim, os possíveis benefícios aos pacientes que poderiam advir de tais informações. A análise dos intervalos R-R permite ao veterinário avaliar a modulação autonômica simpática e parassimpática do coração, compondo o chamado equilíbrio autonômico cardíaco. Vários estados fisiopatológicos levam a profundas alterações no equilíbrio autonômico, especialmente no sistema cardiovascular. Portanto, os métodos de variabilidade da frequência cardíaca representam uma ferramenta valiosa para o diagnóstico e prognóstico de doenças cardiovasculares.
RESUMO
Chronic administration of anabolic androgenic steroids (AAS) in adult rats results in cardiac hypertrophy and increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Molecular analyses demonstrated that hyperactivation of type 1 angiotensin II (AT1) receptor mediates cardiac hypertrophy induced by AAS and also induces down-regulation of myocardial ATP-sensitive potassium channel (KATP), resulting in loss of exercise-induced cardioprotection. Exposure to AAS during adolescence promoted long-term cardiovascular dysfunctions, such as dysautonomia. We tested the hypothesis that chronic AAS exposure in the pre/pubertal phase increases the susceptibility to myocardial ischemia/reperfusion (IR) injury in adult rats. Male Wistar rats (26day old) were treated with vehicle (Control, n=12) or testosterone propionate (TP) (AAS, 5mgkg-1 n=12) 5 times/week during 5 weeks. At the end of AAS exposure, rats underwent 23days of washout period and were submitted to euthanasia. Langendorff-perfused hearts were submitted to IR injury and evaluated for mechanical dysfunctions and infarct size. Molecular analysis was performed by mRNA levels of α-myosin heavy chain (MHC), ßMHC and brain-derived natriuretic peptide (BNP), ryanodine receptor (RyR2) and sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) by quantitative RT-PCR (qRT-PCR). The expression of AT1 receptor and KATP channel subunits (Kir6.1 and SURa) was analyzed by qRT-PCR and Western Blot. NADPH oxidase (Nox)-related reactive oxygen species generation was assessed by spectrofluorimetry. The expression of antioxidant enzymes was measured by qRT-PCR in order to address a potential role of redox unbalance. AAS exposure promoted long-term cardiac hypertrophy characterized by increased expression of ßMHC and ßMHC/αMHC ratio. Baseline derivative of pressure (dP/dt) was impaired by AAS exposure. Postischemic recovery of mechanical properties was impaired (decreased left ventricle [LV] developed pressure and maximal dP/dt; increased LV end-diastolic pressure and minimal dP/dt) and infarct size was larger in the AAS group. Catalase mRNA expression was significantly decreased in the AAS group. In conclusion, chronic administration of AAS during adolescence promoted long-term pathological cardiac hypertrophy and persistent increase in the susceptibility to myocardial IR injury possible due to disturbances on catalase expression.