Increased sympathetic activity in normotensive offspring of malignant hypertensive parents compared to offspring of normotensive parents

Malignant hypertension seems to be the consequence of very high blood pressure. Furthermore, an increase in sympathetic and renin-angiotensin system activity is considered to be the main mechanisms producing malignant hypertension. In the present study, 10 offspring of malignant hypertensive (OMH) parents (age 28 ± 5 years, 7 males, 3 females, 2 white and 8 non-white) and 10 offspring of normotensive (ONT) parents (age 28 ± 6 years, 2 males, 8 females, 3 white and 7 non-white) were evaluated. The OMH group had significantly higher (P < 0.05) casual blood pressure (125 ± 10/81 ± 5 mmHg) compared with ONT (99 ± 13/67 ± 5 mmHg). The increase in blood pressure was greater in OMH (&#916; SBP = 17 ± 2 vs &#916; SBP = 9 ± 1 mmHg in ONT) during cold pressor testing, but they had a lower increase in heart rate (&#916; HR = 13 ± 2 vs &#916; HR = 20 ± 3 bpm in ONT) during isometric exercise (handgrip test). Sympathetic activity, measured by microneurography, was significantly higher (P < 0.05) before exercise in OMH (17 ± 6 vs 11 ± 4 burst/min in ONT) and exhibited a greater increase (&#916; = 18 ± 10 vs &#916; = 8 ± 3 burst/min in ONT) during isometric exercise. This study showed increased sympathetic activity in OMH before exercise and a greater response during isometric exercise, suggesting an autonomic abnormality before exercise and a greater sympathetic response to physical stress in OMH compared to ONT

Association of meningitis and pericarditis in invasive pneumococcal disease : a rare case

Relatar um caso raro de uma criança com meningite associada a pericardite na doença pneumocócica invasiva. Este relato descreve uma evolução clínica desfavorável de um lactente feminino de 6 meses de idade, previamente hígido, que apresentou inicialmente sintomas respiratórios e febre. A radiografia de tórax revelou um aumento da área cardíaca sem alterações radiográficas nos pulmões. Após a identificação do derrame pericárdico, o paciente apresentou convulsões e entrou em coma. Pneumonia foi descartada durante a investigação clínica. Contudo, foi identificado Streptococcus pneumoniae nas culturas de líquor e sangue. O exame neurológico inicial foi compatível com morte encefálica, posteriormente confirmada pelo protocolo. A pericardite purulenta tornou-se uma complicação rara da doença pneumocócica invasiva desde o advento da terapia antibiótica. Pacientes com pneumonia extensa são primariamente predispostos e, mesmo com tratamento adequado e precoce, estão sujeitos a altas taxas de mortalidade. A associação de meningite pneumocócica e pericardite é incomum e, portanto, de difícil diagnóstico. Por isso, uma alta suspeição diagnóstica é necessária para instituir o tratamento precoce e aumentar a sobrevida371126129Toreportararecaseofachildwithinvasivepneumococcal disease that presented meningitis associated with pericarditis. This report describes the unfavorable clinical course of a previously healthy 6-months-old female infant who initially presented symptoms of fever and respiratory problems. A chest X-ray revealed an increased cardiac area with no radiographic changes in the lungs. After identifying a pericardial effusion, the patient experienced seizures and went into coma. Pneumonia was excluded as a possibility during the clinical investigation. However, Streptococcus pneumoniae was identified in the cerebrospinal fluid and blood cultures. An initial neurological examination showed that the patient was brain dead, which was then later confirmed according to protocol. Purulent pericarditis has become a rare complication of invasive pneumococcal disease since the advent of antibiotic therapy. Patients with extensive pneumonia are primarily predisposed and, even with early and adequate treatment, are prone to high mortality rates. The association of pneumococcal meningitis and pericarditis is uncommon, and therefore difficult to diagnose. As such, diagnostic suspicion must be high in order to institute early treatment and increase surviva

Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans

To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 ± 314 vs R5-30 = 7150 ± 326, R35-60 = 6794 ± 349, and R65-90 = 6628 ± 311, P&lt;0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 ± 267 vs 9818 ± 366, P&lt;0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP

Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats

The effect of swimming training (ST) on vagal and sympathetic cardiac effects was investigated in sedentary (S, N = 12) and trained (T, N = 12) male Wistar rats (200-220 g). ST consisted of 60-min swimming sessions 5 days/week for 8 weeks, with a 5% body weight load attached to the tail. The effect of the autonomic nervous system in generating training-induced resting bradycardia (RB) was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. Cardiac hypertrophy was evaluated by cardiac weight and myocyte morphometry. Plasma catecholamine concentrations and citrate synthase activity in soleus muscle were also determined in both groups. Resting heart rate was significantly reduced in T rats (355 ± 16 vs 330 ± 20 bpm). RB was associated with a significantly increased cardiac vagal effect in T rats (103 ± 25 vs 158 ± 40 bpm), since the sympathetic cardiac effect and intrinsic heart rate were similar for the two groups. Likewise, no significant difference was observed for plasma catecholamine concentrations between S and T rats. In T rats, left ventricle weight (13%) and myocyte dimension (21%) were significantly increased, suggesting cardiac hypertrophy. Skeletal muscle citrate synthase activity was significantly increased by 52% in T rats, indicating endurance conditioning. These data suggest that RB induced by ST is mainly mediated parasympathetically and differs from other training modes, like running, that seems to mainly decrease intrinsic heart rate in rats. The increased cardiac vagal activity associated with ST is of clinical relevance, since both are related to increased life expectancy and prevention of cardiac events

Muscle sympathetic nerve activity and hemodynamic alterations in middle-aged obese women

To study the relationship between the sympathetic nerve activity and hemodynamic alterations in obesity, we simultaneously measured muscle sympathetic nerve activity (MSNA), blood pressure, and forearm blood flow (FBF) in obese and lean individuals. Fifteen normotensive obese women (BMI = 32.5 ± 0.5 kg/m²) and 11 age-matched normotensive lean women (BMI = 22.7 ± 1.0 kg/m²) were studied. MSNA was evaluated directly from the peroneal nerve by microneurography, FBF was measured by venous occlusion plethysmography, and blood pressure was measured noninvasively by an autonomic blood pressure cuff. MSNA was significantly increased in obese women when compared with lean control women. Forearm vascular resistance and blood pressure were significantly higher in obese women than in lean women. FBF was significantly lower in obese women. BMI was directly and significantly correlated with MSNA, blood pressure, and forearm vascular resistance levels, but inversely and significantly correlated with FBF levels. Obesity increases sympathetic nerve activity and muscle vascular resistance, and reduces muscle blood flow. These alterations, taken together, may explain the higher blood pressure levels in obese women when compared with lean age-matched women