Blood pressure responses in firefighters reviewed

Blood pressure (BP) responses are controlled by various factors and understanding how BP changes is important to occupational health. This paper presents a review of the literature which reports BP responses in the firefighter population. Hypertension is one of the main risk factors underlying the pathophysiology of cardiovascular disease (CVD), and cardiac incidents remain the leading cause of line-of-duty deaths in firefighters. Risk factors for line-of-duty deaths include obesity, previous or underlying heart disease, and hypertension. The occupation of firefighting is one of the most hazardous and dangerous jobs, yet over 50% of firefighters are volunteers. Tactical operations and the hazardous nature of firefighting are exposures that influence stress responses and therefore affect BP. In fact, hypertension in firefighters often remains undocumented or undiagnosed. CVD risk and elevated BP in tactical populations, like firefighters, may be a combination of physical and emotional stress due to the nature of the job. Cross-sectional studies have reported that firefighters have higher levels of BP and higher rates of hypertension compared to civilians. Interestingly, there is a limited amount of research that reports BP values before and after firefighting-related activities, and very few studies that report on interventional changes in BP. Here we synthesize the literature on firefighting and provide a summary of the studies that report pre- and post- BP levels that relate to CVD risk factors, occupational factors, firefighting activities, and the data on exercise training and BP. More studies are needed that examine BP in firefighters and that report on the changes in BP with occupational activities.

Estimation of Blood Pressure on Postprandial Breakfast, Meal and Dinner among Vegetarians

Background: Blood pressure is the pressure of the blood within the arteries. Based on the circadian rhythm the BP can change. DBP can change according to age. Processed foods, canned soups, snack foods, and condiments may increase BP. The main aim of this study is to estimate the difference in postprandial BP responses during breakfast, lunch and dinner. Materials and Methods: A total of 26 healthy volunteers were randomly selected, men and women aged 17-20 for the study. Systolic blood pressure, Diastolic blood pressure, Heart rate were measured with ambulatory Blood Pressure devices every 10 min before until 90 min after each meal. The measurements were taken to identify the difference in postprandial Blood pressure responses between breakfast, lunch and dinner. Before starting the study, informed consent was taken. Data were collected and analyzed using SPSS software, independent sample T test. Results: In the present study, there was a mild increase observed before and after breakfast, lunch and dinner. There is a difference in BP before and postprandial during breakfast, lunch and dinner. In the present study, there was a mild increase observed before and after breakfast, lunch and dinner. In the morning the body releases hormones such as adrenaline and noradrenaline. These hormones boost energy which raises the BP. So there is decrease in BP before and postprandial during breakfast Conclusion: From this study only a significant difference was observed in SBP, DBP, HR of dinner. There was no significant change seen in breakfast.

The Oslo Ischaemia Study: cohort profile

PurposeThe Oslo Ischaemia Study was designed to investigate the prevalence and predictors of silent coronary disease in Norwegian middle-aged men, specifically validating exercise electrocardiography (ECG) findings compared with angiography. The study has been important in investigating long-term predictors of cardiovascular morbidity and mortality, as well as investigating a broad spectrum of epidemiological and public health perspectives.ParticipantsIn 1972–1975, 2014 healthy men, 40–59 years old, were enrolled in the study. Comprehensive clinical examination included an ECG-monitored exercise test at baseline and follow-ups. The cohort has been re-examined four times during 20 years. Linkage to health records and national health registries has ensured complete endpoint registration of morbidity until the end of 2006, and cancer and mortality until the end of 2017.Findings to dateThe early study results provided new evidence, as many participants with a positive exercise ECG, but no chest pain (‘silent ischaemia’), did not have significant coronary artery stenosis after all. Still, they were over-represented with coronary disease after years of follow-up. Furthermore, participants with the highest physical fitness had lower risk of cardiovascular disease, and the magnitude of blood pressure responses to moderate exercise was shown to influence the risk of cardiovascular disease and mortality. With time, follow-up data allowed the scope of research to expand into other fields of medicine, with the aim of investigating predictors and the importance of lifestyle and risk factors.Future plansRecently, the Oslo Ischaemia Study has been found worthy, as the first scientific study, to be preserved by The National Archives of Norway. All the study material will be digitised, free to use and accessible for all. In 2030, the Oslo Ischaemia Study will be linked to the Norwegian Cause of Death Registry to obtain complete follow-up to death. Thus, a broad spectrum of additional opportunities opens.

Modulation of Sirt1 and FoxO1 on Hypothalamic Leptin‐Mediated Sympathetic Activation and Inflammation in Diet‐Induced Obese Rats

Background Hypothalamic leptin‐mediated signaling contributes to the exaggerated sympatho‐excitation and increased blood pressure in obesity‐associated hypertension. The aim of the study was to investigate the roles of energy‐sensing enzyme sirtuin1 (Sirt1) and forkhead box protein O1 (FoxO1) on the hypothalamic leptin‐mediated high sympathetic nerve activity and inflammation in obesity. Methods and Results Sprague Dawley rats were fed with high‐fat diet (HFD) for 12 weeks. In vivo, the potential of Srit1 and FoxO1 in the sympathetic effects of leptin was investigated via siRNA injection to knockdown Sirt1 or FoxO1 gene in the arcuate nucleus (ARCN) of hypothalamus in rats. In vitro, the effects of Sirt1 or FoxO1 on leptin‐mediated inflammation were observed in proopiomelanocortin (POMC) and microglial cells. Knockdown Sirt1 by siRNA significantly reduced the renal sympathetic nerve activity (RSNA) and blood pressure responses to leptin injection in the ARCN in the HFD rats. Conversely, knockdown FoxO1 significantly enhanced the RSNA and blood pressure responses to leptin injection in the HFD rats. Knockdown Sirt1 reduced the levels of pro‐inflammatory cytokines interleukin 6 (IL‐6), tumor necrosis factor α (TNF‐α), interleukin 1β (IL‐1β), C1q/TNF‐related protein‐1 (CTRP1), and immune cell infiltration in the ARCN in the HFD rats. Knockdown FoxO1 significantly increased the level of IL‐6 in the ARCN of HFD rats. In cultured hypothalamic POMC and microglial cells, knockdown Sirt1 significantly reduced leptin‐induced IL‐6 expression, affected the levels of AMP‐activated protein kinase (AMPK) and serine/threonine‐specific protein kinase (Akt). Knockdown FoxO1 significantly increased leptin‐induced IL‐6 in both POMC cells and microglial cells. Conclusions These data suggest that both Sirt1 and FoxO1 are the key modulators of leptin signaling in the hypothalamus contributed to the over sympathetic activation and inflammation in obesity.