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Night-shift workers may develop poor cardiovascular health. Studies about heart rate variability (HRV) metrics could identify risk factors in this population and be used to examine the effectiveness of interventions for optimizing the health of night-shift workers. The purpose of this review was to examine the use of HRV methodologies in studies about night-shift work. Overall, 34 articles met the selection criteria and underwent a methodological critique. The main conclusion across these studies was that night-shift work could increase the sympathetic influences on the variability between heartbeats. In many cases, however, important methodological details were omitted (e.g., the number and duration of electrocardiogram recordings, sampling rates, R–R segment duration, wavelet transform methods). Recommendations include adding measures of disease outcomes, using ≥250 Hz sampling rates and 600-s R–R segments, and measuring sleep and circadian rhythms. With these approaches, researchers can design investigations that identify therapeutic targets for improving the health of night-shift workers.
Open Medicine
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Multiple sclerosis is still a disease without a cure. Although intensive research efforts have led to the development of drugs that modify the activity of the disease, most of them have various side effects and are expensive. At the same time it is becoming apparent that some remedies usually used to treat somatic and psychic disorders also have immunomodulating properties, and may help manage multiple sclerosis and other autoimmune diseases. We describe here the role of the sympathetic nervous system in the neuro-immune interaction in multiple sclerosis and other immune diseases with increased cellular immunity as well as neurochemical disturbances that take place in these disorders.
The primordia of the sympathetic trunk ganglia were traced on serial sections of 10 embryos at stage 13 (32 postovulatory days). It was found that in all embryos, these primordia were present in the thoracic level T4 to T9 and they appeared as scattered aggregates of cells lying dorsally and laterally to the dorsal aortae. (Folia Morphol 2009; 68, 4: 215–217)
The aim of this experiment was to compare the role of renin-angiotensin and sympathetic nervous system in post-haemorrhagic mechanism of oxytocin release. Oxytocin content in venous dialysates was determined by radioimmunoassay. In control rats the release of oxytocin into dialysates did not change during whole experiment. The injection of captopril induced 2-fold higher oxytocin release, but caused no change in oxytocin release after bleeding. Superior cervical ganglionectomy (SCGx) 20 days before, caused 5-fold higher increase in oxytocin release than in control group. Injection of captopril in rats after SCGx, did not decrease the high level of oxytocin in dialysate. However, bleeding increased oxytocin release and 1 hour after bleeding the highest - 14-fold increase, took place. In the contrary to 14-fold increase in oxytocin release in animals with superior cervical ganglia (SCG), bleeding after SCGx caused only 2-fold higher oxytocin release. When SCGx, bleeding and injection of captopril were done simultaneously, oxytocin release remained on the control concentration level. We assumed that blockade of renin angiotensin system and sympathetic dennervation prevent the increase in oxytocin release after bleeding. On basis of our present experiments, it can be assumed that, in posthaemorrhagic oxytocin release into the blood, sympathetic innervation derived from SCGx, as well as, renin-angiotensin system are involved.
Content available remote Cardiovascular effects of centrally acting orexin A in haemorrhage-shocked rats
Orexin A influences the central cardiovascular regulation, since after intracerebroventricular (icv) administration it evokes short-lasting increases in mean arterial pressure (MAP) and heart rate (HR) in normotensive animals. The aim of the present study was to examine haemodynamic effects of orexin A in haemorrhage-shocked rats. Experiments were carried out in anaesthetized Wistar rats subjected for a critical irreversible haemorrhagic hypotension of 20-25 mmHg, which resulted in the death of all saline icv-treated control animals within 30 min. Orexin A (0.5-1.5 nmol; icv) administered at 5 min of critical hypotension evoked dose-dependent long-lasting increases in MAP, HR and renal, mesenteric and hindquarters blood flows, with a 100% survival of 2 h after treatment (1.5 nmol; icv). Changes in MAP and peripheral haemodynamics were inhibited by intravenous pretreatment with alpha1- and alpha2-adrenoceptor antagonists prazosin (0.5 mg/kg) and yohimbine (1.0 mg/kg), respectively. Moreover, both antagonists significantly decreased the survival rate to 16.6 and 33.3% (P<0.05 vs. orexin A [1.5 nmol]-treated group). In contrast, ß-adrenoceptor antagonist propranolol (1.0 mg/kg) completely blocked orexin A-induced HR changes, without influence on MAP, peripheral blood flows and the survival rate. Therefore, we conclude that centrally acting orexin A evokes the resuscitating effect in haemorrhage-shocked rats due to the activation of the sympathetic nervous system.
The sympathetic nervous system belongs to the essential systems participating in blood pressure (BP) regulation. Inhibitory intervention into the key point of its operation (alfa 1 adrenoceptors) in the prehypertensive period of spontaneously hypertensive rats (SHR) might affect the development of the hypertension in later ontogenic periods. We studied the long-term effect of prazosin administration on the cardiovascular system of young Wistar rats and SHR. Four-week-old animals were used: Wistar rats, SHR, and Wistar rats and SHR receiving prazosin (10 mg/kg/day in tap water) by gavage. Blood pressure (BP) was measured weekly by the plethysmographic method. After six weeks under anaesthesia, the carotid artery was cannulated for BP registration, and the jugular vein was cannulated for administration of drugs. Afterwards, the animals were perfused with a glutaraldehyde fixative at a pressure of 120 mmHg. The septal branch of the left descending coronary artery was processed using electron microscopy. The prazosin administration evoked the following results in both groups: a decrease of BP and heart/body weight ratio, enhancement of hypotensive responses to acetylcholine (0.1 µg, 1 µg, and 10 µg), and an increase in the inner diameter of the coronary artery without changes in wall thickness, cross sectional area (CSA) (tunica intima+media), CSA of smooth muscle cells, and extracellular matrix. In the SHR group, a reduction was observed in BP increase after noradrenaline (1 µg) application. CSA of endothelial cells which was decreased in the SHR (compared to the control Wistar rats) was increased after prazosin treatment (up to control value). Long-term prazosin administration from early ontogeny partially prevented some pathological alterations in the cardiovascular system of SHR.
Content available remote Why study sympathetic nervous system?
Cardiovascular diseases are the most frequent causes of morbidity and mortality around the world. However, during last decades, an improvement was made in diagnosis and therapy of cardiovascular diseases, there was still a need for better understanding of their pathophysiology. Among neurohormonal systems, SNS plays a central role in cardiovascular regulation in both health and disease. Involvement of SNS in pathogenesis of hypertension, coronary artery disease or heart failure is well known and proved. Methods such as microneurography, direct catecholamine measurements, heart rate variability or baroreflex sensitivity assessment allowed studying sympathetic activity and its influence on cardiovascular disorders. Although introduced into scientific practice methods of SNS evaluation are not commonly used in the clinic. However, two of the methods: analysis of heart rate variability (HRV) and baroreflex sensitivity (BRS) were recommended as the diagnostic tools and can be found in clinical guidelines as basic assessment methods.
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