scholarly journals Pathophysiology of Takotsubo Syndrome as A Bridge to Personalized Treatment

2021 ◽  
Vol 11 (9) ◽  
pp. 879
Author(s):  
Monika Budnik ◽  
Radosław Piątkowski ◽  
Dorota Ochijewicz ◽  
Martyna Zaleska ◽  
Marcin Grabowski ◽  
...  
Keyword(s):  
Nervous System ◽  
Genetic Factors ◽  
Personalized Treatment ◽  
Takotsubo Syndrome ◽  
Primary Condition ◽  
Psychiatric Conditions ◽  
Sympathetic Nervous ◽  
Vessel Dissection ◽  
The Brain ◽  
Microcirculation Dysfunction

Takotsubo syndrome (TTS) consists of transient dysfunction of the left and/or right ventricle in the absence of ruptured plaque; thrombus or vessel dissection. TTS may be divided into two categories. Primary TTS occurs when the cause of hospitalization is the symptoms resulting from damage to the myocardium usually preceded by emotional stress. Secondary TTS occurs in patients hospitalized for other medical; surgical; anesthetic; obstetric or psychiatric conditions who have activation of their sympathetic nervous system and catecholamines release- they develop TTS as a complication of their primary condition or its treatment. There are several hypotheses concerning the cause of the disease. They include a decrease in estrogen levels; microcirculation dysfunction; endothelial dysfunction and the hypothesis based on the importance of the brain-heart axis. More and more research concerns the importance of genetic factors in the development of the disease. To date; no effective treatment or prevention of recurrent TTS has been found. Only when the pathophysiology of the disease is fully known; then personalized treatment will be possible.

scholarly journals The Brain-Heart Connection in Takotsubo Syndrome: The Central Nervous System, Sympathetic Nervous System, and Catecholamine Overload

2020 ◽  
Vol 2020 ◽  
pp. 1-5 ◽  
Author(s):  
Xiaopu Wang ◽  
Junyu Pei ◽  
Xinqun Hu
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Physiological Stress ◽  
Acute Chest Pain ◽  
Takotsubo Syndrome ◽  
The Central Nervous System ◽  
Sympathetic Nervous ◽  
As Stress ◽  
Artery Obstruction ◽  
The Brain

Takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of acute heart failure syndrome triggered by intense psychological or physiological stress. TTS typically manifests as acute chest pain, dyspnea or syncope that mimics an acute myocardial infarction but does not involve coronary artery obstruction. The current understanding of the pathogenesis of TTS suggests that sympathetic nervous system (SNS) activation plays a central role. Specifically, stress can activate the SNS and lead to the over-release of catecholamine, which have toxic effects on myocardial tissue when present at excessive levels. However, the brain changes associated with TTS and the connection between the brain and the heart in patients with this disease remain unclear. In recent years, several published reports have revealed the role of this brain-heart connection in the pathogenesis of TTS. This review summarizes recent studies regarding SNS activation, catecholamine overload, and the brain-heart connection in patients with TTS from both pathophysiological and mechanistic aspects.

Attenuation of Haemodynamic Response to Placement of Mayfield Skull Pin Head Holder - Comparison of Dexmedetomidine Versus Propofol Infusion - A Randomized Interventional Trial Done in a Tertiary Centre in Central Kerala

2021 ◽  
Vol 8 (29) ◽  
pp. 2639-2643
Author(s):  
Sruthy Unni ◽  
Ranju Sebastian ◽  
Elizabeth Joseph ◽  
Remani Kelan Kamalakshi ◽  
Jamsheena Muthira Parambath
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Stress Response ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurosurgical Procedures ◽  
Sympathetic Nervous ◽  
The Brain ◽  
Group 1

BACKGROUND Anaesthesia for neurosurgery requires special considerations. The brain is enclosed in a rigid cranium, so the rise in intracranial pressure (ICP) which impairs cerebral perfusion pressure (CPP), results in irrepairable damage to various vital areas in the brain. Stable head position is required in long neurosurgical procedures. This is obtained with the use of clamps which fix the head rigidly. This is done usually under general anaesthesia because it produces intense painful stimuli leading to stimulation of sympathetic nervous system which in turn causes release of vasoconstrictive agents. This can impair perfusion in all organ systems. The increase in blood pressure due to sympathetic nervous system causes increase in blood flow. This causes increases in intracranial pressure which result in reduction in cerebral perfusion pressure once the auto regulatory limits are exceeded. We compared the effects of dexmedetomidine 1 µgm/kg and propofol 100 µgm/kg given as infusion over a period of 10 minutes before the induction of anaesthesia and continued till 5 minutes after pinning to attenuate the stress response while cranial pinning. In this study, we wanted to compare the effects of dexmedetomidine and propofol as infusion to attenuate the stress response while cranial pinning in patients undergoing neurosurgical procedures. METHODS This is a randomized interventional trial. Patients were divided into 2 groups of 20 each. Group 1 receiving dexmedetomidine and group 2 receiving propofol, both drugs given as infusion. Haemodynamic variables were monitored before and after cranial pinning. Data was analysed using IBM statistical package for social sciences (SPSS) statistics. The parameters recorded were analysed with the help of a statistician. RESULTS The two groups were comparable in demographic data. Incidence of tachycardia between group 1 and 2 showed that tachycardia to pinning was better controlled with propofol than dexmedetomidine (P < 0.05) which is statistically significant. There is no statistically significant difference in blood pressure values between group 1 and 2 after pinning. CONCLUSIONS From our study, we came to a conclusion that propofol was superior to dexmedetomidine in attenuating the heart rate response to cranial pinning. The effect of propofol and dexmedetomidine was comparable in attenuating the blood pressure response to cranial pinning. KEYWORDS Cranial Pinning, Dexmedetomidine, Propofol

scholarly journals ULTRASTRUCTURAL IDENTIFICATION OF CATECHOLAMINE-CONTAINING CENTRAL SYNAPTIC TERMINALS

1973 ◽  
Vol 21 (4) ◽  
pp. 333-348 ◽  
Author(s):  
FLOYD E. BLOOM
Keyword(s):  
Nervous System ◽  
Nerve Terminals ◽  
Synaptic Terminals ◽  
Direct Localization ◽  
Sympathetic Nervous ◽  
Neurotransmitter Substances ◽  
6 Hydroxydopamine ◽  
The Brain ◽  
Selective Accumulation ◽  
Peripheral Sympathetic Nervous System

Cytochemical methods for the localization of central catecholamine-containing synaptic terminals have been developed from an extensive foundation of biochemical work and from extrapolation of results on the peripheral sympathetic nervous system. Direct localization of catecholamines in central nerve terminals in some parts of the brain can now be obtained by fixation with permanganates. More broadly applicable, but less direct localizing methods depend upon selective accumulation of tritiated catecholamines for autoradiography or the accumulation of reactive catecholamine congeners which act as markers with conventional fixation. The pattern of acute degenerative changes which result after treatment with 6-hydroxydopamine can also be used to provide an indirect localization of the terminals which had stored catecholamines. When the results of each of the methods are combined, the present techniques indicate that catecholamine-containing terminals in the brain can be identified more confidently than any other system of neurotransmitter substances. Nevertheless, there is considerable need for future cytochemical innovation.

Central and peripheral sympathetic activities in rats during recovery from simulated weightlessness

1995 ◽  
Vol 79 (6) ◽  
pp. 1991-1997 ◽  
Author(s):  
S. Fagette ◽  
L. Somody ◽  
F. Bouzeghrane ◽  
J. M. Cottet-Emard ◽  
C. Gharib ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Activity ◽  
Weight Bearing ◽  
Pressure Control ◽  
Cardiovascular Regulation ◽  
Simulated Weightlessness ◽  
Cell Groups ◽  
Sympathetic Nervous ◽  
The Brain

Rats were tail suspended, keeping their forelimbs weight bearing for 14 days, and then allowed to recover for a short (6-h) or a long (24-h) period to assess the behavior of the sympathetic nervous system after weightless simulation. Sympathetic activity was determined by measuring norepinephrine (NE) turnover in the brain stem cell groups involved in central blood pressure control and in organs playing a key role in the cardiovascular regulation (heart and kidneys). The NE turnover was greatly reduced in the rostral (-56%; P < 0.001) and caudal (-73%; P < 0.001) A2 nucleus of suspended rats but was unchanged in the A1, A5, and A6 cell groups compared with attached rats. The NE turnover in the cardiac atria (-34%; P < 0.001) and ventricles (-35%; P < 0.001) and kidneys (-31%; P < 0.001) was decreased after suspension. The central and peripheral sympathetic activities returned to normal within 24 h of release from suspension, but there was hyperactivity after 6 h of recovery. This raises the problem of interpreting the results obtained in animals killed a few hours after return from spaceflight.

scholarly journals Central Fibroblast Growth Factor 21 Browns White Fat via Sympathetic Action in Male Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (7) ◽  
pp. 2470-2481 ◽  
Author(s):  
Nicholas Douris ◽  
Darko M. Stevanovic ◽  
ffolliott M. Fisher ◽  
Theodore I. Cisu ◽  
Melissa J. Chee ◽  
...  
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Sympathetic Nervous System ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Male Mice ◽  
Sympathetic Nervous ◽  
The Brain

Fibroblast growth factor 21 (FGF21) has multiple metabolic actions, including the induction of browning in white adipose tissue. Although FGF21 stimulated browning results from a direct interaction between FGF21 and the adipocyte, browning is typically associated with activation of the sympathetic nervous system through cold exposure. We tested the hypothesis that FGF21 can act via the brain, to increase sympathetic activity and induce browning, independent of cell-autonomous actions. We administered FGF21 into the central nervous system via lateral ventricle infusion into male mice and found that the central treatment increased norepinephrine turnover in target tissues that include the inguinal white adipose tissue and brown adipose tissue. Central FGF21 stimulated browning as assessed by histology, expression of uncoupling protein 1, and the induction of gene expression associated with browning. These effects were markedly attenuated when mice were treated with a β-blocker. Additionally, neither centrally nor peripherally administered FGF21 initiated browning in mice lacking β-adrenoceptors, demonstrating that an intact adrenergic system is necessary for FGF21 action. These data indicate that FGF21 can signal in the brain to activate the sympathetic nervous system and induce adipose tissue thermogenesis.

Imbalance of central nitric oxide and reactive oxygen species in the regulation of sympathetic activity and neural mechanisms of hypertension

2011 ◽  
Vol 300 (4) ◽  
pp. R818-R826 ◽  
Author(s):  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Koji Sakai ◽  
Akira Takeshita ◽  
Kenji Sunagawa
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brain Stem ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sympathetic Nervous ◽  
The Brain

Nitric oxide (NO) and reactive oxygen species (ROS) play important roles in blood pressure regulation via the modulation of the autonomic nervous system, particularly in the central nervous system (CNS). In general, accumulating evidence suggests that NO inhibits, but ROS activates, the sympathetic nervous system. NO and ROS, however, interact with each other. Our consecutive studies and those of others strongly indicate that an imbalance between NO bioavailability and ROS generation in the CNS, including the brain stem, activates the sympathetic nervous system, and this mechanism is involved in the pathogenesis of neurogenic aspects of hypertension. In this review, we focus on the role of NO and ROS in the regulation of the sympathetic nervous system within the brain stem and subsequent cardiovascular control. Multiple mechanisms are proposed, including modulation of neurotransmitter release, inhibition of receptors, and alterations of intracellular signaling pathways. Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension.

scholarly journals Heterotopic ossification after central nervous system injuries: understanding of pathogenesis

2018 ◽  
Vol 25 (3-4) ◽  
pp. 119-124
Author(s):  
I. F Gareev ◽  
O. A Beylerli ◽  
A. K Vakhitov
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Heterotopic Ossification ◽  
Genetic Factors ◽  
Cellular Interactions ◽  
Heterotopic Ossifications ◽  
The Brain

Available data on the pathogenesis, cellular interactions, role of inflammation, humoral and genetic factors in the formation of heterotopic ossifications resulting from injuries of the brain or spinal cord are presented.

Sign in / Sign up

Export Citation Format

Share Document