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Journal of Biomedical Science Sep 2022Reversible cerebral vasoconstriction syndrome (RCVS) is a complex neurovascular disorder being recognized during the past two decades. It is characterized by multiple... (Review)
Review
Reversible cerebral vasoconstriction syndrome (RCVS) is a complex neurovascular disorder being recognized during the past two decades. It is characterized by multiple abrupt severe headaches and widespread cerebral vasoconstrictions, with potential complications such as ischemic stroke, convexity subarachnoid hemorrhage, intracerebral hemorrhage and posterior reversible encephalopathy syndrome. The clinical features, imaging findings, and dynamic disease course have been delineated. However, the pathophysiology of RCVS remains elusive. Recent studies have had substantial progress in elucidating its pathogenesis. It is now believed that dysfunction of cerebral vascular tone and impairment of blood-brain barrier may play key roles in the pathophysiology of RCVS, which explains some of the clinical and radiological manifestations of RCVS. Some other potentially important elements include genetic predisposition, sympathetic overactivity, endothelial dysfunction, and oxidative stress, although the detailed molecular mechanisms are yet to be identified. In this review, we will summarize what have been revealed in the literature and elaborate how these factors could contribute to the pathophysiology of RCVS.
Topics: Brain; Cerebral Hemorrhage; Humans; Posterior Leukoencephalopathy Syndrome; Vasoconstriction; Vasospasm, Intracranial
PubMed: 36127720
DOI: 10.1186/s12929-022-00857-4 -
Critical Care (London, England) 2015This article presents a personal viewpoint of the shortcoming of conventional hemodynamic resuscitation procedures in achieving organ perfusion and tissue oxygenation...
This article presents a personal viewpoint of the shortcoming of conventional hemodynamic resuscitation procedures in achieving organ perfusion and tissue oxygenation following conditions of shock and cardiovascular compromise, and why it is important to monitor the microcirculation in such conditions. The article emphasizes that if resuscitation procedures are based on the correction of systemic variables, there must be coherence between the macrocirculation and microcirculation if systemic hemodynamic-driven resuscitation procedures are to be effective in correcting organ perfusion and oxygenation. However, in conditions of inflammation and infection, which often accompany states of shock, vascular regulation and compensatory mechanisms needed to sustain hemodynamic coherence are lost, and the regional circulation and microcirculation remain in shock. We identify four types of microcirculatory alterations underlying the loss of hemodynamic coherence: type 1, heterogeneous microcirculatory flow; type 2, reduced capillary density induced by hemodilution and anemia; type 3, microcirculatory flow reduction caused by vasoconstriction or tamponade; and type 4, tissue edema. These microcirculatory alterations can be observed at the bedside using direct visualization of the sublingual microcirculation with hand-held vital microscopes. Each of these alterations results in oxygen delivery limitation to the tissue cells despite the presence of normalized systemic hemodynamic variables. Based on these concepts, we propose how to optimize the volume of fluid to maximize the oxygen-carrying capacity of the microcirculation to transport oxygen to the tissues.
Topics: Capillaries; Hemodynamics; Humans; Microcirculation; Resuscitation; Shock; Vasoconstriction
PubMed: 26729241
DOI: 10.1186/cc14726 -
British Journal of Anaesthesia Aug 2019
Topics: Anesthesia; Hemodynamics; Humans; Perioperative Care; Regional Blood Flow; Vasoconstriction; Vasoconstrictor Agents
PubMed: 31153629
DOI: 10.1016/j.bja.2019.04.052 -
Autonomic Neuroscience : Basic &... Mar 2015Sympathetic vasoconstriction is normally attenuated in exercising muscle by local changes in muscle metabolites and other substances that reduce vascular responsiveness... (Review)
Review
Sympathetic vasoconstriction is normally attenuated in exercising muscle by local changes in muscle metabolites and other substances that reduce vascular responsiveness to α-adrenergic receptor activation. Termed functional sympatholysis, this protective mechanism is thought to optimize muscle blood flow distribution to match perfusion with metabolic demand. Emerging evidence from both animal and human studies indicate that functional sympatholysis is impaired in hypertension and may constitute an important underlying cause of skeletal muscle malperfusion during exercise in this common cardiovascular condition. Findings from studies of animal models of hypertension and patients with essential hypertension will be integrated in this review to provide insight into the underlying mechanisms responsible for inappropriate sympathetic vasoconstriction in exercising muscle and the treatment options that may restore functional sympatholysis and improve muscle perfusion during exercise.
Topics: Animals; Exercise; Humans; Hypertension; Muscle, Skeletal; Sympathetic Nervous System; Vasoconstriction
PubMed: 25458424
DOI: 10.1016/j.autneu.2014.10.019 -
Anesthesiology Apr 2015Hypoxic pulmonary vasoconstriction (HPV) represents a fundamental difference between the pulmonary and systemic circulations. HPV is active in utero, reducing pulmonary... (Review)
Review
Hypoxic pulmonary vasoconstriction (HPV) represents a fundamental difference between the pulmonary and systemic circulations. HPV is active in utero, reducing pulmonary blood flow, and in adults helps to match regional ventilation and perfusion although it has little effect in healthy lungs. Many factors affect HPV including pH or PCO2, cardiac output, and several drugs, including antihypertensives. In patients with lung pathology and any patient having one-lung ventilation, HPV contributes to maintaining oxygenation, so anesthesiologists should be aware of the effects of anesthesia on this protective reflex. Intravenous anesthetic drugs have little effect on HPV, but it is attenuated by inhaled anesthetics, although less so with newer agents. The reflex is biphasic, and once the second phase becomes active after about an hour of hypoxia, this pulmonary vasoconstriction takes hours to reverse when normoxia returns. This has significant clinical implications for repeated periods of one-lung ventilation.
Topics: Anesthetics, Inhalation; Animals; Humans; Hypoxia; Lung; Pulmonary Circulation; Vasoconstriction
PubMed: 25587641
DOI: 10.1097/ALN.0000000000000569 -
Annual Review of Physiology Feb 2023Resistance arteries and arterioles evolved as specialized blood vessels serving two important functions: () regulating peripheral vascular resistance and blood pressure... (Review)
Review
Resistance arteries and arterioles evolved as specialized blood vessels serving two important functions: () regulating peripheral vascular resistance and blood pressure and () matching oxygen and nutrient delivery to metabolic demands of organs. These functions require control of vessel lumen cross-sectional area (vascular tone) via coordinated vascular cell responses governed by precise spatial-temporal communication between intracellular signaling pathways. Herein, we provide a contemporary overview of the significant roles that redox switches play in calcium signaling for orchestrated endothelial, smooth muscle, and red blood cell control of arterial vascular tone. Three interrelated themes are the focus: () smooth muscle to endothelial communication for vasoconstriction, () endothelial to smooth muscle cell cross talk for vasodilation, and () oxygen and red blood cell interregulation of vascular tone and blood flow. We intend for this thematic framework to highlight gaps in our current knowledge and potentially spark interest for cross-disciplinary studies moving forward.
Topics: Humans; Microcirculation; Vasodilation; Vasoconstriction; Oxidation-Reduction; Oxygen
PubMed: 36763969
DOI: 10.1146/annurev-physiol-031522-021457 -
Journal of Neurology Feb 2023Reversible cerebral vasoconstriction syndrome may be underdiagnosed. It can be accompanied by various complications, mainly intracerebral hemorrhage and ischemic stroke.... (Review)
Review
BACKGROUND/OBJECTIVE
Reversible cerebral vasoconstriction syndrome may be underdiagnosed. It can be accompanied by various complications, mainly intracerebral hemorrhage and ischemic stroke. The clinical presentation of this condition varies according to its localization. The aims of this review are to raise awareness of the disease, especially in the presence of corresponding risk factors; to connect its precipitating factors, pathophysiology, and complications; and to compare various differential diagnoses of vasoconstriction.
METHODS
A review of the literature in PubMed/MEDLINE and Google Scholar was conducted from May 1997 until May 2022.
RESULTS
Reversible cerebral vasoconstriction syndrome, which is a clinical-radiological syndrome, is mainly characterized by the occurrence of thunderclap headache and widespread vasoconstriction. The most common precipitating factors are the use of vasoactive substances and postpartum status. The pathophysiology is currently assumed to include two mechanisms: sympathetic overactivity and endothelial dysfunction. From these mechanisms, it is possible to derive potential complications as well as the most important differential diagnoses: posterior reversible encephalopathy syndrome, convexity subarachnoid hemorrhage, ischemic and hemorrhagic stroke, and primary angiitis of the central nervous system.
CONCLUSION
In general, the outcome of reversible cerebral vasoconstriction syndrome is very good. Vasospasm as well as thunderclap headache attacks can be fully reversible, and > 90% of patients are functionally independent at discharge.
Topics: Female; Humans; Vasospasm, Intracranial; Posterior Leukoencephalopathy Syndrome; Cerebrovascular Disorders; Headache Disorders, Primary; Vasoconstriction
PubMed: 36305970
DOI: 10.1007/s00415-022-11425-z -
Transactions of the American Clinical... 2017Cirrhosis leads to portal hypertension and vascular abnormalities in multiple vascular beds. There is intense vasoconstriction in the liver and the kidneys, but also... (Review)
Review
Cirrhosis leads to portal hypertension and vascular abnormalities in multiple vascular beds. There is intense vasoconstriction in the liver and the kidneys, but also vasodilation in the other vascular beds, including the periphery, lungs, brain, and mesentery. The derangement in each of these beds leads to specific clinical disease. The vasoconstrictive phenotype in the liver ultimately leads to clinical portal hypertension, and is caused by an imbalance of vasoconstrictive and vasorelaxing molecules, which will be the focus of this review.
Topics: Animals; Endothelial Cells; Gene Expression Regulation; Hepatic Stellate Cells; Humans; Hypertension, Portal; Liver Cirrhosis; Vasoconstriction; Vasodilation
PubMed: 28790516
DOI: No ID Found -
Experimental Physiology Feb 2021This short review was prompted by The Physiological Society's recent online symposium on variability. It does not deal with a specific methodology, but rather with the...
This short review was prompted by The Physiological Society's recent online symposium on variability. It does not deal with a specific methodology, but rather with the myth that certain environmentally-induced clinical conditions can be identified, quantified, simplified and monitored with a single methodology. Although this might be possible with some clinical conditions, others resist the prevailing reductionist approach of minimizing rather than exploring variation in pathogenesis and pathology, and will not be understood fully until the variation in cause and effect are embraced. This is likely to require comprehensive methodologies and collaboration.
Topics: Adaptation, Physiological; Animals; Cold Injury; Humans; Vasoconstriction
PubMed: 33174651
DOI: 10.1113/EP089147 -
Communications Biology Sep 2022Human and animal studies have reported widespread reductions in cerebral blood flow associated with chronic cocaine exposures. However, the molecular and cellular...
Human and animal studies have reported widespread reductions in cerebral blood flow associated with chronic cocaine exposures. However, the molecular and cellular mechanisms underlying cerebral blood flow reductions are not well understood. Here, by combining a multimodal imaging platform with a genetically encoded calcium indicator, we simultaneously measured the effects of acute cocaine on neuronal and astrocytic activity, tissue oxygenation, hemodynamics and vascular diameter changes in the mouse cerebral cortex. Our results showed that cocaine constricted blood vessels (measured by vessel diameter Φ changes), decreasing cerebral total blood volume (HbT) and temporally reducing tissue oxygenation. Cellular imaging showed that the mean astrocytic Ca dependent fluorescence [Formula: see text] increase in response to cocaine was weaker but longer lasting than the mean neuronal Ca dependent fluorescence [Formula: see text] changes. Interestingly, while cocaine-induced [Formula: see text] increase was temporally correlated with tissue oxygenation change, the [Formula: see text] elevation after cocaine was in temporal correspondence with the long-lasting decrease in arterial blood volumes. To determine whether the temporal association between astrocytic activation and cocaine induced vasoconstriction reflected a causal association we inhibited astrocytic Ca using GFAP-DREADD(Gi). Inhibition of astrocytes attenuated the vasoconstriction resulting from cocaine, providing evidence that astrocytes play a critical role in cocaine's vasoconstrictive effects in the brain. These results indicate that neurons and astrocytes play different roles in mediating neurovascular coupling in response to cocaine. Our findings implicate neuronal activation as the main driver of the short-lasting reduction in tissue oxygenation and astrocyte long-lasting activation as the driver of the persistent vasoconstriction with cocaine. Understanding the cellular and vascular interaction induced by cocaine will be helpful for future putative treatments to reduce cerebrovascular pathology from cocaine use.
Topics: Animals; Astrocytes; Cerebrovascular Circulation; Cocaine; Cocaine-Related Disorders; Humans; Mice; Vasoconstriction
PubMed: 36097038
DOI: 10.1038/s42003-022-03877-w