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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 -
International Journal of Stroke :... Dec 2023Reversible segmental narrowing of the intracranial arteries has been described since several decades in numerous clinical settings, using variable nosology. Twenty-one... (Review)
Review
Reversible segmental narrowing of the intracranial arteries has been described since several decades in numerous clinical settings, using variable nosology. Twenty-one years ago, we tentatively proposed the unifying concept that these entities, based on similar clinical-imaging features, represented a single cerebrovascular syndrome. This "reversible cerebral vasoconstriction syndrome" or RCVS has now come of age. A new International Classification of Diseases code, (ICD-10, I67.841) has been established, enabling larger-scale studies. The RCVS2 scoring system provides high accuracy in confirming RCVS diagnosis and excluding mimics such as primary angiitis of the central nervous system. Several groups have characterized its clinical-imaging features. RCVS predominantly affects women. Recurrent worst-ever (thunderclap) headaches are typical at onset. While initial brain imaging is often normal, approximately one-third to half develop complications such as convexity subarachnoid hemorrhages, lobar hemorrhages, ischemic strokes located in arterial "watershed" territories and reversible edema, alone or in combination. Vasoconstriction evolves over hours to days, first affecting distal and then the more proximal arteries. An overlap between RCVS and primary thunderclap headache, posterior reversible encephalopathy syndrome, Takotsubo cardiomyopathy, transient global amnesia, and other conditions has been recognized. The pathophysiology remains largely unknown. Management is mostly symptomatic: headache relief with analgesics and oral calcium-channel blockers, removal of vasoconstrictive factors, and avoidance of glucocorticoids that can significantly worsen outcome. Intra-arterial vasodilator infusions provide variable success. Overall, 90-95% of admitted patients achieve complete or major resolution of symptoms and clinical deficits within days to weeks. Recurrence is exceptional, although 5% can later develop isolated thunderclap headaches with or without mild cerebral vasoconstriction.
Topics: Humans; Female; Vasoconstriction; Posterior Leukoencephalopathy Syndrome; Stroke; Cerebrovascular Disorders; Headache; Vasospasm, Intracranial
PubMed: 37246916
DOI: 10.1177/17474930231181250 -
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 -
Der Anaesthesist Jul 1996Hypoxic pulmonary vasoconstriction (HPV) was first described by von Euler and Liljestrand in 1946 and is still the only known vascular feedback control mechanism in the... (Review)
Review
Hypoxic pulmonary vasoconstriction (HPV) was first described by von Euler and Liljestrand in 1946 and is still the only known vascular feedback control mechanism in the lung. This technique results in a redistribution of blood flow away from poorly ventilated areas into better ventilated regions, thus reducing shunt. HPV functions as a local mechanism that acts in response to alveolar hypoxia but in the smallest areas of the lung, making it an important mechanism in all situations where ventilation perfusion mismatch occurs. to be effective, HPV needs normal pulmonary areas into which blood flow can be diverted. This explains why the efficacy of the treatment depends on the area that is vasoconstricted. The effect on PaO2 is maximal when the amount of the hypoxic lung ist 30-70%. If the area in vasoconstriction is small, the influence on PaO2 is negligible. On the other hand, when most of the lung is hypoxic, there is no significant normoxic region to which the hypoxic region can divert flow. In that case it does not matter, in terms of PaO2, whether the hypoxic region has active hypoxic pulmonary vasoconstriction or not. In this situation HPV becomes a rather detrimental mechanism, because it causes an increase in pulmonary arterial pressure. At some stage a turning point, where the gain in PaO2 is lost due to an increase in right ventricular after-load, inducing a decrease in CO. The reaction is diminished by exogenous manipulations, drugs (inhalation anesthetics, direct vasodilators), endotoxin, very low PaO2 values, vasodilating mediators and changes in the acid-base balance. Acidosis and alkalosis inhibit HPV. Factors like spontaneous or mechanical ventilation, PEEP, open or closed chest, and the type of hypoxia (atelectasis or nitrogen) have no influence on HPV. The small arteries, those less than 500 microns in diameter, were identified as the location of the hypoxic constriction. Pulmonary vascular smooth muscle cells in pure culture undergo reversible and repeated hypoxic constriction. Examination of a histological lung section emphasizes that the small arteries are closely surrounded by alveoli gas on the outside and by mixed venous blood on the inside. Thus, the response is believed to be accounted for by each smooth muscle cell in the pulmonary arterial wall responding proportionally to the local oxygen tension in its vicinity and depending on alveolar as well as mixed venous oxygen pressure. The biochemical intracellular mechanism remains unknown.
Topics: Critical Care; Humans; Hypoxia; Pulmonary Circulation; Vasoconstriction
PubMed: 8765866
DOI: 10.1007/s001010050298 -
Journal of Biomedical Optics Aug 2023Corticosteroids-commonly prescribed medications for skin diseases-inhibit the secretion of vasodilators, such as prostaglandin, thereby exerting anti-inflammatory action...
SIGNIFICANCE
Corticosteroids-commonly prescribed medications for skin diseases-inhibit the secretion of vasodilators, such as prostaglandin, thereby exerting anti-inflammatory action by constricting capillaries in the dermis. The effectiveness of corticosteroids is determined by the degree of vasoconstriction followed by skin whitening, namely, the blanching effect. However, the current method of observing the blanching effect indirectly evaluates the effects of corticosteroids.
AIM
In this study, we employed optical-resolution photoacoustic (PA) microscopy (OR-PAM) to directly visualize the blood vessels and quantitatively evaluate vasoconstriction.
APPROACH
Using OR-PAM, the vascular density in mice skin was monitored for 60 min after performing each experimental procedure for four groups, and the vasoconstriction was quantified. Volumetric PA data were segmented into the papillary dermis, reticular dermis, and hypodermis based on the vascular characteristics obtained through OR-PAM. The vasoconstrictive effect of each skin layer was quantified according to the dermatological treatment method.
RESULTS
In the case of corticosteroid topical application, vasoconstriction was observed in the papillary ( ) and reticular ( ) dermis. For corticosteroid subcutaneous injection, constriction was observed solely in the reticular ( ) dermis. In contrast, no vasoconstrictions were observed with nonsteroidal topical application.
CONCLUSIONS
Our results indicate that OR-PAM can quantitatively monitor the vasoconstriction induced by corticosteroids, thereby validating OR-PAMs potential as a practical evaluation tool for predicting the effectiveness of corticosteroids in dermatology.
Topics: Animals; Mice; Anti-Inflammatory Agents; Skin; Adrenal Cortex Hormones; Vasoconstriction; Spectrum Analysis; Photoacoustic Techniques
PubMed: 36844430
DOI: 10.1117/1.JBO.28.8.082805 -
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 -
Critical Care (London, England) 2001Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical... (Review)
Review
Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical mechanism and its exact physiological function. Recent work suggests an important role for pulmonary arteriolar smooth muscle cell oxygen-sensitive voltage-dependent potassium channels. Inhibition of these channels by decreased PO2 inhibits outward potassium current, causing membrane depolarization, and calcium entry through voltage-dependent calcium channels. Endothelium-derived vasoconstricting and vasodilating mediators modulate this intrinsic smooth muscle cell reactivity to hypoxia. However, refined modeling of hypoxic pulmonary vasoconstriction operating as a feedback mechanism in inhomogeneous lungs, using more realistic stimulus-response curves and confronted with direct measurements of regional blood flow distribution, shows a more effective than previously assessed ability of this remarkable intrapulmonary reflex to improve gas exchange and arterial oxygenation. Further studies could show clinical benefit of pharmacological manipulation of hypoxic pulmonary vasoconstriction, in circumstances of life-threatening hypoxemia.
Topics: Acute Disease; Anesthesia; Humans; Hypoxia; Oxygen; Pulmonary Artery; Pulmonary Veins; Respiratory Insufficiency; Vasoconstriction
PubMed: 11299064
DOI: 10.1186/cc989 -
Journal of Molecular and Cellular... Jun 2006Hypoxic pulmonary vasoconstriction (HPV) and pulmonary hypertension present a common and formidable clinical problem for practicing intensivists, thoracic, transplant,... (Review)
Review
Hypoxic pulmonary vasoconstriction (HPV) and pulmonary hypertension present a common and formidable clinical problem for practicing intensivists, thoracic, transplant, and trauma surgeons. The Redox Theory for the mechanisms of HPV has provided researchers with a new understanding of the etiology behind HPV that has opened the door to many new avenues of therapy for the disease. Potassium channels have been proposed to be the main mediator contributing to HPV, and treatment concepts that attempt to manipulate the function and number of those channels have been explored. Additionally, attempts to transfer genes that express the formation of specific potassium channels directly into pulmonary hypertensive lungs have proven to be very promising. Finally, rho kinase (ROK) has been discovered to play a very central role in the formation of hypoxia-induced pulmonary hypertension, and the advent of very specific ROK inhibitors has shown positive clinical results. The purposes of this review are to: (1) briefly discuss some of the basic mechanisms that undergird HPV, including the Redox Theory for the mechanisms of HPV; (2) address current research involving treatments concepts related to ion channels; (3) report on research involving gene therapy to combat pulmonary hypertension; and (4) examine potential therapeutic avenues associated with inhibition of rho kinase.
Topics: Humans; Hypoxia; Ion Channels; Lung; Muscle Contraction; Muscle, Smooth; Vasoconstriction
PubMed: 16697004
DOI: 10.1016/j.yjmcc.2006.03.431 -
The Netherlands Journal of Medicine Jun 2001Acute pulmonary embolism with haemodynamic instability has a high mortality rate. Death results from an acute increase in right ventricular afterload, and the commonly... (Review)
Review
Acute pulmonary embolism with haemodynamic instability has a high mortality rate. Death results from an acute increase in right ventricular afterload, and the commonly held view is that mechanical obstruction of the pulmonary vascular bed is largely responsible for this increase. In accordance, recent treatment guidelines for severe pulmonary embolism focus exclusively on interventions aimed at relieving this mechanical obstruction, either by thrombolysis or (catheter) embolectomy. However, there is evidence to indicate that vasoconstriction is a very important contributor to the initial increase in pulmonary vascular resistance after pulmonary embolism. This is consistent with the observation that the degree of mechanical obstruction correlates at best poorly with haemodynamic manifestations. Thromboxane A(2) and serotonin are probably mainly responsible for pulmonary vasoconstriction. Cyclooxygenase inhibitors and serotonin antagonists have been shown in animal experiments to attenuate the haemodynamic response to acute pulmonary embolism and to reduce mortality. In addition, reports of a favourable response to pulmonary vasodilators in animals and in humans with acute severe pulmonary embolism have been published. In this paper, it is argued that we may need to reconsider our current therapeutic approach to patients with acute severe pulmonary embolism. Antagonising pulmonary vasoconstrictive mediators or administering pulmonary vasodilators may prove to be life-saving interventions in these patients.
Topics: Animals; Embolectomy; Fibrinolytic Agents; Hemodynamics; Humans; Pulmonary Embolism; Vasoconstriction; Vasodilator Agents
PubMed: 11395221
DOI: 10.1016/s0300-2977(01)00117-6 -
Interventional Cardiology Clinics Jul 2020Passing contrast media through the renal vascular bed leads to vasoconstriction. The perfusion decrease leads to ischemia of tubular cells. Through ischemia and direct... (Review)
Review
Passing contrast media through the renal vascular bed leads to vasoconstriction. The perfusion decrease leads to ischemia of tubular cells. Through ischemia and direct toxicity to renal tubular cells, reactive oxygen species formation is increased, enhancing the effect of vasoconstrictive mediators and decreasing the bioavailability of vasodilative mediators. Reactive oxygen species formation leads to oxidative damage to tubular cells. These interacting pathways lead to tubular necrosis. In the pathophysiology of contrast-induced acute kidney injury, low osmolar and iso-osmolar agents have theoretic advantages and disadvantages; however, clinically the difference in incidence of contrast-induced acute kidney injury has not changed.
Topics: Acute Kidney Injury; Contrast Media; Drug-Related Side Effects and Adverse Reactions; Humans; Incidence; Kidney; Kidney Tubules; Necrosis; Osmolar Concentration; Reactive Oxygen Species; Vasoconstriction
PubMed: 32471670
DOI: 10.1016/j.iccl.2020.03.001