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Blood Sep 2020
Topics: Anemia, Sickle Cell; Asthma; Humans; Primary Dysautonomias; Vasoconstriction
PubMed: 32882017
DOI: 10.1182/blood.2020007070 -
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 -
Stroke Jul 2016To compare hemorrhagic and nonhemorrhagic reversible cerebral vasoconstriction syndromes (RCVS) with a view to understand mechanisms.
BACKGROUND AND PURPOSE
To compare hemorrhagic and nonhemorrhagic reversible cerebral vasoconstriction syndromes (RCVS) with a view to understand mechanisms.
METHODS
This single-center retrospective study included 162 patients with RCVS. Clinical, brain imaging, and angiography data were analyzed.
RESULTS
The mean age was 44±13 years, 78% women. Hemorrhages occurred in 43% including 21 patients with intracerebral hemorrhage (ICH) and 62 with convexal subarachnoid hemorrhage (cSAH). The frequency of triggers (eg, vasoconstrictive drugs) and risk factors (eg, migraine) were not significantly different between hemorrhagic and nonhemorrhagic RCVS or between subgroups (ICH versus non-ICH, isolated cSAH versus normal scan). Hemorrhagic lesions occurred within the first week, whereas infarcts and vasogenic edema accumulated during 2 to 3 weeks (P<0.001). Although all ICHs occurred before cSAH, their time course was not significantly different (P=0.11). ICH and cSAH occurred earlier than infarcts (P≤0.001), and ICH earlier than vasogenic edema (P=0.009). Angiogram analysis showed more severe vasoconstriction in distal versus proximal segments in all lesion types (ICH, cSAH, infarction, vasogenic edema, and normal scan). The isolated infarction group had more severe proximal vasoconstriction, and those with normal imaging had significantly less vasoconstriction. Multivariable analysis failed to uncover independent predictors of hemorrhagic RCVS; however, female sex predicted ICH (P=0.048), and angiographic severity predicted infarction (P=0.043).
CONCLUSIONS
ICH and cSAH are common complications of RCVS. Triggers and risk factors do not predict lesion subtype but may alter central vasomotor control mechanisms resulting in centripetal angiographic evolution. Early distal vasoconstriction is associated with lobar ICH and cSAH, and delayed proximal vasoconstriction with infarction.
Topics: Adult; Cerebral Angiography; Cerebral Arterial Diseases; Cerebral Hemorrhage; Female; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Retrospective Studies; Risk Factors; Syndrome; Vasoconstriction; Vasospasm, Intracranial
PubMed: 27272485
DOI: 10.1161/STROKEAHA.116.013136 -
Clinical Neurophysiology : Official... Jan 2015Skin wrinkling upon water immersion has been used as an indicator of limb nerve function for more than 80years. Until recently, routine use of the test has been hampered... (Review)
Review
Skin wrinkling upon water immersion has been used as an indicator of limb nerve function for more than 80years. Until recently, routine use of the test has been hampered by a poor understanding of the physiology and lack of standardization. The process underlying stimulated skin wrinkling has been recently identified as dependent on digital vasoconstriction mediated via sympathetic nerve fibers. Vasoconstriction is postulated to drive wrinkling through loss of digit volume, which induces a negative pressure in the digit pulp and exerts a downward pull on the overlying skin and ultimately results in wrinkles. Improved test standardization has been achieved through substituting water with EMLA for inducing skin wrinkling. This has made testing much easier and has helped implement stimulated skin wrinkling as a practical routine clinical bedside test. A literature search identified 10 studies of sufficient quality for evaluating stimulated skin wrinkling as a diagnostic test of sympathetic under or over function. Seven studies provide level 1 or 2 evidence as a diagnostic test of small fiber neuropathy and three provide level 1 or 2 evidence for cystic fibrosis. There is reasonable evidence allowing the test to be employed as a simple and effective marker for small fiber neuropathy and cystic fibrosis.
Topics: Autonomic Nervous System Diseases; Extremities; Humans; Skin; Skin Aging; Skin Physiological Phenomena; Sympathetic Nervous System; Vasoconstriction; Water
PubMed: 25216595
DOI: 10.1016/j.clinph.2014.08.007 -
Neuroscience May 2016The brain possesses two intricate mechanisms that fulfill its continuous metabolic needs: cerebral autoregulation, which ensures constant cerebral blood flow over a wide... (Review)
Review
The brain possesses two intricate mechanisms that fulfill its continuous metabolic needs: cerebral autoregulation, which ensures constant cerebral blood flow over a wide range of arterial pressures and functional hyperemia, which ensures rapid delivery of oxygen and glucose to active neurons. Over the past decade, a number of important studies have identified astrocytes as key intermediaries in neurovascular coupling (NVC), the mechanism by which active neurons signal blood vessels to change their diameter. Activity-dependent increases in astrocytic Ca(2+) activity are thought to contribute to the release of vasoactive substances that facilitate arteriole vasodilation. A number of vasoactive signals have been identified and their role on vessel caliber assessed both in vitro and in vivo. In this review, we discuss mechanisms implicating astrocytes in NVC-mediated vascular responses, limitations encountered as a result of the challenges in maintaining all the constituents of the neurovascular unit intact and deliberate current controversial findings disputing a main role for astrocytes in NVC. Finally, we briefly discuss the potential role of pericytes and microglia in NVC-mediated processes.
Topics: Animals; Astrocytes; Calcium Signaling; Microglia; Neurovascular Coupling; Pericytes; Vasoconstriction; Vasodilation
PubMed: 25843438
DOI: 10.1016/j.neuroscience.2015.03.064 -
Comprehensive Physiology Mar 2018This review concentrates on the determinants of gas exchange abnormalities in liver-induced pulmonary vascular disorders, more specifically in the hepatopulmonary... (Review)
Review
This review concentrates on the determinants of gas exchange abnormalities in liver-induced pulmonary vascular disorders, more specifically in the hepatopulmonary syndrome. Increased alveolar-arterial O difference, with or without different levels of arterial hypoxemia, and reduced diffusing capacity represent the most characteristic gas exchange disturbances in the absence of cardiac and pulmonary comorbidities. Pulmonary gas exchange abnormalities in the hepatopulmonary syndrome are unique encompassing all three pulmonary factors determining arterial PO , that is, ventilation-perfusion imbalance, increased intrapulmonary shunt and oxygen diffusion limitation that, combined, interplay with two relevant nonpulmonary determinants, that is, increased total ventilation and high cardiac output. Behind the complexity of this lung-liver association there is an abnormal pulmonary vascular tone that combines inhibition of hypoxic pulmonary vasoconstriction with a reduced (or blunted) hypoxic vascular response. The pathology and pathobiology include the presence of intrapulmonary vascular dilatations with or without pulmonary vascular remodeling, i.e. angiogenesis. Liver transplantation, the only effective therapeutic approach to successfully improve and resolve the vast majority of complications induced by the hepatopulmonary syndrome, along with a large list of frustrating pharmacologic interventions, are also reviewed. Another liver-induced pulmonary vascular disorder with less gas exchange involvement, such as portopulmonary hypertension, is also considered. © 2018 American Physiological Society. Compr Physiol 8:711-729, 2018.
Topics: Hemodynamics; Hepatopulmonary Syndrome; Humans; Liver Transplantation; Pressure; Pulmonary Gas Exchange; Vasoconstriction; Ventilation-Perfusion Ratio
PubMed: 29687908
DOI: 10.1002/cphy.c170020 -
The Journal of Physiology Jan 2023
Topics: Humans; Vasoconstriction; Hypoxia
PubMed: 36524431
DOI: 10.1113/JP284057 -
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 -
Advances in Pharmacology (San Diego,... 2017Potassium channels importantly contribute to the regulation of vascular smooth muscle (VSM) contraction and growth. They are the dominant ion conductance of the VSM cell... (Review)
Review
Potassium channels importantly contribute to the regulation of vascular smooth muscle (VSM) contraction and growth. They are the dominant ion conductance of the VSM cell membrane and importantly determine and regulate membrane potential. Membrane potential, in turn, regulates the open-state probability of voltage-gated Ca channels (VGCC), Ca influx through VGCC, intracellular Ca, and VSM contraction. Membrane potential also affects release of Ca from internal stores and the Ca sensitivity of the contractile machinery such that K channels participate in all aspects of regulation of VSM contraction. Potassium channels also regulate proliferation of VSM cells through membrane potential-dependent and membrane potential-independent mechanisms. VSM cells express multiple isoforms of at least five classes of K channels that contribute to the regulation of contraction and cell proliferation (growth). This review will examine the structure, expression, and function of large conductance, Ca-activated K (BK) channels, intermediate-conductance Ca-activated K (K3.1) channels, multiple isoforms of voltage-gated K (K) channels, ATP-sensitive K (K) channels, and inward-rectifier K (K) channels in both contractile and proliferating VSM cells.
Topics: Animals; Humans; Membrane Potentials; Muscle, Smooth, Vascular; Potassium Channels; Vasoconstriction
PubMed: 28212804
DOI: 10.1016/bs.apha.2016.07.001 -
Journal of Cerebral Blood Flow and... Jan 2018Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebral event that kills or debilitates the majority of those afflicted. The blood that spills into the... (Review)
Review
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebral event that kills or debilitates the majority of those afflicted. The blood that spills into the subarachnoid space stimulates profound cerebral artery vasoconstriction and consequently, cerebral ischemia. Thus, once the initial bleeding in SAH is appropriately managed, the clinical focus shifts to maintaining/improving cerebral perfusion. However, current therapeutic interventions largely fail to improve clinical outcome, because they do not effectively restore normal cerebral artery function. This review discusses emerging evidence that perturbed cerebrovascular "myogenic reactivity," a crucial microvascular process that potently dictates cerebral perfusion, is the critical element underlying cerebral ischemia in SAH. In fact, the myogenic mechanism could be the reason why many therapeutic interventions, including "Triple H" therapy, fail to deliver benefit to patients. Understanding the molecular basis for myogenic reactivity changes in SAH holds the key to develop more effective therapeutic interventions; indeed, promising recent advancements fuel optimism that vascular dysfunction in SAH can be corrected to improve outcome.
Topics: Cerebral Arteries; Cerebrovascular Circulation; Humans; Muscle, Smooth, Vascular; Subarachnoid Hemorrhage; Vasoconstriction
PubMed: 29135346
DOI: 10.1177/0271678X17742548