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Annual Review of Physiology Feb 2019Maintenance of a homeostatic body core temperature is a critical brain function accomplished by a central neural network. This orchestrates a complex behavioral and... (Review)
Review
Maintenance of a homeostatic body core temperature is a critical brain function accomplished by a central neural network. This orchestrates a complex behavioral and autonomic repertoire in response to environmental temperature challenges or declining energy homeostasis and in support of immune responses and many behavioral states. This review summarizes the anatomical, neurotransmitter, and functional relationships within the central neural network that controls the principal thermoeffectors: cutaneous vasoconstriction regulating heat loss and shivering and brown adipose tissue for heat production. The core thermoregulatory network regulating these thermoeffectors consists of parallel but distinct central efferent pathways that share a common peripheral thermal sensory input. Delineating the neural circuit mechanism underlying central thermoregulation provides a useful platform for exploring its functional organization, elucidating the molecular underpinnings of its neuronal interactions, and discovering novel therapeutic approaches to modulating body temperature and energy homeostasis.
Topics: Animals; Body Temperature; Body Temperature Regulation; Humans; Neural Pathways; Neurons; Vasoconstriction
PubMed: 30256726
DOI: 10.1146/annurev-physiol-020518-114546 -
Chest Jan 2017Hypoxic pulmonary vasoconstriction (HPV) is a homeostatic mechanism that is intrinsic to the pulmonary vasculature. Intrapulmonary arteries constrict in response to... (Review)
Review
Hypoxic pulmonary vasoconstriction (HPV) is a homeostatic mechanism that is intrinsic to the pulmonary vasculature. Intrapulmonary arteries constrict in response to alveolar hypoxia, diverting blood to better-oxygenated lung segments, thereby optimizing ventilation/perfusion matching and systemic oxygen delivery. In response to alveolar hypoxia, a mitochondrial sensor dynamically changes reactive oxygen species and redox couples in pulmonary artery smooth muscle cells (PASMC). This inhibits potassium channels, depolarizes PASMC, activates voltage-gated calcium channels, and increases cytosolic calcium, causing vasoconstriction. Sustained hypoxia activates rho kinase, reinforcing vasoconstriction, and hypoxia-inducible factor (HIF)-1α, leading to adverse pulmonary vascular remodeling and pulmonary hypertension (PH). In the nonventilated fetal lung, HPV diverts blood to the systemic vasculature. After birth, HPV commonly occurs as a localized homeostatic response to focal pneumonia or atelectasis, which optimizes systemic Po without altering pulmonary artery pressure (PAP). In single-lung anesthesia, HPV reduces blood flow to the nonventilated lung, thereby facilitating thoracic surgery. At altitude, global hypoxia causes diffuse HPV, increases PAP, and initiates PH. Exaggerated or heterogeneous HPV contributes to high-altitude pulmonary edema. Conversely, impaired HPV, whether due to disease (eg, COPD, sepsis) or vasodilator drugs, promotes systemic hypoxemia. Genetic and epigenetic abnormalities of this oxygen-sensing pathway can trigger normoxic activation of HIF-1α and can promote abnormal metabolism and cell proliferation. The resulting pseudohypoxic state underlies the Warburg metabolic shift and contributes to the neoplasia-like phenotype of PH. HPV and oxygen sensing are important in human health and disease.
Topics: Humans; Hypoxia; Hypoxia-Inducible Factor 1, alpha Subunit; Oxygen Consumption; Pulmonary Circulation; Pulmonary Gas Exchange; Vasoconstriction
PubMed: 27645688
DOI: 10.1016/j.chest.2016.09.001 -
Autonomic Neuroscience : Basic &... Apr 2016Cold exposure in humans causes specific acute and chronic physiological responses. This paper will review both the acute and long-term physiological responses and... (Review)
Review
Cold exposure in humans causes specific acute and chronic physiological responses. This paper will review both the acute and long-term physiological responses and external factors that impact these physiological responses. Acute physiological responses to cold exposure include cutaneous vasoconstriction and shivering thermogenesis which, respectively, decrease heat loss and increase metabolic heat production. Vasoconstriction is elicited through reflex and local cooling. In combination, vasoconstriction and shivering operate to maintain thermal balance when the body is losing heat. Factors (anthropometry, sex, race, fitness, thermoregulatory fatigue) that influence the acute physiological responses to cold exposure are also reviewed. The physiological responses to chronic cold exposure, also known as cold acclimation/acclimatization, are also presented. Three primary patterns of cold acclimatization have been observed, a) habituation, b) metabolic adjustment, and c) insulative adjustment. Habituation is characterized by physiological adjustments in which the response is attenuated compared to an unacclimatized state. Metabolic acclimatization is characterized by an increased thermogenesis, whereas insulative acclimatization is characterized by enhancing the mechanisms that conserve body heat. The pattern of acclimatization is dependent on changes in skin and core temperature and the exposure duration.
Topics: Acclimatization; Adaptation, Physiological; Animals; Body Temperature Regulation; Cold Temperature; Fatigue; Humans; Vasoconstriction
PubMed: 26924539
DOI: 10.1016/j.autneu.2016.02.009 -
Arteriosclerosis, Thrombosis, and... Sep 2019While the opioid epidemic has garnered significant attention, the use of methamphetamines is growing worldwide independent of wealth or region. Following overdose and... (Review)
Review
While the opioid epidemic has garnered significant attention, the use of methamphetamines is growing worldwide independent of wealth or region. Following overdose and accidents, the leading cause of death in methamphetamine users is cardiovascular disease, because of significant effects of methamphetamine on vasoconstriction, pulmonary hypertension, atherosclerotic plaque formation, cardiac arrhythmias, and cardiomyopathy. In this review, we examine the current literature on methamphetamine-induced changes in cardiovascular health, discuss the potential mechanisms regulating these varied effects, and highlight our deficiencies in understanding how to treat methamphetamine-associated cardiovascular dysfunction.
Topics: Arrhythmias, Cardiac; Atherosclerosis; Cardiomyopathies; Cardiovascular Diseases; Humans; Hypertension, Pulmonary; Methamphetamine; Vasoconstriction
PubMed: 31433698
DOI: 10.1161/ATVBAHA.119.312461 -
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 -
Continuum (Minneapolis, Minn.) Oct 2021This article describes the causes, clinical and imaging features, management, and prognosis of posterior reversible encephalopathy syndrome (PRES) and reversible... (Review)
Review
PURPOSE OF REVIEW
This article describes the causes, clinical and imaging features, management, and prognosis of posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS), in which the underlying pathophysiology is related to reversible dysregulation of the cerebral vasculature.
RECENT FINDINGS
PRES and RCVS are descriptive terms, each bringing together conditions with similar clinical-imaging manifestations. Headache, visual symptoms, seizures, and confusion occur in both syndromes. RCVS is usually heralded by recurrent thunderclap headaches, whereas encephalopathy and seizures are typical in PRES. In PRES, brain imaging shows reversible vasogenic edema that is typically symmetric and located in subcortical regions (mostly posterior predominant). In RCVS, brain imaging is often normal; cerebral angiography shows segmental vasoconstriction-vasodilatation affecting the circle of Willis arteries and their branches. Aside from shared clinical features, significant imaging overlap exists. Both PRES and RCVS can be complicated by ischemic and hemorrhagic brain lesions; angiographic abnormalities frequently occur in PRES and vasogenic edematous lesions in RCVS. Common triggers (eg, eclampsia, vasoconstrictive and chemotherapeutic agents) have been identified. Abnormal cerebrovascular tone and endothelial dysfunction may explain both syndromes. Management of these syndromes includes the removal of identified triggers, symptomatic treatment of headache or seizures, and moderate blood pressure control. Both syndromes are self-limited, with clinical recovery occurring within days to weeks. Long-term deficits and mortality are uncommon.
SUMMARY
PRES and RCVS have been well characterized and acknowledged to have significant overlap. Advances in our understanding of pathophysiology and risk factors for poor outcome are expected to optimize the management of these not uncommon syndromes.
Topics: Cerebral Angiography; Cerebrovascular Disorders; Female; Headache Disorders, Primary; Humans; Posterior Leukoencephalopathy Syndrome; Pregnancy; Vasoconstriction
PubMed: 34618761
DOI: 10.1212/CON.0000000000001037 -
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 -
Physiological Reviews Jul 2023The pulmonary circulation is a low-resistance, low-pressure, and high-compliance system that allows the lungs to receive the entire cardiac output. Pulmonary arterial... (Review)
Review
The pulmonary circulation is a low-resistance, low-pressure, and high-compliance system that allows the lungs to receive the entire cardiac output. Pulmonary arterial pressure is a function of cardiac output and pulmonary vascular resistance, and pulmonary vascular resistance is inversely proportional to the fourth power of the intraluminal radius of the pulmonary artery. Therefore, a very small decrease of the pulmonary vascular lumen diameter results in a significant increase in pulmonary vascular resistance and pulmonary arterial pressure. Pulmonary arterial hypertension is a fatal and progressive disease with poor prognosis. Regardless of the initial pathogenic triggers, sustained pulmonary vasoconstriction, concentric vascular remodeling, occlusive intimal lesions, in situ thrombosis, and vascular wall stiffening are the major and direct causes for elevated pulmonary vascular resistance in patients with pulmonary arterial hypertension and other forms of precapillary pulmonary hypertension. In this review, we aim to discuss the basic principles and physiological mechanisms involved in the regulation of lung vascular hemodynamics and pulmonary vascular function, the changes in the pulmonary vasculature that contribute to the increased vascular resistance and arterial pressure, and the pathogenic mechanisms involved in the development and progression of pulmonary hypertension. We focus on reviewing the pathogenic roles of membrane receptors, ion channels, and intracellular Ca signaling in pulmonary vascular smooth muscle cells in the development and progression of pulmonary hypertension.
Topics: Humans; Hypertension, Pulmonary; Pulmonary Arterial Hypertension; Ion Channels; Lung; Vasoconstriction; Calcium Signaling; Myocytes, Smooth Muscle
PubMed: 36422993
DOI: 10.1152/physrev.00030.2021 -
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 -
Seminars in Respiratory and Critical... Oct 2023The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary... (Review)
Review
The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary capillary bed enabling gas exchange. The distribution of pulmonary blood flow is regulated by several factors including effects of vascular branching structure, large-scale forces related to gravity, and finer scale factors related to local control. Hypoxic pulmonary vasoconstriction is one such important regulatory mechanism. In the face of local hypoxia, vascular smooth muscle constriction of precapillary arterioles increases local resistance by up to 250%. This has the effect of diverting blood toward better oxygenated regions of the lung and optimizing ventilation-perfusion matching. However, in the face of global hypoxia, the net effect is an increase in pulmonary arterial pressure and vascular resistance. Pulmonary vascular resistance describes the flow-resistive properties of the pulmonary circulation and arises from both precapillary and postcapillary resistances. The pulmonary circulation is also distensible in response to an increase in transmural pressure and this distention, in addition to recruitment, moderates pulmonary arterial pressure and vascular resistance. This article reviews the physiology of the pulmonary vasculature and briefly discusses how this physiology is altered by common circumstances.
Topics: Humans; Vasoconstriction; Vascular Resistance; Lung; Pulmonary Circulation; Hypoxia; Blood Pressure
PubMed: 37816344
DOI: 10.1055/s-0043-1770059