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Respirology (Carlton, Vic.) Feb 2013Opioids are widely used for their analgesic properties for the management of acute and chronic pain related to a variety of illnesses. Opioid usage is associated with... (Review)
Review
Opioids are widely used for their analgesic properties for the management of acute and chronic pain related to a variety of illnesses. Opioid usage is associated with adverse effects on respiration which are often attributed to depression of the central nervous system. Recent data indicate that opioid use has increased over the last two decades. There is also increasing evidence that opioids have a variety of effects on the lungs besides suppression of respiration. Opioids can affect immune cells function, increase histamine release causing bronchospasm, vaso-constriction and hypersensitivity reactions. Together, these actions have a variety of effects on lung function. Here, we provide a comprehensive review of the effects of opioids on the lungs including the respiratory centre, immune function, airways and pulmonary vasculature.
Topics: Analgesics, Opioid; Histamine; Humans; Immune System; Lung; Respiratory Hypersensitivity; Respiratory Mechanics; Vasoconstriction
PubMed: 23066838
DOI: 10.1111/j.1440-1843.2012.02307.x -
Developmental Neuroscience 2009The pathophysiology of the effects of cocaine on fetal development has been described along 2 major pathways: neurochemical effects and vasoconstrictive effects.... (Review)
Review
The pathophysiology of the effects of cocaine on fetal development has been described along 2 major pathways: neurochemical effects and vasoconstrictive effects. Following a summary of these effects, we suggest a 'third pathophysiology' in which altered fetal programming affects the acute and long-term adverse effects of in utero cocaine exposure. We describe how cocaine as a stressor alters the expression of key candidate genes, increasing exposure to catecholamines and fetal cortisol-altering neuroendocrine (hypothalamic-pituitary-adrenal axis) activity, leading to infant behavioral dysregulation, poor behavioral control and emotion regulation during childhood and phenotypes that confer vulnerability to substance use in adolescence. This model is discussed in relation to follow-up studies of the effects of in utero cocaine exposure and maturational changes in brain development.
Topics: Animals; Behavior; Brain Chemistry; Cocaine-Related Disorders; Female; Fetus; Humans; Pregnancy; Prenatal Exposure Delayed Effects; Vasoconstriction
PubMed: 19372684
DOI: 10.1159/000207491 -
Experimental Physiology Aug 2021What is the central question of this study? Sympathetically mediated vasoconstriction is preserved during hypoxaemia in humans, but our understanding of vascular control...
NEW FINDINGS
What is the central question of this study? Sympathetically mediated vasoconstriction is preserved during hypoxaemia in humans, but our understanding of vascular control comes from predominantly male cohorts. We tested the hypothesis that young women attenuate sympathetically mediated vasoconstriction during steady-state hypoxaemia, whereas men do not? What is the main finding and its importance? Sympathetically mediated vasoconstriction is preserved or even enhanced during steady-state hypoxia in young men, and the peripheral vascular response to sympathetic activation during hypoxaemia is attenuated in young women. These data advance our understanding of sex-related differences in hypoxic vascular control.
ABSTRACT
Activation of the sympathetic nervous system causes vasoconstriction and a reduction in peripheral blood flow. Sympathetically mediated vasoconstriction may be attenuated during systemic hypoxia to maintain oxygen delivery; however, in predominantly male participants sympathetically mediated vasoconstriction is preserved or even enhanced during hypoxaemia. Given the potential for sex-specific differences in hypoxic vascular control, prior results are limited in application. We tested the hypothesis that young women attenuate sympathetically mediated vasoconstriction during steady-state hypoxaemia, whereas men do not. Healthy young men (n = 13, 25 ± 4 years) and women (n = 11, 24 ± 4 years) completed two trials consisting of a 2-min cold pressor test (CPT, a well-established sympathoexcitatory stimulus) during baseline normoxia and steady-state hypoxaemia. Beat-to-beat blood pressure (finger photoplethysmography) and forearm blood flow (venous occlusion plethysmography) were measured continuously. Total and forearm vascular conductance (TVC and FVC, respectfully) were calculated. A change (Δ) in TVC and FVC from steady-state during the last 1 min of CPT was calculated and differences between normoxia and systemic hypoxia were assessed. In men, the reduction in TVC during CPT was greater during hypoxia compared to normoxia (ΔTVC, P = 0.02), whereas ΔTVC did not differ between conditions in women (P = 0.49). In men, ΔFVC did not differ between normoxia and hypoxia (P = 0.92). In women, the reduction in FVC during CPT was attenuated during hypoxia (ΔFVC, P < 0.01). We confirm sympathetically mediated vasoconstriction is preserved or enhanced during hypoxaemia in young men, whereas peripheral vascular responsiveness to sympathetic activation during hypoxaemia is attenuated in young women. The results advance our understanding of sex-related differences in hypoxic vascular control.
Topics: Blood Pressure; Female; Forearm; Humans; Hypoxia; Male; Regional Blood Flow; Sex Characteristics; Sympathetic Nervous System; Vasoconstriction
PubMed: 34187092
DOI: 10.1113/EP089461 -
American Journal of Physiology. Lung... Nov 2004
Topics: Acute Disease; Humans; Hypoxia; Pulmonary Circulation; Vasoconstriction
PubMed: 15475491
DOI: 10.1152/classicessays.00004.2004 -
Haematologica Jan 2020Vaso-occlusive crisis (VOC) is a hallmark of sickle cell disease (SCD) and occurs when deoxygenated sickled red blood cells occlude the microvasculature. Any stimulus,...
Vaso-occlusive crisis (VOC) is a hallmark of sickle cell disease (SCD) and occurs when deoxygenated sickled red blood cells occlude the microvasculature. Any stimulus, such as mental stress, which decreases microvascular blood flow will increase the likelihood of red cell entrapment resulting in local vaso-occlusion and progression to VOC. Neurally mediated vasoconstriction might be the physiological link between crisis triggers and vaso-occlusion. In this study, we determined the effect of mental stress on microvascular blood flow and autonomic nervous system reactivity. Sickle cell patients and controls performed mentally stressful tasks, including a memory task, conflict test and pain anticipation test. Blood flow was measured using photoplethysmography, autonomic reactivity was derived from electrocardiography and perceived stress was measured by the State-Trait Anxiety Inventory questionnaire. Stress tasks induced a significant decrease in microvascular blood flow, parasympathetic withdrawal and sympathetic activation in all subjects. Of the various tests, pain anticipation caused the highest degree of vasoconstriction. The magnitude of vasoconstriction, sympathetic activation and perceived stress was greater during the Stroop conflict test than during the N-back memory test, indicating the relationship between magnitude of experimental stress and degree of regional vasoconstriction. Baseline anxiety had a significant effect on the vasoconstrictive response in sickle cell subjects but not in controls. In conclusion, mental stress caused vasoconstriction and autonomic nervous system reactivity in all subjects. Although the pattern of responses was not significantly different between the two groups, the consequences of vasoconstriction can be quite significant in SCD because of the resultant entrapment of sickle cells in the microvasculature. This suggests that mental stress can precipitate a VOC in SCD by causing neural-mediated vasoconstriction.
Topics: Anemia, Sickle Cell; Autonomic Nervous System; Humans; Stress, Psychological; Vascular Diseases; Vasoconstriction
PubMed: 30975906
DOI: 10.3324/haematol.2018.211391 -
Revista Medica de Chile Jun 2023Pulmonary arterial hypertension is characterized by increased mean pulmonary arterial pressure, resistance, and pathological remodeling of pulmonary arteries. Calcium... (Review)
Review
Pulmonary arterial hypertension is characterized by increased mean pulmonary arterial pressure, resistance, and pathological remodeling of pulmonary arteries. Calcium entry from the extracellular to the intracellular space through voltage-dependent and -independent channels play a major role in the increase of contractility of pulmonary arteries and in the loss of regulation of the proliferative behavior of the cells from the different layers of the pulmonary arterial wall. In doing so, these channels contribute to enhanced vasoconstriction of pulmonary arteries and their pathological remodeling. This review aims to summarize the evidence obtained from animal and cellular models regarding the involvement of the main plasma membrane calcium channels in these key pathophysiological processes for pulmonary arterial hypertension, discussing the potential value as pharmacological targets for therapies in the present and the future.
Topics: Humans; Hypertension, Pulmonary; Calcium Channels; Animals; Calcium Signaling; Calcium Channel Blockers; Signal Transduction; Pulmonary Artery; Vasoconstriction
PubMed: 38801384
DOI: 10.4067/s0034-98872023000600753 -
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 -
Experimental Physiology Sep 2007
Review
Topics: Animals; Humans; Hypoxia; Pulmonary Circulation; Reactive Oxygen Species; Vasoconstriction
PubMed: 17591681
DOI: 10.1113/expphysiol.2007.038414 -
Journal of Applied Physiology... Jul 2017Sex differences in the neurovascular control of blood pressure and vascular resistance have been reported. However, the mechanisms underlying the modulatory influence of...
Sex differences in the neurovascular control of blood pressure and vascular resistance have been reported. However, the mechanisms underlying the modulatory influence of sex have not been fully elucidated. Nitric oxide (NO) has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle, and estrogen modulates NO synthase (NOS) expression and NO bioavailability. Therefore NO-mediated inhibition of sympathetic vasoconstriction may be enhanced in females. Thus the purpose of the present study was to investigate the hypothesis that sympathetic vasoconstrictor responsiveness would be blunted and NO-mediated inhibition of sympathetic vasoconstriction would be enhanced in females compared with males. Male (M; = 8) and female (F; = 10) Sprague-Dawley rats were anesthetized and surgically instrumented for measurement of arterial blood pressure and femoral artery blood flow and stimulation of the lumbar sympathetic chain. The percentage change of femoral vascular conductance in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction before (control) and after NOS blockade [-nitro-l-arginine methyl ester (l-NAME), 10 mg/kg iv]. At rest, sympathetic vasoconstrictor responsiveness was augmented ( < 0.05) in female compared with male rats at 2 Hz [F: -33 ± 8% (SD); M: -26 ± 6%] but was not different at 5 Hz (F: -55 ± 7%; M: -47 ± 7%). During muscle contraction, evoked vasoconstriction was similar ( > 0.05) in females and males at 2 Hz (F: -12 ± 5%; M: -13 ± 5%) but was blunted ( < 0.05) in females compared with males at 5 Hz (F: -24 ± 5%; M: -34 ± 8%). l-NAME increased ( < 0.05) sympathetic vasoconstrictor responsiveness in both groups at rest and during contraction. Contraction-mediated inhibition of vasoconstriction (sympatholysis) was enhanced ( < 0.05) in females compared with males; however, sympatholysis was not different ( > 0.05) between males and females in the presence of NOS blockade, indicating that NO-mediated sympatholysis was augmented in female rats. These data suggest that sex modulates sympathetic vascular control in resting and contracting skeletal muscle and that a portion of the enhanced sympatholysis in female rats was NO dependent. Sex differences in the neurovascular regulation of blood pressure and vascular resistance have been documented. However, our understanding of the underlying mechanisms that mediate these differences is incomplete. The present study demonstrates that female rats have an enhanced capacity to inhibit sympathetic vasoconstriction during exercise (sympatholysis) and that NO mediates a portion of the enhanced sympatholysis.
Topics: Adrenergic Fibers; Animals; Female; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Rats; Rats, Sprague-Dawley; Sex Characteristics; Vasoconstriction; Vasoconstrictor Agents
PubMed: 28473610
DOI: 10.1152/japplphysiol.00139.2017 -
Acta Ophthalmologica Dec 2018To investigate the effects of intravitreal neuropeptide Y (NPY) treatment following acute retinal ischaemia in an in vivo porcine model. In addition, we evaluated the...
PURPOSE
To investigate the effects of intravitreal neuropeptide Y (NPY) treatment following acute retinal ischaemia in an in vivo porcine model. In addition, we evaluated the vasoconstrictive potential of NPY on porcine retinal arteries ex vivo.
METHODS
Twelve pigs underwent induced retinal ischaemia by elevated intraocular pressure clamping the ocular perfusion pressure at 5 mmHg for 2 hr followed by intravitreal injection of NPY or vehicle. After 4 weeks, retinas were evaluated functionally by standard and global-flash multifocal electroretinogram (mfERG) and histologically by thickness of retinal layers and number of ganglion cells. Additionally, the vasoconstrictive effects of NPY and its involved receptors were tested using wire myographs and NPY receptor antagonists on porcine retinal arteries.
RESULTS
Intravitreal injection of NPY after induced ischaemia caused a significant reduction in the mean induced component (IC) amplitude ratio (treated/normal eye) compared to vehicle-treated eyes. This reduction was accompanied by histological damage, where NPY treatment reduced the mean thickness of inner retinal layers and number of ganglion cells. In retinal arteries, NPY-induced vasoconstriction to a plateau of approximately 65% of potassium-induced constriction. This effect appeared to be mediated via Y1 and Y2, but not Y5.
CONCLUSION
In seeming contrast to previous in vitro studies, intravitreal NPY treatment caused functional and histological damage compared to vehicle after a retinal ischaemic insult. Furthermore, we showed for the first time that NPY induces Y1- and Y2- but not Y5-mediated vasoconstriction in retinal arteries. This constriction could explain the worsening in vivo effect induced by NPY treatment following an ischaemic insult and suggests that future studies on exploring the neuroprotective effects of NPY might focus on other receptors than Y1 and Y2.
Topics: Acute Disease; Animals; Disease Models, Animal; Electroretinography; Female; Intravitreal Injections; Ischemia; Neuropeptide Y; Retinal Diseases; Retinal Ganglion Cells; Retinal Vessels; Swine; Vasoconstriction
PubMed: 30218483
DOI: 10.1111/aos.13806