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Clinical Medicine (London, England) 2007
Review
Topics: Cardiac Output; Homeostasis; Humans; Vasoconstriction; Veins; Venous Pressure
PubMed: 17348572
DOI: 10.7861/clinmedicine.7-1-35 -
Journal of Healthcare Engineering 2014Photoplethysmograph (PPG) has been widely used to investigate various cardiovascular conditions. Previous studies demonstrated effects of temperature of the measurement...
Photoplethysmograph (PPG) has been widely used to investigate various cardiovascular conditions. Previous studies demonstrated effects of temperature of the measurement environment; however, an integrated evaluation has not been established in environments with gradual air temperature variation. The purpose of this study is to investigate variations and relationships of blood pressure (BP), PPG and cardiovascular parameters such as heart rate (HR), stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR), by changing skin surface temperature (SST). Local mild cooling and heating was conducted on 16 healthy subjects. The results showed that local SST changes affected Finometer blood pressures (Finger BP), PPG components and TPR, but not the oscillometric blood pressure (Central BP), HR, SV and CO, and indicated that temperature must be maintained and monitored to reliably evaluate cardiovascular conditions in temperature-varying environments.
Topics: Adult; Humans; Photoplethysmography; Skin; Skin Temperature; Vasoconstriction; Vasodilation; Young Adult
PubMed: 25516126
DOI: 10.1260/2040-2295.5.4.429 -
The Journal of Physiology Apr 2012
Topics: Cardiac Output; Female; Humans; Male; Sympathetic Nervous System; Syncope; Vasoconstriction
PubMed: 22532643
DOI: 10.1113/jphysiol.2012.231282 -
American Journal of Physiology. Heart... Jan 2011Erythrocyte free hemoglobin (Hb) induces vasoconstriction due to nitric oxide (NO) scavenging, limiting the NO available for vascular smooth muscle. The central...
Erythrocyte free hemoglobin (Hb) induces vasoconstriction due to nitric oxide (NO) scavenging, limiting the NO available for vascular smooth muscle. The central objective of this study was to restore NO bioavailability using long-lived circulating NO-releasing nanoparticles (NO-np) to reverse the vasoconstriction and hypertension induced by polymerized bovine Hb (PBH) NO scavenging. PBH (13 g/dl) was infused in a volume equal to 10% of the animal blood volume. Intravascular NO supplementation was provided with an infusion of NO-np (10 and 20 mg/kg body wt). This study was performed using the hamster window chamber model to concurrently access systemic and microvascular hemodynamics. Infusion of PBH increased blood pressure and induced vasoconstriction. Treatment with 10 and 20 mg/kg NO-np reduced the blood pressure and vasoconstriction induced by PBH. Moreover, the higher dose of NO-np decreased blood pressure and induced vasodilation compared with baseline, respectively. Treatment with NO-np to decrease PBH-induced vasoconstriction increased methemoglobin levels and plasma nitrite and nitrate. In conclusion, NO-np counteracted both systemic hypertension and decreased the vasoconstrictor effects of PBH infusion, improving systemic and microvascular function. Based on the observed physiological properties, NO-np has clear potential as a therapeutic agent to replenish NO in situations where NO production is impaired, insufficient, or consumed, thereby preventing vascular complications.
Topics: Analysis of Variance; Animals; Blood Pressure; Cricetinae; Heart Rate; Hemoglobins; Male; Mesocricetus; Microcirculation; Nanoparticles; Nitric Oxide; Random Allocation; Vasoconstriction
PubMed: 21057038
DOI: 10.1152/ajpheart.00665.2010 -
American Journal of Physiology. Lung... Dec 2004Pulmonary arteries exhibit a marked vasoconstriction when exposed to hypoxic conditions. Although this may be an adaptive response to match lung ventilation with...
Pulmonary arteries exhibit a marked vasoconstriction when exposed to hypoxic conditions. Although this may be an adaptive response to match lung ventilation with perfusion, the potential consequences of sustained pulmonary vasoconstriction include pulmonary hypertension and right heart failure. Concomitant production of proinflammatory mediators during hypoxia may exacerbate acute increases in pulmonary vascular resistance. We hypothesized that acute hypoxia causes pulmonary arterial contraction and increases the pulmonary artery tissue expression of proinflammatory cytokines via a protein kinase C (PKC)-mediated mechanism. To study this, isometric force displacement was measured in isolated rat pulmonary artery rings during hypoxia in the presence and absence of the PKC inhibitors calphostin C or chelerythrine. In separate experiments, pulmonary artery rings were treated with the PKC activator thymeleatoxin for 60 min. After hypoxia, with or without PKC inhibition, or PKC activation alone, pulmonary artery rings were subjected to mRNA analysis for TNF-alpha and IL-1beta via RT-PCR. Our results showed that, in isolated pulmonary arteries, hypoxia caused a biphasic contraction and increased expression of TNF-alpha and IL-1beta mRNA. Both effects were inhibited by PKC inhibition. PKC activation resulted in pulmonary artery contraction and increased the pulmonary artery expression of TNF-alpha and IL-1beta mRNA. These findings suggest that hypoxia induces the expression of inflammatory cytokines and causes vasoconstriction via a PKC-dependent mechanism. We conclude that PKC may have a central role in modulating hypoxic pulmonary vasoconstriction, and further elucidation of its involvement may lead to therapeutic application.
Topics: Alkaloids; Animals; Benzophenanthridines; Cell Hypoxia; Cytokines; Enzyme Inhibitors; In Vitro Techniques; Muscle Contraction; Muscle, Smooth, Vascular; Phenanthridines; Protein Kinase C; Pulmonary Artery; Rats; Vasoconstriction
PubMed: 15321786
DOI: 10.1152/ajplung.00179.2004 -
Journal of Applied Physiology... Nov 2009Despite recent advances in the design of hemoglobin (Hb)-based oxygen carriers (HBOCs), vasoconstriction, presumably caused by nitric oxide (NO) scavenging, vessel wall...
Despite recent advances in the design of hemoglobin (Hb)-based oxygen carriers (HBOCs), vasoconstriction, presumably caused by nitric oxide (NO) scavenging, vessel wall hyperoxygenation, and/or extravasation, has been identified as the principal road block hampering commercial development of HBOCs. This study was designed to analyze systemic and microvascular responses to the molecular mass and plasma concentration of tense (T)-state polymerized bovine Hb (PolybHb) solutions. Experiments were performed using the hamster window chamber model subjected to successive hypervolemic infusions of T-state PolybHb solutions. PolybHb plasma concentrations were evaluated, namely, 0.5, 1.0 and 1.5 g/dl, respectively. Infusion of PolybHb solutions with molecular mass >500 kDa elicited hypertension and vasoconstriction proportional to the plasma concentration and inversely proportional to the PolybHb cross-link density. However, two high-molecular mass PolybHb solutions, PolybHb(40:1)(high) PolybHb(50:1)(high), did not elicit vasoconstriction at all concentrations studied, whereas PolybHb(50:1)(high) only elicited moderate hypertension at the highest concentration studied. In contrast, infusion of PolybHb solutions with molecular mass <500 kDa elicited significant hypertension and vasoconstriction compared with PolybHb solutions with molecular mass >500 kDa that was proportional to the plasma concentration and inversely proportional to the PolybHb cross-link density. We present promising results for highly cross-linked T-state PolybHb solutions with molecular mass >500 kDa [PolybHb(40:1)(high) PolybHb(50:1)(high)], which supports the concept that HBOC size/molecular mass influences its proximity to the vascular endothelium and molecular diffusivity. The hemodynamics of HBOC within the plasma layer surrounding the abluminal side endothelium regulates NO production and consumption, vessel oxygen flux, and extravasation. Although mechanistically attractive, neither of these hypotheses can be directly tested in vivo and will require further investigation.
Topics: Animals; Blood Pressure; Blood Substitutes; Cattle; Cricetinae; Dose-Response Relationship, Drug; Hemoglobins; Infusions, Intra-Arterial; Molecular Weight; Vasoconstriction
PubMed: 19745190
DOI: 10.1152/japplphysiol.00622.2009 -
Neurosurgery May 2021The trigeminal nerve directly innervates key vascular structures both centrally and peripherally. Centrally, it is known to innervate the brainstem and cavernous sinus,...
BACKGROUND
The trigeminal nerve directly innervates key vascular structures both centrally and peripherally. Centrally, it is known to innervate the brainstem and cavernous sinus, whereas peripherally the trigemino-cerebrovascular network innervates the majority of the cerebral vasculature. Upon stimulation, it permits direct modulation of cerebral blood flow (CBF), making the trigeminal nerve a promising target for the management of cerebral vasospasm. However, trigeminally mediated cerebral vasodilation has not been applied to the treatment of vasospasm.
OBJECTIVE
To determine the effect of percutaneous electrical stimulation of the infraorbital branch of the trigeminal nerve (pTNS) on the cerebral vasculature.
METHODS
In order to determine the stimulus-response function of pTNS on cerebral vasodilation, CBF, arterial blood pressure, cerebrovascular resistance, intracranial pressure, cerebral perfusion pressure, cerebrospinal fluid calcitonin gene-related peptide (CGRP) concentrations, and the diameter of cerebral vessels were measured in healthy and subarachnoid hemorrhage (SAH) rats.
RESULTS
The present study demonstrates, for the first time, that pTNS increases brain CGRP concentrations in a dose-dependent manner, thereby producing controllable cerebral vasodilation. This vasodilatory response appears to be independent of the pressor response induced by pTNS, as it is maintained even after transection of the spinal cord at the C5-C6 level and shown to be confined to the infraorbital nerve by administration of lidocaine or destroying it. Furthermore, such pTNS-induced vasodilatory response of cerebral vessels is retained after SAH-induced vasospasm.
CONCLUSION
Our study demonstrates that pTNS is a promising vasodilator and increases CBF, cerebral perfusion, and CGRP concentration both in normal and vasoconstrictive conditions.
Topics: Animals; Calcitonin Gene-Related Peptide; Cerebrovascular Circulation; Electric Stimulation; Male; Rats; Trigeminal Nerve; Vasoconstriction; Vasodilation; Vasospasm, Intracranial
PubMed: 33677599
DOI: 10.1093/neuros/nyab053 -
Anesthesiology Oct 1990To determine the extent to which thermoregulatory vasoconstriction decreases heat loss to the environment, we measured regional heat flux, average skin temperature, and...
To determine the extent to which thermoregulatory vasoconstriction decreases heat loss to the environment, we measured regional heat flux, average skin temperature, and tympanic membrane temperature before and after thermoregulatory vasoconstriction in five minimally clothed volunteers maintained in a 30.8 +/- 0.1 degrees C environment. Thermoregulatory vasoconstriction was induced by central venous infusion of cooled fluid. Peripheral cutaneous blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Laser Doppler flowmetry was used to measure vasoconstriction in centrally located skin. This model mimics the common clinical situation in which patients in a warm environment are centrally cooled by administration of cold intravenous fluids or by lavage of internal cavities with cold fluids. Tympanic membrane temperature decreased 1.5 +/- 0.3 degrees C in the first 15 min after the cold fluid infusion was started and remained approximately 1 degrees C below control values during the rest of the study. Average skin-surface temperature decreased slowly to approximately 0.7 degrees C below control. Flow in capillaries of centrally distributed skin, determined with laser Doppler flowmetry, decreased only approximately 40%. Total heat flux, and flux from the arms and legs decreased approximately 25% (15.5 +/- 0.3 W). Heat loss from the trunk and head decreased only 17%, whereas, loss from the hands and feet (10.5% of the body surface area) decreased approximately 50%. All measured values decreased significantly following vasoconstriction (P less than 0.01). Therefore, thermoregulatory vasoconstriction in a thermoneutral environment appears to decrease cutaneous loss of metabolic heat approximately 25%.
Topics: Adult; Body Temperature Regulation; Female; Humans; Male; Skin; Skin Temperature; Vasoconstriction
PubMed: 2221434
DOI: 10.1097/00000542-199010000-00011 -
British Journal of Pharmacology Oct 19991. An investigation was performed in pentobarbitone anaesthetized rats to compare the renal vasoconstrictor actions of endothelin-1 (ET-1), endothelin-3 (ET-3) and...
1. An investigation was performed in pentobarbitone anaesthetized rats to compare the renal vasoconstrictor actions of endothelin-1 (ET-1), endothelin-3 (ET-3) and sarafotoxin 6c and their dependency on NO production. 2. Intra-renal arterial infusion of ET-1 and ET-3, from 1 - 1000 ng had no effect on blood pressure, but reduced renal blood flow maximally by 82 and 81% with EC50 values of 510+/-18 and 1113+/-17 ng, respectively and correspondingly increased renal vascular resistance and decreased conductance. 3. Direct renal arterial administration of sarafotoxin 6c was without effect on blood pressure but caused a maximum reduction in renal blood flow of 56% at 300 ng and had an EC50 of 86+/-4 ng. 4. Administration of the selective ETA receptor antagonist FR139317 at 0.3 and 1.0 mg kg-1 had no effect on basal levels of blood pressure, renal vascular resistance or renal blood flow. The lower dose of FR139317 had no effect on the ET-1 dose-response curve for renal blood flow while at 1.0 mg kg-1, FR139317 reduced the EC50 to 363+/-32 ng (P<0.05). 5. Infusion of L-NAME, 10 microg kg-1 min-1 increased blood pressure by approximately 15%, increased renal vascular resistance and decreased renal blood flow by some 40%. The EC50 values for renal blood flow were reduced to 358+/-68 ng (P<0.05) for ET-1, 638+/-69 ng (P<0.05) for ET-3 and 55+/-10 ng (P<0.01) for sarafotoxin 6c. The maximal reduction in renal blood flow induced by sarafotoxin 6c was raised (P<0.01) from 56% to approximately 100% and renal vascular resistance increased when NO production was blocked. 6. These results showed that the vasoconstrictor actions of ET-1 and ET-3 on resistance vessels controlling renal blood flow are mediated via ETB rather than ETA receptors. Moreover, both ET-1 and ET-3 dependent vasoconstrictions are slightly attenuated by concomitant NO production. By contrast, sarafotoxin 6c appears much more potent at the renal resistance vasculature and is much more powerfully modulated by NO.
Topics: Anesthesia; Animals; Endothelins; Kidney; Male; NG-Nitroarginine Methyl Ester; Rats; Rats, Wistar; Regional Blood Flow; Vasoconstriction; Viper Venoms
PubMed: 10516666
DOI: 10.1038/sj.bjp.0702846 -
Physiology (Bethesda, Md.) Jun 2010Calcium-activated nonselective cationic currents have been known for 30 years, but their physiological implications have remained unresolved until the recent cloning of... (Review)
Review
Calcium-activated nonselective cationic currents have been known for 30 years, but their physiological implications have remained unresolved until the recent cloning of the TRPM4 ion channel. Since then, TRPM4 has been identified as a key modulator of numerous calcium-dependent mechanisms such as the immune response, insulin secretion, cerebral artery constriction, respiratory rhythm, and cardiac conduction.
Topics: Heart Conduction System; Humans; Immunity; Respiratory Mechanics; Signal Transduction; TRPM Cation Channels; Vasoconstriction
PubMed: 20551229
DOI: 10.1152/physiol.00004.2010