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Aviation, Space, and Environmental... Jan 2013The goal of this study was to investigate the contribution of splanchnic volume redistribution and lower limb vasoconstriction in the maintenance of blood pressure... (Clinical Trial)
Clinical Trial
BACKGROUND
The goal of this study was to investigate the contribution of splanchnic volume redistribution and lower limb vasoconstriction in the maintenance of blood pressure during progressive central hypovolemia induced by graded lower body negative pressure (LBNP). It was hypothesized that splanchnic blood volume loss during LBNP would buffer decreases in thoracic blood volume.
METHODS
There were 15 healthy subjects (8 men, 7 women) who participated in the study. We used LBNP of -10, -20, -30, and -40 mmHg with segmental impedance analysis to determine central and splanchnic volume changes, and near infrared spectroscopy (NIRS) to assess calf venous volume changes and vasoconstrictor tone.
RESULTS
In relation to baseline, LBNP to -40 mmHg resulted in a 57% increase in deoxygenated blood in the calf, indicating venous pooling in the lower limbs. These events led to a decrease in venous return and a 28% decline in cardiac output. Total upper body impedance increased by 6.6% with a 2.4% change in thoracic and a 13.1% increase in splanchnic impedance with progressive LBNP. Splanchnic blood volume contributed to more than 50% of the volume redistribution to the thoracic compartment during hypovolemia. Both men and women increased their heart rate, but only men vasoconstricted (4.4%) with increasing LBNP. The net result of these events was the maintenance of mean arterial blood pressure with no presyncopal symptoms in these subjects.
DISCUSSION
Our results suggest that splanchnic blood volume redistribution--rather than leg vasoconstriction--plays an important role in blood pressure regulation during central hypovolemia.
Topics: Blood Pressure; Blood Volume; Cardiac Output; Female; Humans; Hypovolemia; Leg; Lower Body Negative Pressure; Male; Spectroscopy, Near-Infrared; Splanchnic Circulation; Vasoconstriction
PubMed: 23305001
DOI: 10.3357/asem.3424.2013 -
Heart and Vessels 1999We previously showed that deformation of the cardiac tissue surrounding a dilated coronary artery changes its hydraulic resistance depending on the direction of stretch.... (Comparative Study)
Comparative Study
We previously showed that deformation of the cardiac tissue surrounding a dilated coronary artery changes its hydraulic resistance depending on the direction of stretch. Stretch parallel, but not perpendicular, to the vessel axis increased the hydraulic resistance. This asymmetric dependence of resistance on the direction of stretch was found at a low perfusion pressure only, presumably because this was the state in which surrounding fibers were sufficiently stretched to be able to exert their effects. When the vessel is vasoconstricted and its diameter decreases, this might alter the coupling between tissue and vessel. On the other hand, the stiffer vessel wall would be more difficult to deform, making the coupling less evident. The aim of this study was to test the hypothesis that, at this low perfusion pressure, the asymmetric resistance response to strain differs between the vasodilated and vasoconstricted states. We compared how the hydraulic resistance of an in situ segment of a vasodilated and then vasoconstricted epicardial coronary artery was affected by stretching the surrounding tissue by 10% in a direction parallel and then perpendicular to the vessel axis. Vasoconstriction increased the unstretched resistance of the vessel, demonstrating that the vessel diameter was decreased. In both vasomotor states the relative resistance changes to parallel and perpendicular tissue stretches were found to be similar. Thus, the effects of subtle differences in vessel cross-sectional shape underlying the resistance changes to tissue stretch in the vasodilated state - that should have been altered by vasoconstriction - were seemingly counterbalanced by increased vessel wall stiffness that decreased the manifestation of coupling between the vessel and the surrounding tissue.
Topics: Animals; Coronary Circulation; Coronary Vessels; Dogs; Female; In Vitro Techniques; Ischemic Preconditioning, Myocardial; Male; Myocardial Reperfusion; Vascular Resistance; Vasoconstriction
PubMed: 10543309
DOI: 10.1007/BF02481738 -
Journal of Applied Physiology... May 1991Endotoxin [lipopolysaccharide (LPS)] has been reported to reduce hypoxic pulmonary vasoconstriction and thus increases venous admixture. The time course of this failure...
Endotoxin [lipopolysaccharide (LPS)] has been reported to reduce hypoxic pulmonary vasoconstriction and thus increases venous admixture. The time course of this failure of pulmonary blood flow regulation was investigated in six chronically instrumented unanesthetized sheep after infusion of Escherichia coli LPS (1 microgram/kg). The change in left pulmonary arterial blood flow (LPBF, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N2 alternately to the left and right lungs) was compared before and at various time intervals after the administration of LPS. During baseline conditions, LPBF was 33% of total cardiac output and decreased to 15% when the left lung was ventilated with a hypoxic gas mixture. One hour after endotoxin infusion, LPBF remained at 33% of total cardiac output yet only decreased to 28% during the hypoxic challenge. The response to one-lung hypoxia was still significantly depressed 10 h post-LPS administration. It is concluded that hypoxic pulmonary vasoconstriction is almost completely abolished for a prolonged time period after a small dose of LPS.
Topics: Animals; Endotoxins; Female; Hypoxia; Pulmonary Circulation; Sheep; Time Factors; Toxemia; Vascular Resistance; Vasoconstriction
PubMed: 1864794
DOI: 10.1152/jappl.1991.70.5.2120 -
Cardiovascular Research Nov 1994Physiological and pathophysiological roles of endothelins are still unclear. One reason is that circulating endothelin levels in normal and pathological states are much... (Review)
Review
Physiological and pathophysiological roles of endothelins are still unclear. One reason is that circulating endothelin levels in normal and pathological states are much lower than the concentrations necessary to elicit contractions in vitro. It is usually assumed that endothelin accumulates in diseased tissues and that, because of its degradation, only a small fraction of it reaches the systemic circulation. Such a hypothesis does not fit with recent observations showing that low circulating endothelin levels may be active. We show here that most of the current inferences about the actions of endothelin assume that the peptide acts in the vessel wall under conditions known as non-stoichiometric binding conditions, that is, under conditions in which the receptor concentration in tissues ([Ro]) is smaller than the equilibrium dissociation constant of endothelin receptor complexes (Kd). Under stoichiometric binding conditions (defined by the condition [Ro] > Kd), most ligand molecules are bound to receptors and cannot be present in a free form. Estimates of [Ro] and Kd from the literature suggests that in vivo endothelin probably binds stoichiometrically to its receptors. Under this condition, most of tissue endothelin is probably bound to receptors. It is therefore suggested that plasma endothelin levels are low probably because tissue free endothelin levels are low, and this is not inconsistent with the presence of high tissue levels of active (that is, bound) endothelin. When the topology of the vessels with respect to the site of production (or of delivery) of endothelin is considered, stoichiometric binding may also account for the higher sensitivity to Et-1 of in vivo preparations. It also suggests that autocrine and paracrine actions of Et-1 are favoured at low and high secretory rates respectively, thus providing an explanation for the dual (vasodilator and vasoconstricting) actions of endothelin. Finally, the stoichiometric binding model predicts that functional receptors also act as clearance receptors and provides an explanation for the observation that antagonists of endothelin receptors are also clearance antagonists.
Topics: Endothelins; Humans; Protein Binding; Receptors, Endothelin; Vasoconstriction; Vasodilation
PubMed: 7842453
DOI: 10.1093/cvr/28.11.1613 -
Cell and Tissue Research Apr 1998The endothelins (ETs) are regulatory peptides, distributed in many organ systems and with potent physiological effects. ETs represent the most powerful vasoconstrictive... (Review)
Review
The endothelins (ETs) are regulatory peptides, distributed in many organ systems and with potent physiological effects. ETs represent the most powerful vasoconstrictive substances known today. They also act as growth factors and seem to be involved in fetal development. Much data support a pathophysiological role for ETs, especially in diseases of the vascular system, such as hypertension, preeclampsia, ischemic heart disease, subarachnoidal haemorrhage, and cerebral ischemia. The development of drugs affecting ET-receptors and the biosynthesis of ETs presently attract great interest for the establishment of new treatments of diseases in which ETs are involved. Hopefully, the elaboration of more specific ET-receptor ligands will fulfill some of these expectations.
Topics: Amino Acid Sequence; Animals; Endothelins; Growth Substances; Humans; Molecular Sequence Data; Peptides; Vasoconstriction
PubMed: 9506906
DOI: 10.1007/s004410051028 -
The American Journal of Cardiology Nov 1992Prolonged exposure to organic nitrates has been shown to lead to the rapid development of tolerance to the peripheral and coronary vasodilatory effects of these drugs.... (Review)
Review
Prolonged exposure to organic nitrates has been shown to lead to the rapid development of tolerance to the peripheral and coronary vasodilatory effects of these drugs. As a result of this phenomenon, the hemodynamic and anti-ischemic effects of nitrates may be rapidly attenuated in patients with ischemic heart disease, congestive heart failure, or both. This nitrate tolerance appears to be both dose- and time-dependent. Likely mechanisms proposed for its development are multifactorial and include depletion of sulfhydryl groups, a nitrate-mediated increase in blood volume, and neurohormonal stimulation with activation of vasoconstrictive mechanisms.
Topics: Coronary Circulation; Drug Tolerance; Hemodynamics; Humans; Nitrates; Vasoconstriction
PubMed: 1449100
DOI: 10.1016/0002-9149(92)90026-u -
Anesthesia and Analgesia Sep 1996Intraoperative hypothermia results largely from anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction. Sufficient hypothermia, however, triggers... (Clinical Trial)
Clinical Trial Comparative Study Randomized Controlled Trial
Intraoperative hypothermia results largely from anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction. Sufficient hypothermia, however, triggers peripheral vasoconstriction, which usually prevents further decrease in core temperature. The thermoregulatory effects of all volatile anesthetics have been tested in adults and/or children, but different anesthetics have not been directly compared. We therefore evaluated thermoregulatory responses during enflurane, isoflurane, and halothane administration. Anesthesia was maintained with 1 minimum alveolar anesthetic concentration (MAC) of halothane, isoflurane, or enflurane in 27 patients undergoing intraabdominal surgery. Patients were maintained normovolemic and normocapnic but were allowed to cool passively. A forearm minus fingertip, skin-temperature gradient of 4 degrees C identified significant vasoconstriction; the core temperature triggering vasoconstriction identified the threshold. Morphometric characteristics, initial core temperatures, ambient operating room temperatures, blood pressures, and anesthetic potencies were similar in each group. All eight patients given halothane vasoconstricted at a core temperature of 35.5 +/- 0.6 degrees C. Eight of the patients given isoflurane vasoconstricted at a core temperature of 35.2 +/- 0.5 degrees C. However, two others did not at minimum core temperatures of 34.0 and 33.8 degrees C. Only one patient given enflurane vasoconstricted at a core temperature of 34.6 degrees C. The other six patients never vasoconstricted, at minimum core temperatures of 33.6 +/- 0.4 degrees C. Our data indicate that enflurane profoundly inhibits thermoregulatory responses in children. The mechanism for this extraordinary inhibition remains unknown but does not result from any obvious anesthetic pharmacology or thermoregulatory physiology. We conclude that unwarmed pediatric patients will become colder when anesthetized with enflurane than with halothane or isoflurane.
Topics: Anesthetics, Inhalation; Body Temperature Regulation; Child, Preschool; Enflurane; Female; Halothane; Humans; Hypothermia; Intraoperative Complications; Isoflurane; Male; Vasoconstriction
PubMed: 8780288
DOI: 10.1097/00000539-199609000-00028 -
Nan Fang Yi Ke Da Xue Xue Bao = Journal... Mar 2014To investigate the effect of dexmedetomidine on 5-HT-induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms.
OBJECTIVE
To investigate the effect of dexmedetomidine on 5-HT-induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms.
METHODS
Lung tissue was obtained from patients undergoing surgery for lung carcinoma. Intrapulmonary arteries were dissected and cut into rings, which were mounted in a Multi Myograph system to determine the effect of dexmedetomidine (0.3-3 nmol/L) on 5-HT-induced vasoconstrictions. The influences of the endothelium removal and various drugs including L-NAME, yohimbine and indomethacin were tested on the effects of dexmedetomidine.
RESULTS
Dexmedetomidine (0.1-100 nmol/L) did not obviously affect the resting tension of endothelium-intact human intrapulmonary arteries. 5-HT induced concentration-dependent contraction in endothelium-intact intrapulmonary arteries [pD2: 6.11∓0.05, Emax: (102.10∓1.96)%]. In the rings with intact endothelium, dexmedetomidine (0.3-3 nmol/L) significantly attenuated the Emax and pD2 of 5-HT-induced vasoconstriction [pD2: 5.94∓0.03, Emax: (79.96∓1.31)%]. 5-HT also induced concentration-dependent contraction in endothelium-denuded intrapulmonary arteries [pD2: 6.10∓0.07, Emax: (107.40∓3.20)%]. Dexmedetomidine produced no significant effects on the rings with denuded endothelium. The effects of dexmedetomidine on 5-HT-induced vasoconstriction was suppressed by L-NAME and yohimbine, but not by indomethacin.
CONCLUSION
Dexmedetomidine can inhibit 5-HT-induced vasoconstriction of isolated human intrapulmonary arteries probably through α2-adrenergic acceptor and NO released from the endothelium.
Topics: Adult; Aged; Dexmedetomidine; Female; Humans; In Vitro Techniques; Male; Middle Aged; Pulmonary Artery; Serotonin; Vasoconstriction
PubMed: 24670438
DOI: No ID Found -
Anesthesia and Analgesia Nov 1990The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor response was studied in six closed-chest dogs anesthetized with pentobarbital and paralyzed... (Comparative Study)
Comparative Study
The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor response was studied in six closed-chest dogs anesthetized with pentobarbital and paralyzed with pancuronium. The right lung was ventilated continuously with 100% O2; the left lung was ventilated either with 100% O2 ("hyperoxia") or with an hypoxic gas mixture ("hypoxia": end-tidal oxygen tension = 60.3 +/- 0.6 mm Hg). On two consecutive days, each dog received either almitrine (Vectarion, Servier Lab) or malic acid. Consecutive almitrine doses of 0.003, 0.03, 0.3, and 3.0 micrograms.kg-1.min-1, or the equivalent volumes of malic acid without almitrine, were administered intravenously as a constant peripheral infusion for 15 min. Percent blood flow to each lung was calculated based on a variation of the traditional shunt equation. The change in percent left lung blood flow (delta %QL-VA) increased significantly between the hypoxia-no drug and the hypoxia-almitrine (3.0 micrograms.kg-1.min-1) phase. No significant changes occurred during the other almitrine doses or the respective malic acid control phases. The change in arterial oxygen tension (delta PaO2) also increased significantly between the hypoxia-no drug and the hypoxia-almitrine (3.0 micrograms.kg-1.min-1) phase. No significant changes occurred during the other almitrine doses or the respective malic acid control phases. It is concluded that in dogs low-dose almitrine enhances hypoxic pulmonary vasoconstriction and that this enhancement is dose-related.
Topics: Almitrine; Animals; Dogs; Dose-Response Relationship, Drug; Female; Hypoxia; Infusions, Intravenous; Lung; Malates; Stimulation, Chemical; Vasoconstriction
PubMed: 2221407
DOI: 10.1213/00000539-199011000-00004 -
Hypertension (Dallas, Tex. : 1979) Jan 1993The effects of dietary supplementation with marine oils on vascular reactivity in human forearm resistance arteries were studied. Healthy male adults (six to nine... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
The effects of dietary supplementation with marine oils on vascular reactivity in human forearm resistance arteries were studied. Healthy male adults (six to nine subjects per group) were given either maxEPA capsules (content: eicosapentaenoic acid, 0.178 g/g; docosahexaenoic acid, 0.116 g/g) at doses of 20, 10, or 5 g/day or placebo capsules at 20 g/day for 28 days. Capsule compliance was confirmed by measurement of platelet membrane incorporation of n-3 fatty acids. Blood pressure was not affected by either maxEPA or placebo. The influence of treatment interventions on forearm vasoconstrictive responses to local infusions of angiotensin II and norepinephrine was examined using venous occlusion plethysmography before and after treatment. Responses to both agonists were significantly suppressed by 20 g/day maxEPA (slopes before and after maxEPA, respectively: angiotensin II, 3.34 and 0.89; norepinephrine, 0.91 and 0.41). When analyzed as difference in area under the dose-response curves, the suppressive effects of maxEPA were clearly dose dependent (angiotensin II: 20 g area reduced by 72%, 10 g by 67%, 5 g by 33%). Similarly, responses to norepinephrine were dose-dependently suppressed by maxEPA (20 g area reduced by 61%, 10 g by 63%, and 5 g by 33%). Placebo had no effect on the responses to either constrictor. The responses to both agonists returned to preoil levels after 2 months' discontinuation of 20 g/day maxEPA. We conclude that the suppressive effects of marine oils on vascular reactivity may, in part, contribute to their cardioprotective influence in humans.
Topics: Adolescent; Adult; Blood Platelets; Blood Pressure; Dose-Response Relationship, Drug; Fatty Acids, Omega-3; Forearm; Humans; Male; Membrane Lipids; Vascular Resistance; Vasoconstriction
PubMed: 8418020
DOI: 10.1161/01.hyp.21.1.22