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Query: UMLS:C0085383 (hypocapnia)
1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the metabolic and ventilatory effects of anemia, which is characterized by a decrease in blood O2 content with no changes in arterial PO2 (PaO2). Anemia was obtained in conscious chronically instrumented adult male rats by substituting blood with equal volumes of Ringer lactate solution via the tail artery. Three hours later, we measured resting O2 consumption (VO2) by an open flow method and ventilation (VE) by the barometric method. Hemodilution to 80-90, 70-80, or 60-70% of the starting hematocrit and hemoglobin values had no major effects on VO2, VE, or mean arterial blood pressure (MAP). A 50-60% hemodilution reduced VO2 and MAP, with a modest increase in VE; the rats were hypocapnic, with normal PaO2. Infusion of vasopressin in a dosage sufficient to increase MAP to the basal value resulted in a reduction in VE, a further drop in VO2, and a return to normocapnia. Three days after hemodilution, hematocrit and hemoglobin were still low but ventilatory and metabolic parameters were normal. In conclusion, in this rat model of anemic hypoxia, 1) hypometabolism occurred without a drop in PaO2, implying that its manifestation does not require activation of the carotid body, and 2) the transient hypocapnia resulted from the VE stimulating effects of the hypotension.
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PMID:Metabolic and ventilatory responses to anemic hypoxia in conscious rats. 783 5

Near-infrared spectroscopy is a noninvasive bedside technique for monitoring hemoglobin saturation (HbO2%) in brain vasculature. The method linearly relates the optical signal detected from the surface of the head to HbO2%. To do so, the method relies on constant transcranial optical pathlength and light scattering as well as minimal interference by tissues overlying the brain. This study examined these premises. Optical signals from a dual-wavelength, near-infrared spectrometer were correlated with sagittal sinus HbO2% in 7 anesthetized piglets subjected to 7 different physiological conditions: normoxia, moderate and severe hypoxia, hyperoxia, hypocapnia, hypercapnic hyperoxia, and hypotension. These conditions were induced by varying the inspired O2 concentration (7-100%), ventilatory rate (5-35 breaths/min), and blood pressure (phlebotomy 20 ml/kg) to force HbO2% over a wide range (5-93%). To evaluate interference by tissues overlying the brain, correlations were repeated after the scalp and skull were rendered ischemic. Transcranial optical pathlength was measured by phase-modulated spectroscopy. Linear relationships between optical signals and sagittal sinus HbO2% were found with correlation coefficients ranging from -0.89 to -0.99 (p < 0.05) among animals; however, slope and intercept had coefficients of variability of approximately 15 and 333%, respectively. Almost identical linear expressions were observed whether scalp and skull were ischemic or perfused. Transcranial optical pathlength was constant in each animal, but ranged from 10 to 18 cm among animals. The data indicate that the assumptions underlying near infrared spectroscopy are reasonably accurate in a given animal, but that the constants for transcranial optical pathlength and light scattering are not the same in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Near-infrared monitoring of the cerebral circulation. 834 68

Near-infrared spectroscopy may allow continuous and noninvasive monitoring of regional brain hemoglobin oxygen saturation by measuring the differential absorption of infrared light by oxyhemoglobin and deoxyhemoglobin. We have previously examined the correlation between the spectroscopic signal generated by a prototype cerebral oximeter (Invos 3100; Somanetics, Troy, MI), and global brain hemoglobin oxygen saturation calculated from arterial and jugular venous bulb oxygen saturations. Because the technology does not distinguish between arterial and venous hemoglobin saturation, changes in the proportion of cerebral arterial and venous blood volume, which may result from changes in blood flow or venous distending pressure, may confound measurements. In eight conscious volunteers breathing hypoxic oxygen mixtures, we examined the influence of supine, 20 degrees Trendelenburg, and 20 degrees reverse Trendelenburg positions on the correlation of the spectroscopic measurement of cerebral oxygen saturation in the field assessed by the probe (CSfO2) and the calculated brain hemoglobin oxygen saturation (CScombO2), estimated as 0.25 x arterial saturation plus 0.75 x jugular venous bulb oxygen saturation. We found that changes in position did not influence the association between CSfO2 and CScombO2 (r2 = 0.69-0.885) during hypoxic challenge. In a second set of eight volunteers, we studied the influence of hypercapnia and hypocapnia and body position on the association between CSfO2 and CScombO2, and found that they were less well correlated (r2 = 0.366-0.976) in individual patients. Because changes in body position and Paco2 confound the relationship between CSfO2 and CScombO2, changes in CSfO2 can best be assessed if position and Paco2 are constant.
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PMID:The influence of carbon dioxide and body position on near-infrared spectroscopic assessment of cerebral hemoglobin oxygen saturation. 856 27

With the use of isolated perfused rabbit lungs (n = 152), roles of endothelium-derived relaxing factor (EDRF) in pulmonary vascular responses to hypocapnia and hypercapnia were studied. Lungs were ventilated with a gas mixture containing 1, 5, or 10% CO2 and 21% O2, adjusting the perfusate pH to 7.8, 7.4, or 7.1, respectively. Methemoglobin (MetHb), hemoglobin (Hb), methylene blue (MB), and L-argininosuccinic acid (L-ASA) were used as modulators of EDRF. To eliminate augmented shear stress, we used papaverine during hypercapnia. As a measure of EDRF, we spectrophotometrically examined nitric oxide (NO) metabolites in the perfusate. Hypocapnia and hypercapnia evoked, respectively, unsustainable vasodilatation and vasoconstriction. Hb, MB, and L-ASA, but not MetHb, produced an increase in baseline pulmonary arterial pressure (Ppa). These agents also exacerbated vasoconstriction during hypercapnia. Hypercapnia and hypocapnia caused an increase and decrease, respectively, in EDRF production. L-ASA suppressed EDRF production in hypercapnic lungs. Papaverine did not suppress EDRF production under hypercapnia. In conclusion, 1) the effects of pH on pulmonary circulation are transient, 2) the increase in Ppa caused by hypercapnia is modulated by EDRF, and 3) the pulmonary EDRF genesis is activated by hypercapnic acidosis but suppressed by hypocapnic alkalosis.
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PMID:Endothelial modulation of pH-dependent pressor response in isolated perfused rabbit lungs. 876 59

To evaluate the effect of prostagrandin E1 (PGE1)-induced hypotension on cerebral blood flow (CBF) and carbon dioxide (CO2) reactivity of CBF, regional cerebral hemoglobin oxygen saturation (rSo2) was measured in non-neurosurgical patients (n = 10) under sevoflurane-anesthesia using near infrared spectroscopy. PGE1 was infused intravenously to maintain arterial pressure at a level of about 75% of the MAP (hypotensive group) under sevoflurane-anesthesia alone (normotensive group). Ventilation was controlled to adjust PaCO2 to hypocapnia (25-30 mmHg), normocapnia (35-40 mmHg) and hypercapnia (45-50 mmHg) in both normotensive and hypotensive groups. rSo2 during hypotension did not change by hypocapnia and normocapnia, but significantly increased by hypercapnia, compared with rSo2 during normotension. Significant correlations between rSo2 and PaCO2 during both normotensive and hypotensive groups were observed. Slope of the regression line of rSo2 and PaCO2 did not differ between the normotensive and hypotensive groups. When arterial oxygen content and cerebral metabolic rate of oxygen are constant, changes in rSo2 correlate with those of CBF. Therefore, CBF and CO2 reactivity of CBF that indicates autoregulation in response to changes in CO2 during hypotension were maintained as those during normotension. The results show that PGE2-induced hypotension maintains CBF and CO2 reactivity well in non-neurosurgical patients under sevoflurane anesthesia.
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PMID:[Prostagrandin E1-induced hypotension well maintains cerebral circulation and carbon dioxide reactivity in non-neurosurgical patients under sevoflurane-anesthesia]. 907 Nov 2

Bright-field and dark-field illumination techniques for in vivo measurements of reduced pyridine nucleotide fluorescence were compared in 15 rats during periods of normocapnia, hypocapnia, hypercapnia, and anoxia. Parameters investigated included fluorescence, cortical reflectance, cortical blood flow, and electroencephalograms. In normal brain, with preserved autoregulation, reduced pyridine nucleotide fluorescence was constant through a wide range in Pa(CO2), cortical blood flow, and cerebral blood volume in animals studied using vertical illumination (bright-field) techniques. There was a marked increase in reduced pyridine nucleotide fluorescence at death from anoxia. Artifacts were reduced by monochromators for excitation, emission, and reflected light; low-intensity vertical excitation energy and high-sensitivity recording instrumentation; and a small avascular (123 microns) field. Potential sources of error include photodecomposition, hemoglobin interference from absorption and reflectance, and light scattering. Vertical excitation techniques using a small field appeared to give more reliable and reproducible results than circumferential techniques using a larger field of observation.
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PMID:Comparison of dark-field and bright-field incident illumination for in vivo measurements of reduced pyridine nucleotides. 976 36

We tested whether the leftward shift of the oxygen dissociation curve of hemoglobin with hyperpnea delays the oxygen uptake (VO(2)) response to the onset of exercise. Six male subjects performed cycle ergometer exercise at a work rate corresponding to 80% of the ventilatory threshold (VT) VO(2) of each individual after 3 min of 20-W cycling under eupnea [control (Con) trial]. A hyperpnea procedure (minute ventilation = 60 l/min) was undertaken for 2 min before and during 80% VT exercise in hypocapnia (Hypo) and normocapnia (Normo) trials. In the Normo trial, the inspired CO(2) fraction was 3% to prevent hypocapnia. The subjects completed two repetitions of each trial. To determine the kinetic variables of VO(2) and heart rate (HR) at the onset of exercise, a nonlinear least-squares fitting was applied to the data averaged from two repetitions by a monoexponential model. The end-tidal CO(2) partial pressure before the onset of exercise was significantly lower in the Hypo trial than in the Con and Normo trials (22 +/- 1 vs. 38 +/- 3 and 36 +/- 1 mmHg, respectively, P < 0.05). The time constant of VO(2) and HR was significantly longer in the Normo trial (28 +/- 7 and 39 +/- 18 s, respectively) than in the Con trial (21 +/- 7, 34 +/- 16 s, respectively, P < 0.05). The VO(2) time constant of the Hypo trial (37 +/- 12 s) was significantly longer than that of the Normo trial, although no significant difference in the HR time constant was seen (Hypo, 41 +/- 28 s). These findings suggested that respiratory alkalosis delayed the kinetics of oxygen diffusion in active muscle as a result of the leftward shift of the oxygen dissociation curve of hemoglobin. This supports an important role for hemoglobin-O(2) offloading in setting the VO(2) kinetics at exercise onset.
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PMID:Impeding O(2) unloading in muscle delays oxygen uptake response to exercise onset in humans. 1056 97

The effect of transfusing a nonextravasating, zero-link polymer of cell-free hemoglobin on pial arteriolar diameter, cerebral blood flow (CBF), and O2 transport (CBF x arterial O2 content) was compared with that of transfusing an albumin solution at equivalent reductions in hematocrit (approximately 19%) in anesthetized cats. The influence of viscosity was assessed by coinfusion of a high-viscosity solution of polyvinylpyrrolidone (PVP), which increased plasma viscosity two- to threefold. Exchange transfusion of a 5% albumin solution resulted in pial arteriolar dilation, increased CBF, and unchanged O2 transport, whereas there were no significant changes over time in a control group. Exchange transfusion of a 12% polymeric hemoglobin solution resulted in pial arteriolar constriction and unchanged CBF and O2 transport. Coinfusion of PVP with albumin produced pial arteriolar dilation that was similar to that obtained with transfusion of albumin alone. In contrast, coinfusion of PVP with hemoglobin converted the constrictor response to a dilator response that prevented a decrease in CBF. Pial arteriolar dilation to hypercapnia was unimpaired in groups transfused with albumin or hemoglobin alone but was attenuated in the largest vessels in albumin and hemoglobin groups coinfused with PVP. Unexpectedly, hypocapnic vasoconstriction was blunted in all groups after transfusion of albumin or hemoglobin alone or with PVP. We conclude that 1) the increase in arteriolar diameter after albumin transfusion represents a compensatory response that prevents decreased O2 transport at reduced O2-carrying capacity, 2) the decrease in diameter associated with near-normal O2-carrying capacity after cell-free polymeric hemoglobin transfusion represents a compensatory mechanism that prevents increased O2 transport at reduced blood viscosity, 3) pial arterioles are capable of dilating to an increase in plasma viscosity when hemoglobin is present in the plasma, 4) decreasing hematocrit does not impair pial arteriolar dilation to hypercapnia unless plasma viscosity is increased, and 5) pial arteriolar constriction to hypocapnia is impaired at reduced hematocrit independently of O2-carrying capacity.
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PMID:Cerebrovascular response to decreased hematocrit: effect of cell-free hemoglobin, plasma viscosity, and CO2. 1281 46

Microcirculatory changes in the window chamber preparation in Syrian golden hamsters, secondary to chronic hypoxia adaptation, are presented herein. Adaptation was attained by keeping animals in a 10% oxygen environment for 1 wk and 5% the following week. The following groups were studied: group 1, adapted to chronic hypoxia and kept in a 5% oxygen environment throughout the experiment; group 2, adapted to chronic hypoxia and kept in a 21% oxygen environment 24 h before and during the experiment; and group 3, control. Adaptation caused venule enlargement and hematocrit increase (68.6 +/- 2.44 in group 1, 70 +/- 2.66 in group 2, and 43.27 +/- 2.30 in group 3; P < 0.05). Whereas heart rate decreased in adapted animals, blood pressure remained constant. Group 1 presented alkalosis, hypocapnia, and hypoxemia. The adapted groups had decreased blood flow velocity in arterioles and veins. We found no difference in microvasculature oxygen tension between groups 2 and 3; however, the number of capillaries with flow was markedly reduced in group 1 but significantly increased in group 2. Our findings suggest that, as an adaptation to hypoxia, erythropoiesis may prove beneficial by increasing blood viscosity and shear stress, leading to vasodilatation, in addition to the increase in oxygen-carrying capacity. Calculations show that oxygen extraction in the tissue of the window chamber model was significantly lowered in adapted animals breathing 5% oxygen, but was unchanged from the control when breathing 21% oxygen, even though blood hemoglobin content was increased from 14.5 +/- 0.07 g/dl at control to 21.04 +/- 1.24 g/dl in the adapted animals (P < 0.05).
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PMID:Microcirculatory changes during chronic adaptation to hypoxia. 1456 80

We composed a model, combining oxygen transport system from blood to tissue with the oxygen consumption system at the tissue. The aim of this study is to apply it to the brain tissue under conditions when two or more oxygen transport parameters are affected simultaneously. The following values were assumed. Critical tissue P(O)(2) (Pcrit(O)(2)) 2 mmHg; oxygen consumption above this level 3 ml.min(-1).100 g(-1); diffusion coefficient from blood vessel to tissue (Dvt) 0.2 ml.min(-1).mmHg(-1).100 g(-1); cerebral bloow flow (CBF) 50 ml.min(-1).100 g(-1); hemoglobin 15 g.100 ml(-1). The Hill equation was used for oxygen dissociation curve with n of 2.7 and P(50) of 27.0 mmHg. The changes of oxygen consumption of the brain (V(O)(2)) were analyzed when 2 or more of 5 parameters, Pa(O)(2), CBF, Dvt, P(50) and hemoglobin decreased simultaneously from their respective normal values. As the number of parameters affected increased, the level at which oxygen consumption begins to be affected became higher. With all five parameters combined, a reduction down to 78 per cent of normal resulted in tissue hypoxia. We conclude that the oxygen consumption of the brain is fairly resistant when only one parameter is affected, but it becomes increasingly vulnerable when several parameters are affected simultaneously. A clinically important finding is that the brain is particularly vulnerable to a combination of hypocapnia and a decreased level of 2,3DPG.
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PMID:Analysis of oxygen transport to the brain when two or more parameters are affected simultaneously. 1527 41


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