UMLS:C0432222 - FACTA Search

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Query: UMLS:C0432222 (SEM)
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The pulmonary artery pressure (Ppa) responses to short runs of acute hypoxia at two different levels of end-tidal CO2 were measured in nine normal subjects and in 20 patients with moderate to severe obstructive sleep apnea (OSA). In normal subjects the mean increase in Ppa in response to eucapnic hypoxia was 8 +/- 2 mm Hg (SEM) and was not different from the response to hypercapnic hypoxia (9 +/- 2 mm Hg, p > 0.2). In patients with OSA, the mean increase of Ppa was 8 +/- 1 mm Hg to eucapnic hypoxia, and the response to hypercapnic hypoxia was higher at 10 +/- 1 mm Hg (p = 0.01). Pulmonary pressor response to hypoxia was augmented (> 10 mm Hg) by hypercapnia in four of 20 patients with OSA but in none of the normal subjects. Normoxic hypercapnia alone was a weak stimulus, increasing Ppa by > 5 mm Hg in only two of nine patients with OSA studied. In conclusion, Ppa increases in both normal subjects and patients with OSA exposed to a ramp of acute isocapnic hypoxia. There were clear interindividual differences in pulmonary artery response. Hypercapnia did not produce clinical significant changes in Ppa in either group.
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PMID:Pulmonary artery pressure response to hypoxia in sleep apnea. 900 11

We examined the role of respiratory control during O2-induced hypercarbia in patients with chronic obstructive pulmonary disease (COPD), by comparing the observed change in ventilation (delta VEobs) with the delta VE predicted (delta VEpred) from the patients' ventilatory drive and the O2-induced delta PaCO2 and delta SaO2. Eleven stable hypoxemic COPD patients (mean +/- SD: FEV1 = 1.00 +/- 0.25 L, FVC = 2.33 +/- 0.38 L; room air PaCO2 = 52.7 +/- 7.9 mm Hg, SaO2 87.7 +/- 5.1%) were studied. Using standard rebreathing methods, we measured the ventilatory responses to hypercapnia (delta VE/PCO2 = 0.76 +/- 0.55 L/min/mm Hg) and to hypoxia (delta VE/delta SaO2 = -0.74 +/- 0.31 L/min/%). After breathing 100% O2 for 15 min, the mean delta VEobs was -0.08 +/- 0.62 (SEM) L/min (p = NS), the delta SaO2 was 7.6 +/- 3.6% (p < 0.001), and the delta PaCO2 was 6.6 +/- 3.3 mm Hg (p < 0.001). The delta VEpred was expressed as the sum of a decrease in ventilation due to suppression of hypoxic drive [calculated as the product (delta VE/SaO2) x delta SaO2] and an increase in ventilation due to the O2-induced hypercarbia [calculated as the production (delta VE/delta PCO2) x delta PaCO2]. The mean delta VEpred [-0.96 +/- 0.68 (SEM)] did not differ significantly from mean delta VEobs. We conclude that the O2-induced delta VEobs is equal to that expected from the ventilatory drives and the changes in PaCO2 and SaO2; and that O2-induced hypercarbia does not indicate a failure of respiratory control mechanisms in the maintenance of PaCO2 homeostasis.
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PMID:O2-induced change in ventilation and ventilatory drive in COPD. 903 2

The fetoscopic approach to fetal intervention is a promising minimally invasive technique for correcting congenital anomalies in utero. However, expansion of the amniotic cavity with CO2 to visualize the fetus causes fetal hypercarbia and acidosis. We assessed whether maternal hyperventilation during intrauterine CO2 insufflation could attenuate the fetal hypercarbic acidosis. Seven fetal lambs of 105 +/- 2 days (mean +/- SEM) gestation (term = 145 days) were instrumented with a carotid arterial catheter in utero. After 7 +/- 1 days of recovery, fetoscopic exposure was obtained with intrauterine insufflation of CO2 at 10 mmHg of intraamniotic pressure. After 30 min, the ewe was hyperventilated at a mean respiratory rate of 23/min for 30 min under continuous insufflation. The uterus was then deflated and following 1 hr of stabilization, and the same protocol of CO2 pneumometrium was repeated. Fetal and maternal arterial blood was sampled at baseline and at 15 min intervals. Fetal PaCO2 increased during 30 min of CO2 insufflation (50.8 +/- 2.8 vs. 72.3 +/- 5.0 mmHg, P < 0.01); however, this change was reversed (to 51.5 +/- 3.0 mmHg, P < 0.01) by 30 min of maternal hyperventilation. The fetus developed acidosis after 30 min of CO2 pneumometrium (pH 7.350 +/- 0.012 vs. 7.236 +/- 0.026, P < 0.01); this was also reversed (to 7.366 +/- 0.019, P < 0.01) by maternal hyperventilation. These results were reproducible during the second CO2 insufflation challenge. Fetal hypercarbic acidosis during fetoscopy with CO2 insufflation is reduced by maternal hyperventilation.
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PMID:Reducing the deleterious effects of intrauterine CO2 during fetoscopic surgery. 920 46

The aim of the study was to evaluate whether the Heidelberg retina flowmeter (HRF), a new device for retinal and anterior optic nerve blood flow assessment, can gauge, at least semiquantitatively, a known effect such as an increase in optic nerve blood flow by hypercapnia or a decrease in optic nerve blood flow by hyperoxia or high intraocular pressure (IOP). Measurements with the HRF were obtained at the papilla of three groups of 5 young healthy subjects (1) at baseline and after breathing 5% carbogen, (2) at baseline and after breathing 100% oxygen and (3) at baseline and after increasing IOP to 20 and 50 mm Hg. The changes in the value of the HRF parameter 'flow' were analyzed by means of a paired Student's t test. Breathing 100% oxygen for 7 min resulted in a statistically significant decrease of 34.7+/-2.5% (mean+/-SEM) in HR parameter 'flow' (p < 0.01) at the papilla. Breathing 5% carbogen for 7 min resulted in a statistically significant increase of 18.3+/-2.6% in HRF parameter 'flow' (p = 0.024). Increasing IOP to 20 mm Hg did not result in a statistically significant change in HRF parameter 'flow' (-9.6+/-7.4%; p = 0.13). Increasing IOP from 20 to 50 mm Hg, however, resulted in a statistically significant decrease of 40.1+/-6.6% in HRF parameter 'flow' (p = 0.003). With the applied stimuli, the HRF parameter 'flow' changed in the expected direction, i.e. an increase with hypercapnia and a decrease with hyperoxia or high IOP. The simplicity of use of the HRF instrument suggests that it might be well suited for a non-invasive, at least semiquantitative, assessment of changes in blood flow at the papilla.
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PMID:Effect of carbogen, oxygen and intraocular pressure on Heidelberg retina flowmeter parameter 'flow' measured at the papilla. 956 85

We investigated whether blood flow determined by a flow probe situated on one common carotid artery provided an accurate estimation of unilateral cerebral blood flow (CBF) in piglets. In eight anesthetized, mechanically ventilated piglets, blood flow determined by an ultrasonic flow probe placed on the right common carotid artery was correlated with CBF determined by microspheres under two experimental conditions: 1) before ligation of the right external carotid artery with both the right external and internal carotid circulations intact [common carotid artery blood flow (CCABF) condition], and 2) after ligation of the right external carotid artery (ipsilateral to the flow probe) with all residual right-sided carotid artery blood flow directed through the right internal carotid artery [internal carotid artery blood flow (ICABF) condition]. The left carotid artery was not manipulated in any way in either protocol. Independent correlations of unilateral CCABF and ICABF with microsphere-determined unilateral CBF were highly significant over a 5-fold range of CBF induced by hypercarbia or hypoxia (r = 0.94 and 0.92, respectively; both p < 0.001). The slope of the correlation of unilateral CCABF versus unilateral CBF was 1.68 +/- 0.19 (SEM), suggesting that CCABF overestimated CBF by 68%. The slope of the correlation of unilateral ICABF versus unilateral CBF did not differ significantly from unity (1.06 +/- 0.15), and the y intercept did not differ significantly from zero [-1.3 +/- 5.2 (SEM) mL]. Consequently, unilateral ICABF determined by flow probe accurately reflected unilateral CBF determined by microspheres under these conditions. Flow probe assessments of CCABF and ICABF in piglets may provide information about dynamic aspects of vascular control in the cerebral circulation that has heretofore been unavailable.
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PMID:Correlation of flow probe determinations of common carotid artery blood flow and internal carotid artery blood flow with microsphere determinations of cerebral blood flow in piglets. 1008 49

Before and 7-12 days after an Himalayan expedition CO2 equilibration curves were determined in the blood plasma of 12 mountaineers by in vitro and in vivo CO2 titration; in vivo osmolality changes (delta Osm x deltaPCO2(-1), deltaOsm x delta pH(-1), where PCO2 is the partial pressure of CO2) during the latter experiments yielded estimates of whole body CO2 storage. In vitro -delta[HCO3-] x delta pH(-1) [nonbicarbonate buffer capacity (beta) of blood] was increased 7 days after descent [before 31.3 (SEM 0.4) mmol x kgH2O(-1), after 38.3 (SEM 3.9) mmol x kgH2O(-1); P<0.05] resulting from an increased proportion of young erythrocytes; in additional experiments an augmented beta was found in young (low density cells) compared to old cells [<1.097 g x ml(-1): 0.216 (SEM 0.028) mmol x gHb(-1), >1.100 g x ml(-1): 0.145 (SEM 0.013) mmol x gHb(-1), where Hb is haemoglobin; P < 0.02]. In spite of increased Hb mass in vivo delta[CO2total] x deltaPCO2(-1) [0.192 (SEM 0.010) mmol x kgH2O(-1) x mmHg(-1)] and -delta[HCO3-] x delta pH(-1) [17.9 (SEM 1.0) mmol x kgH2O(-1)] as indicators of extracellular beta rose only slightly after altitude (7 days +16%, P<0.02; +7%, NS) because of haemodilution. The deltaOsm x deltaPCO2(-1) [0.230 (SEM 0.015) mosmol x kgH2O(-1) x mmHg(-1)] remained unchanged. Prealtitude differences in deltaOsm x delta pH(-1) between hypercapnia [-41 (SEM 5) mosmol x kgH2O(-1)] and hypocapnia [-20 (SEM 3) mosmol x kgH2O(-1); P<0.01] disappeared temporarily after return since the former slope was reduced. The high value during hypercapnia before ascent probably resulted from mechanisms stabilizing intracellular pH during moderate hypercapnia which were attenuated after descent.
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PMID:Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition. 1020 56

Cerebrovascular reactivity is severely affected by ischemia, and changes in vascular responses have been reported after cortical spreading depression and head trauma as well. Cortical depolarization (CD) occurs during ischemia, cortical spreading depression, and head trauma, but its effects on cerebrovascular reactivity are unclear. We tested the hypothesis that CD induced by KCl diminishes the vascular responsiveness to various vasodilatory stimuli in piglets. Responses of pial arterioles were determined by changes in vascular diameter by use of a closed cranial window and intravital microscopy. Baseline arteriolar diameters were 105 +/- 3 microm (mean +/- SEM, n = 27). CD was elicited by topical administration of 1 mol/L KCl for 3 min. Vascular responses were measured before and 1 h after CD. KCl elicited CD and constricted arterioles by 54 +/- 4% (n = 27). N-methyl-D-aspartate induced dose-dependent vasodilation that was unaffected by CD; the percent changes were 9 +/- 1 versus 8 +/- 1 (before and after CD) at 10(-5) mol/L, 19 +/- 2 versus 18 +/- 3 at 5 x 10(-5) mol/L, and 29 +/- 2 versus 26 +/- 3 at 10(-4) mol/L (n = 9). Hypercapnic vasodilation was not diminished by CD; the percent changes were 15 +/- 2 versus 16 +/- 4 at 5%, and 27 +/- 5 versus 27 +/- 6 at 10% inspired CO2 (n = 8). Aprikalim and forskolin caused dilation that was also resistant to prior CD; the percent change values were 21 +/- 4 versus 18 +/- 3 and 16 +/- 2 versus 16 +/- 4 at 10(-6) mol/L, 36 +/- 5 versus 34 +/- 5 and 34 +/- 7 versus 37 +/- 7 at 10(-5) mol/L (n = 8), respectively. Finally, calcitonin gene-related peptide-induced vasodilation was unaffected by CD; percent changes were 15 +/- 3 versus 16 +/- 2 at 10(-7) mol/L and 26 +/- 4 versus 22 +/- 3 at 10(-6) mol/L (n = 8). The intact vascular responses after CD suggest that this component is not responsible for decreased cerebrovascular reactivity after ischemia, head trauma, or cortical spreading depression.
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PMID:Cerebrovascular reactivity remains intact after cortical depolarization in newborn piglets. 1036 74

We have determined the influence of 0.1 minimum alveolar concentration (MAC) of sevoflurane on ventilation, the acute ventilatory response to a step change in end-tidal carbon dioxide and the ventilatory response to sustained hypercapnia in 10 healthy adult volunteers. Subjects undertook a preliminary 10-min period of breathing air without sevoflurane to determine their normal ventilation and natural end-tidal PCO2. This 10-min period was repeated while breathing 0.1 MAC of sevoflurane. Subjects then undertook two procedures: end-tidal PO2 was maintained at 13.3 kPa and end-tidal PCO2 at 1.3 kPa above the subject's normal value for 30 min of data collection, first with and then without 0.1 MAC of sevoflurane. A dynamic end-tidal forcing system was used to generate these gas profiles. Sevoflurane did not significantly change ventilation: 10.1 (SEM 1.0) litre min-1 without sevoflurane, 9.6 (0.9) litre min-1 with sevoflurane. The response to acute hypercapnia was also unchanged: mean carbon dioxide response slopes were 20.2 (2.7) litre min-1 kPa-1 without sevoflurane and 18.8 (2.7) litre min-1 kPa-1 with sevoflurane. Sustained hypercapnia caused a significant gradual increase in ventilation and tidal volume over time and significant gradual reduction in inspiratory and expiratory times. Sevoflurane did not affect these trends during sustained hypercapnia. These results suggest that 0.1 MAC of sevoflurane does not significantly affect the acute ventilatory response to hypercapnia and does not modify the progressive changes in ventilation and pattern of breathing that occur with sustained hypercapnia.
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PMID:Effects of subanaesthetic sevoflurane on ventilation. 1: Response to acute and sustained hypercapnia in humans. 1061 28

1. Exogenously administered endothelin (ET) modulates the activity of cardiovascular and respiratory neurons in the central nervous system (CNS) and, thus, affects arterial blood pressure (ABP) and ventilation. However, a physiological role(s) for endogenous ET in the CNS has not been elucidated. To address this question, we examined ABP and ventilation in mutant mice deficient in ET-1, ETA and ETB receptors and endothelin-converting enzyme-1, which were made by gene targeting. 2. Respiratory frequency and volume was measured in mice by whole body plethysmography when animals breathed normal room air and hypoxic and hypercapnic gas mixtures. A few days after respiratory measurements, a catheter was implanted into the femoral artery under halothane anaesthesia. On the following day, the ABP of awake mice was measured through the indwelling catheter and heart rate was calculated from the ABP signal. After 2 h ABP measurement, arterial blood was collected through the catheter and pH and the partial pressures of O2 and CO2 were measured by a blood gas analyser. 3. Compared with corresponding controls, the mean (+/- SEM) ABP in ET-1+/- and ETB-deficient mice was significantly higher (118 +/- 2 vs 106 +/- 3 mmHg for ET-1+/- (n = 22) and ET-1+/+ (n = 17) mice, respectively; 127 +/- 3 vs 109 +/- 4 mmHg for ETB-/s (n = 9) and ETB+/s (n = 9) mice, respectively; P < 0.05 for both). In ET-1+/- mice, PCO2 tended to be higher and PO2 was significantly lower than corresponding values in ET-1+/+ mice. Under resting conditions, there was no significant difference in respiratory parameters between mutants and their corresponding controls. However, reflex increases of ventilation to hypoxia and hypercapnia were significantly attenuated in ET-1+/-, ET-1-/- and ETA-/- mice. 4. In another series of experiments in ET-1+/- mice, we found that sympathetic nerve activity (SNA) was augmented and reflex excitation of phrenic nerve activity (PNA) in response to hypoxia and hypercapnia was blunted. Attenuation of the reflex PNA response to hypercapnia was also observed in the medulla-spinal cord preparation from ET-1-/- mice. 5. Elevation of ABP in ETB-deficient mice was most likely due to a peripheral mechanism, because SNA and respiratory reflexes were not different from those in control animals. 6. We conclude that endogenous ET-1 plays an important role in the central neural control of circulation and respiration and that ETA receptors mediate this mechanism.
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PMID:Endothelin in the central control of cardiovascular and respiratory functions. 1062 68

It has been demonstrated previously that isohydric hypercapnia (IH) does not affect agonist-induced tension development in pulmonary arteries. The aim of the present study was to examine the effects of IH on depolarisation-induced, steady state tension in the isolated rat pulmonary artery. Rings were submaximally contracted with high KCl under control conditions (5% CO(2)-95% air). IH was achieved by switching to a modified PSS (isosmotic substitution of NaHCO(3) for NaCl), equilibrated with 10% CO(2) in air. On switching to IH, a significant increase in mean (+/-SEM) tension (25.3+/-6.3% Tmax) was observed in endothelium intact rings (n=6). Endothelial removal significantly reduced this response. Non-specific inhibition of nitric oxide synthase (NOS) isoenzymes (L-NAME, 10(-3) M) abolished the IH-induced increase in tension while inhibition of neuronal NOS (TRIM, 10(-5) M) was without effect. The relaxant response to the nitric oxide donor sodium nitroprusside was similar in IH and control conditions. These results suggest that IH caused an endothelium-dependent increase in depolarisation-induced tension by reducing NO production.
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PMID:Hypercapnia-induced contraction in isolated pulmonary arteries is endothelium-dependent. 1085 24

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