Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of a stepwise decrease in PaCO2 from 3.9-1.6 kPa on rCBF, rCMRO2, tissue PO2 and concentrations of glucose, lactate, pyruvate, ATP, ADP, AMP and phosphocreatine in the brain cortex was studied in cats lightly anaesthetized with sodium pentobarbital. 1. Moderate lowering of PaCO2 to 2.5 kPa induced in all animals a homogeneous decrease of rCBF in corresponding areas of the right and left hemisphere. Mean rCBF fell from 129.2 to 103.1 ml X 100 g-1 X min-1, while rCMRO2 remained unchanged (12.7-12.9 ml X 100 g-1 X min-1). The tissue PO2 frequency histograms showed a shift to lower values without indicating the presence of brain tissue hypoxia. 2. Severe arterial hypocapnia (PaCO2 = 1.6 kPa) caused an inhomogeneous blood flow reaction. Both further decreased as well as increased rCBF values were measured simultaneously in the brain cortex of individual animals (mean rCBF = 97.6 ml X 100 g-1 X min-1). At the same time tissue PO2 measurements and metabolite assays indicated the presence of pronounced brain tissue hypoxia. The tissue concentrations of lactate and pyruvate and the lactate/pyruvate ratio were significantly increased, while the phosphocreatine concentration was significantly reduced. In addition, rCMRO2 decreased to 11.3 ml X 100 g-1 X min-1. The results provide conclusive evidence that severe arterial hypocapnia leads to an insufficient O2 supply of the brain cortex, which in turn seems to counteract the influence of hypocapnia on cortical blood flow regulation.
Pflugers Arch 1981 Sep
PMID:Effects of severe arterial hypocapnia on regional blood flow regulation, tissue PO2 and metabolism in the brain cortex of cats. 681 15

The influence of respired gas density on ventilatory control during cycle-ergometer exercise was investigated in six healthy subjects. They underwent constant-load exercise for 10 min both at 50% and 90% of the anaerobic threshold, inhaling air for the first 5 min followed abruptly by 80% helium-20% oxygen (He-O2) for the remaining 5 min (and vice versa). The He-O2 breathing elicited no discernible effect on ventilation (VI) or mean alveolar PCO2 (PACO2) at rest or at the lower work rate. However, at the higher work rate, He-O2 breathing resulted in a clear and sustained hyperventilation in all subjects. A compensatory response to the hypocapnia, consequent to the helium-induced hyperventilation, was not evident even though all subjects demonstrated a normal ventilatory responsiveness to inhaled CO2 while in this condition. These observations suggest that turbulent airflow normally imposes a constraint on the magnitude of the hyperpnea of high-intensity exercise.
Respir Physiol 1982 Sep
PMID:Density-dependent airflow and ventilatory control during exercise. 681 52

Changes in cerebral blood volume (CBV) after head injury may be an important determinant of intracranial pressure (ICP). To determine the normal response of CBV to hypoxemia, hypercapnia, and hypocapnia, eight normal subjects (5 males and 3 females; ages 25 to 43) were studied under these conditions. Cerebral blood volume was measured using an external collimated gamma detector to determine 99m-Tc-labeled red blood cell (RBC) activity in the intracranial vascular pool, and cerebral blood flow (CBF) was determined by internal carotid artery duplex scanning. Hypocapnia (Paco2 = 26.0 +/- 1.7 mm Hg, mean +/- SE) was achieved by hyperventilation, hypercapnia (Paco2 = 47.8 +/- 1.5 mm Hg) was achieved by inhalation of 6% CO2, and hypoxemia (Pao2 = 38.1 +/- 1.1 mm Hg, O2 saturation = 76.7 +/- 2.0%) was achieved by inhalation of 10% O2. Changes in CBF and CBV were determined by comparing the values in each condition to the immediately preceding period of normoxia and normocapnia. For conditions of hypocapnia, hypercapnia, and hypoxemia, the percentage of change in CBV was: -7.2 +/- 0.01, 12.8 +/- 0.01, and 5.2 +/- 0.03, respectively. The simultaneous percentage of change in CBF for the same conditions was -30.7 +/- 4.0, 29.5 +/- 9.2, and 18.4 +/- 6.9, respectively. For all conditions, changes in CBF were greater than changes in CBV; however, this was most pronounced during hypocapnia induced by hyperventilation. Because the change in CBV reflects the potential change in ICP in response to treatment, therapeutic hyperventilation may impair CBF to a greater degree than it reduces ICP.(ABSTRACT TRUNCATED AT 250 WORDS)
J Trauma 1995 Sep
PMID:Cerebral blood flow and blood volume in response to O2 and CO2 changes in normal humans. 747 10

Glutamate (GLU) is a neurotransmitter. Massive release of GLU and glycine (GLY) into the brain's extracellular space may be triggered by ischemia, and may result in acute neuronal lysis or delayed neuronal death. The aim of this study was to evaluate the possible relationship between hyperventilation and the level of GLU and GLY during brain ischemia. Rabbits were anesthetized with halothane and oxygen. Group 1 was allowed to hyperventilate (PaCO2 25-35 mmHg). PaCO2 was maintained throughout the study. Group 2 was a normal control group that maintained normocapnia. Two global cerebral ischemic episodes were produced. Microdialysate was collected during the periischemic and reperfusion periods from the dorsal hippocampus. GLU and GLY concentrations were determined using high-performance liquid chromatography. In the control group, GLU and GLY were significantly elevated during each episode of ischemia; these levels returned to baseline within 10 minutes after reperfusion. In contrast, in the hyperventilation group GLU and GLY concentrations increased during ischemia, but they were not statistically significant. Two way ANOVA for the periischemic periods (t = 15,80; p = 0.06) revealed lower GLU values for the hyperventilated animals. A similar analysis for periischemic GLY concentrations revealed significantly lower values in the hyperventilated group (t = 10,15,75,80: p = 0.03) as compared to normal controls. We were able to demonstrate that hypocapnia during periischemic period lowered extracellular GLU and GLY concentrations. These results can explain a part of the protective action of hypocapnia during cerebral ischemia.
Ann N Y Acad Sci 1995 Sep 15
PMID:Effect of hypocapnia on extracellular glutamate and glycine concentrations during the periischemic period in rabbit hippocampus. 748 47

We have investigated the maximum tolerance and the ventilatory responses of a bat, P. poliocephalus (PP), to normobaric hypoxic stress. PP can tolerate inspired PO2s (PiO2) down to 30 torr. This bat is one of the most hypoxia-tolerant non-hibernating species of mammals known, and has a tolerance which lies within the range of PiO2s reported for different birds. Unlike most mammals in its size range, PP maintains its normoxic oxygen consumption rate even in deep hypoxia. The maximum hypoxic ventilatory response (HVR), the air convection requirement (Vi/MO2), and the lung oxygen extraction (EL) ability of PP in deep hypoxia are all greater than those of other mammals. These and other data indicate that PP has a superior mammalian tolerance for hypocapnia. The magnitudes of both the V1/MO2 and the EL value of PP fall between those reported for Pekin ducks at corresponding PiO2s, and are inferior to the maximum capabilities of bar-headed geese. Thus, the tolerance and ventilatory adjustments of PP to deep hypoxia are intermediate between those of typical non-flying mammals and the most tolerant avian species, and suggest that at least some of this bat's respiratory adaptations for flight may serve as preadaptations for withstanding acute hypoxic stress.
Comp Biochem Physiol A Physiol 1995 Sep
PMID:Metabolic and ventilatory adjustments and tolerance of the bat Pteropus poliocephalus to acute hypoxic stress. 755 35

CO2 cerebrovascular reactivity has been recorded in 12 healthy volunteers and 10 patients with unilateral > 70% extracranial internal carotid artery (ICA) stenosis, using non invasive techniques. The relative changes of middle cerebral artery blood flow velocity (VMCA) and velocity waveform pulsatility (PIMCA) after that hypocapnia was induced by spontaneous hyperventilation were recorded. 35.5% average VMCA reduction and 63% PIMCA increment of basal values was produced in healthy subjects after hyperventilation. The percentage variation of CO2 Reactivity Index (RI), expressed in terms of VMCA (V-RI) and PIMCA (PI-RI), per mmHg change in pCO2, presents a good right-left side correlation (r = 0.82 and r = 0.83 respectively) in healthy subjects, while a dissociation between V-RI and PI-RI was found in our patients. A significant reduction of PI-RI was also recorded in the group of patients on the side of ICA stenosis. From our data CO2 reactivity index recorded in terms of PI seems to allow a better separation between pathology and normality, without the need to assume a close relationship between velocity and blood flow under the condition considered. Furthermore, PI-RI seems to be a valid index in the evaluation of some attribute pertaining to the distal vascular bed.
J Neurosurg Sci 1994 Sep
PMID:Non invasive recording of CO2 cerebrovascular reactivity in normal subjects and patients with unilateral internal carotid artery stenosis. 778 59

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.
J Appl Physiol (1985) 1994 Sep
PMID:Metabolic and ventilatory responses to anemic hypoxia in conscious rats. 783 5

A whole body plethysmograph was used to determine the minute ventilation-to-CO2 production ratio (VE/VCO2) of intact unrestrained unanesthetized adult male Sprague-Dawley rats during 7 days of hypoxemia (arterial PO2 approximately 50 Torr). In one set of rats, normocapnia (arterial PCO2 approximately 40 Torr) was maintained. Arterial blood gases and acid-base status were determined, and arterial PCO2 was used to calculate alveolar ventilation-to-VCO2 ratio (VA/VCO2) in all situations when inhaled CO2 was not elevated. In normoxia VE/VCO2 = 25 +/- 1 (mean +/- 95% confidence limits); after 12 h of hypoxemia, VE/VCO2 was maximal, 61 +/- 5 in hypoxemic hypocapnia and 200 +/- 55 in hypoxemic normocapnia. Between 2 and 7 days of hypoxemia, VE/VCO2 had plateaued, 42 +/- 3 in hypoxemic hypocapnia and 95 +/- 19 in hypoxemic normocapnia. Dead space-to-tidal volume ratio (VD/VT) = (VE/VCO2 - VA/VCO2)/(VE/VCO2), and in normoxia VD/VT = 0.17 +/- 0.04. In hypoxemic hypocapnia, VD/VT measured between 1 and 5 h was 0.38 +/- 0.04. It remained elevated at 0.29 +/- 0.04 after 24 h, but after 4-7 days in hypoxemic hypocapnia, VD/VT had recovered to 0.15 +/- 0.03. It is postulated that the disproportionate increase in VE/VCO2 observed during the first 24 h of exposure to hypoxemic normocapnia (compared with elevated steady-state plateau levels maintained from 2 to 7 days sojourn) reflects an immediate transient increase of physiological dead space on exposure to hypoxemia.
J Appl Physiol (1985) 1994 Sep
PMID:Physiological dead space increases during initial hours of chronic hypoxemia with or without hypocapnia. 783 60

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.
Am J Physiol 1994 Sep
PMID:Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. 809 53

To understand the interplay between microcirculatory control and carotid body (CB) function, we simultaneously measured carotid body microvascular PO2 (CBM PO2) and chemosensory activity in the cat in vivo under several experimental conditions. Cats were anesthetized with pentobarbital sodium, paralyzed, and artificially ventilated. CBs were exposed, and steady-state CBM PO2 was measured by the O2-dependent quenching of the phosphorescence of Pd-meso-tetra-(4-carboxyphenyl)porphine, which was administered intravenously. A few fibers of the carotid sinus nerve were used to record chemosensory discharges. At arterial PO2 (PaO2) of 103.4 +/- 4.1 Torr, CBM PO2 was 52.5 +/- 3.6 Torr (n = 9). Graded lowering of PaO2 from 160 to 50 Torr resulted in nearly proportional decreases in CBM PO2, but at lower PaO2 the decrease in CBM PO2 became more substantial. As PaO2 decreased, chemosensory discharge increased in parallel with CBM PO2. Hypercapnia and hypocapnia did not significantly change the relationship between PaO2 and CBM PO2, although the chemosensory discharge responded significantly. CBM PO2 and chemosensory discharge were not affected by hemorrhagic hypotension until arterial blood pressure fell below approximately 50 Torr and then CBM PO2 decreased and chemosensory discharge increased. The lack of a significant effect of hemorrhagic hypotension indicated that O2 delivery to CB was almost independent of the systemic blood pressure. Taken together, the observations suggest that CB microcirculation and PO2 are subject to control by intrinsic mechanisms and that CBM PO2 is compatible with oxidative metabolism playing a role in O2 chemoreception during hypoxia.
J Appl Physiol (1985) 1993 Sep
PMID:Contribution of in vivo microvascular PO2 in the cat carotid body chemotransduction. 822 9


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>