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

Regional cerebral blood flow was simultaneously determined using the stable xenon computed tomographic and the radioactive microsphere techniques over a wide range of blood flow rates (less than 10-greater than 300 ml/100 g/min) in 12 baboons under conditions of normocapnia, hypocapnia, and hypercapnia. A total of 31 pairs of determinations were made. After anesthetic and surgical preparation of the baboons, cerebral blood flow was repeatedly determined using the stable xenon technique during saturation with 50% xenon in oxygen. Concurrently, cerebral blood flow was determined before and during xenon administration using 15-microns microspheres. In Group 1 (n = 7), xenon and microsphere determinations were made repeatedly during normocapnia. In Group 2 (n = 5), cerebral blood flow was determined using both techniques in each baboon during hypocapnia (PaCO2 = 20 mm Hg), normocapnia (PaCO2 = 40 mm Hg), and hypercapnia (PaCO2 = 60 mm Hg). Xenon and microsphere values in Group 1 were significantly correlated (r = 0.69, p less than 0.01). In Group 2, values from both techniques also correlated closely across all levels of PaCO2 (r = 0.92, p less than 0.001). No significant differences existed between the slopes or y intercepts of the regression lines for either group and the line of identity. Our data indicate that the stable xenon technique yields cerebral blood flow values that correlate well with values determined using radioactive microspheres across a wide range of cerebral blood flow rates.
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PMID:Stable xenon versus radiolabeled microsphere cerebral blood flow measurements in baboons. 251 92

In this study, we tested the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension. The hypothesis took origin from the following two considerations: alveolar hypoxia constricts the pulmonary vessels by enhancing the Ca2+ penetration across sarcolemma of the smooth muscle cells and systemic high blood pressure is associated with an elevation of tone and reactivity of the lung vessels, which seems to depend on an excessive cytosol free Ca2+ concentration due to alterations in sodium handling and in the Na+-Ca2+ exchange system. These considerations suggest the possibility that the disorders in the biochemistry of smooth muscle contraction in hypertension facilitate the rise of cytosol Ca2+ concentration during alveolar hypoxia, thus resulting in a potentiation of the vasoconstrictor properties of this stimulus. In 43 hypertensive and 17 normotensive men, pulmonary arteriolar resistance has been evaluated during air respiration and after 15 minutes of breathing 17%, 15%, and 12% oxygen in nitrogen. Curves relating changes in pulmonary arteriolar resistance to oxygen breathing contents had similar configuration in the two populations but in hypertension were steeper and significantly shifted to the left, reflecting a lower threshold and an enhanced reactivity. This pattern was not related to differences in severity of the hypoxic stimulus, plasma catecholamine concentration, or hypocapnia and respiratory alkalosis induced by hypoxia and probably was not mediated through alpha-receptor activation. Calcium channel blockade with nifedipine was able to almost abolish both the normotensive and the hypertensive pulmonary vasoconstriction reaction. These findings support the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension.
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PMID:Enhanced hypoxic pulmonary vasoconstriction in hypertension. 256 42

Sixteen patients with supratentorial cerebral tumours were subjected to craniotomy under thiopentone, fentanyl, nitrous oxide, halothane anaesthesia during moderate hypocapnia (PaCO2 level 4.0 kPa). The arterio-venous oxygen content difference (AVDO2) was measured peroperatively, and repeatedly during the first three hours after extubation. Peroperatively the level of AVDO2 averaged 8.0 vol% during opening of the dura, and decreased to 7.0 vol% during closure of the dura (P less than 0.05). Immediately after extubation the AVDO2 decreased to 4.3 vol% (P less than 0.05), and during the next 3 hours a gradual increase to 5.8 vol% (P less than 0.05) was disclosed. In individual cases the postoperative changes in AVDO2 correlated fairly well with changes in mean arterial blood pressure (MABP), but other factors including duration of the operation, age of the patients, size of the tumour, level of PaCO2 and adaptation to prolonged hyperventilation during operation are supposed to be responsible for the low levels of AVDO2 observed in the postoperative period.
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PMID:Per- and postoperative changes in the arterio-venous oxygen content difference (AVDO2) in patients subjected to craniotomy for cerebral tumours. 260 75

In the proximal tubules, fractional reabsorption remains essentially unchanged during variations in glomerular filtration rate (GFR). Glomerulotubular balance (GTB), defined as the linear relationship between proximal tubular reabsorption and GFR, is quantitatively the most important regulator of tubular reabsorption, which may be stopped by inhibiting Na, K-ATPase activity completely. However, ouabain in doses inhibiting 80% of the Na, K-ATPases, exerts no effect on proximal reabsorption of water, NaCl and NaHCO3. At constant plasma pH, the same relationship between filtered and reabsorbed bicarbonate is obtained whether bicarbonate reabsorption is altered by varying GFR or plasma concentration of bicarbonate. In contrast, a selective rise in plasma NaCl concentration at constant plasma pH (hypernatremia) reduces NaHCO3 reabsorption and fails to stimulate NaCl reabsorption. Other characteristics of proximal tubular reabsorption are that nonreabsorbable solutes, such as mannitol, inhibit water and NaCl reabsorption with little or no change in NaHCO3 reabsorption and renal oxygen consumption. Mannitol reduces the slope of the GTB curve for NaCl but not for NaHCO3. Hypertonic NaHCO3 exerts an osmotic effect on proximal water and NaCl reabsorption comparable to that of mannitol, whereas hypertonic NaCl is without osmotic effect. By reducing plasma pH (hypercapnia at high plasma bicarbonate concentration), the slope of the GTB curves for NaCl and NaHCO3 can be greatly increased. By raising plasma pH either by hypocapnia or bicarbonate loading, proximal reabsorption of NaHCO3 and NaCl is greatly depressed and remains almost unaltered during variations of GFR (abolished GTB). Similarly, carbonic anhydrase inhibitors, such as acetazolamide, reduce the reabsorption of NaCl and NaHCO3 in the same proportion as a rise in plasma pH, and abolish GTB. Examinations of proximal tubular oxygen consumption indicate that the energy requirement for NaHCO3 reabsorption is as expected for transcellular transport by Na, K-ATPases, whereas proximal NaCl reabsorption requires no additional energy. These data indicate that transcellular energy-requiring NaHCO3 reabsorption provides the main osmotic force across the tight junction for paracellular reabsorption of proximal tubular fluid containing NaCl and other solutes of low reflection coefficient. The main factors influencing GTB are the filtered load of bicarbonate, plasma pH and nonreabsorbable solutes in the proximal tubular fluid.
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PMID:Essentials of glomerulotubular balance. 267 97

Experiments on dogs have shown that hyperthermia intensifies respiration, increases oxygen consumption, induces pronounced discrepancy of the alveolar ventilation to carbon dioxide elimination, severe hypocapnia and decompensated respiratory alkalosis.
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PMID:[External respiration, gas exchange and blood acid-base status in dogs with hyperthermia]. 271 67

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.
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PMID:Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure. 273 78

The clinical value of noninvasive continuous monitoring of conjunctival oxygen tension for assessment of cerebral perfusion during carotid endarterectomy performed under general anaesthesia has been evaluated. The patients (n = 17; mean age 62.5 +/- 1.7 years) were monitored as follows: conjunctival oxygen tension (PcjO2); internal jugular venous oxygen tension at the skull base level (PcijvO2); arterial blood pressure; arterial and internal jugular venous blood gases; acid-base data and lactate, pyruvate levels; end-tidal CO2 concentration. The mean preanaesthetic PcjO2 level of 4.86 +/- 0.40 kPa was significantly lower than PaO2(PcjO2)/PaO2 ratio of 0.48). Following anaesthesia, a larger PcjO2-PaO2 gradient (ratio 0.32) was seen in spite of the hyperoxic situation (FiO2 = 0.40) due to vasoconstriction induced by slight hypocapnia (reduction of PaCO2 from 5.13 +/- 0.08 to 4.64 +/- 0.10 kPa). The carotid artery crossclamping resulted in a rapid and pronounced decrease of PcjO2, while PcijvO2 remained unchanged. No relationship between PcjO2 and stump pressure was found, while a significant correlation (P less than 0.02) between PcjO2 and lactate in effluent venous blood from the brain was demonstrable. It is concluded that PcjO2 monitoring seems a clinically useful trend indicator of cerebral perfusion in the individual patient. Due to large interindividual variations in basal PcjO2 readings and in PcjO2 changes during carotid artery clamping, however, transconjunctival oxygen tension monitoring does not seem to allow early and accurate recognition of impending cerebral ischaemia during carotid endarterectomy, and its routine use therefore seems of limited value.
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PMID:Continuous conjunctival oxygen tension (PcjO2) monitoring for assessment of cerebral oxygenation and metabolism during carotid artery surgery. 281 41

1. Interstitial pH (pHo) was measured with ion-selective microelectrodes in the fascia dentata of rats anaesthetized with urethane, while CO2 levels were controlled by varying pulmonary ventilation and CO2 content of inspired air. In the CA1 sector of hippocampal tissue slices in vitro pHo was similarly measured and altered by varying CO2 in the gas phase, or by adding HCl or NaOH to the artificial cerebrospinal fluid (ACSF) of the bath, or by changing the concentration of HCO3-. 2. Orthodromically evoked compound action potentials ('population spikes') were depressed in hypercapnia and increased in hypocapnia. In the fascia dentata of intact brains the population spike of the granule cells varied on average by more than 40% of control amplitude for each 0.1 change of pHo. In the CA1 zone of tissue slices in vitro, the change of population spike amplitude was approximately 30% per pH change of 0.1 caused by altered CO2 or HCO3- concentration, but only about 15% per pH change of 0.1 when HCl or NaOH were administered. 3. In anaesthetized rats the focal synaptic potential (FEPSP) evoked by a given stimulus intensity was weakly influenced by varying [CO2]; in tissue slices weak effects on FEPSP were inconsistent. In hippocampus both in situ and in vitro the population spike triggered by a given magnitude of FEPSP increased in hypocapnia and decreased in hypercapnia. This suggests that the main effect of CO2 is on the electric excitability of postsynaptic cells, with minor or no effect on transmitter release and on the interaction of the transmitter with its receptors. 4. Hypercapnia of anaesthetized rats was usually associated with a slight increase of [K+]o in the fascia dentata. Tissue [Ca2+]o changed little and not consistently. Neither of these two ions, nor concomitant changes of blood pressure or tissue partial pressure of oxygen, (Pt, O2), could account for the effects of pH on neuronal excitability. 5. The results show that increasing the extracellular concentration of H+ ions has a moderately depressant effect on the firing threshold of hippocampal neurones. The more powerful effects of elevated [CO2] and of lowered [HCO3-] may probably be explained by a direct effect on the neuronal membrane. The brain, by regulating breathing, controls its own excitability.
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PMID:Concentration of carbon dioxide, interstitial pH and synaptic transmission in hippocampal formation of the rat. 284 90

Propofol like thiopental and etomidate, suppresses cortical electrical activity in a dose-related manner, which leads to a 36% decrease in cerebral oxygen uptake and a 51% decrease in cerebral blood flow after an induction dose of 2 mg/kg followed by a maintenance dose of 0.2 mg/kg per min. In this study, the effects of propofol and varying paCO2 values on cerebral energy and amino acid metabolism were examined. METHODS. Eleven male patients between 49 and 63 years of age who were about to undergo coronary artery bypass surgery were studied. Measurements were performed with the patient awake (I), during steady-state maintenance anesthesia after propofol 2 mg/kg as an induction dose with 0.2 mg/kg per min by infusion with normocapnia (paCO2 39.9 +/- 3.1 mm Hg) (II), during hypocapnia (paCO2 29.9 +/- 2.6 mmHg) (III), and during hypercapnia (paCO2 50.6 +/- 3.3 mmHg) (IV). Cerebral blood flow was measured using the argon wash-in technique. A catheter was advanced into the superior bulb of the right internal jugular vein for measurement of cerebral oxygen, glucose, lactate, and amino acid uptake and release, which were calculated by multiplying the arterial-cerebral venous oxygen and substrate difference by the cerebral blood flow. Lactate/glucose index was calculated from the equation. Formula: see text. where a-vD lactate and a-vD glucose represent the arterial-cerebral venous substrate differences in mmol/l. Cerebral electrical activity was recorded by Fourier analysis of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Energy and amino acid metabolism in the human brain under Disoprivan anesthesia with various paCO2 values]. 289 87

We have recently demonstrated an increase in myocardial blood-flow (MBF) during systemic hypercapnia independent of myocardial oxygen consumption. During hypocapnia no significant decrease of MBF was observed; however, a significant increase of myocardial oxygen extraction resulted. The present study was undertaken to examine whether these effects were caused by changes in the sympathoadrenal activity. During beta-adrenoceptor blockade and combined alpha- and beta-blockade the effects of hypocapnia and hypercapnia on MBF and haemodynamics were examined. Closed-chest dogs were anaesthetized with pentobarbital and hypocapnia was induced by hyperventilation. Carbon dioxide was added to the inspiratory gas to create normocapnia and hypercapnia. Hypocapnia did not result in any changes of MBF, coronary vascular resistance or myocardial oxygen extraction, neither during beta-adrenoceptor blockade nor during combined alpha- and beta-blockade. Hypercapnia did not increase MBF, neither during beta-blockade nor during combined alpha- and beta-blockade. However, both myocardial oxygen consumption and mechanical performance of the heart were reduced during hypercapnia. Thus, a relative myocardial overperfusion, indicated by decreased coronary vascular resistance and myocardial oxygen extraction, was observed during hypercapnia. In conclusion, the unaltered MBF during hypocapnia and the coronary overperfusion during hypercapnia were not related to changes in the sympathoadrenal activity.
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PMID:Hypocapnia and hypercapnia in the dog: effects on myocardial blood-flow and haemodynamics during beta- and combined alpha- and beta-adrenoceptor blockade. 302 3


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