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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An isolated perfused lung (IPL) preparation was used to investigate the influence of acute environmental stress on lung substrate metabolism. The IPL apparatus consists of four perfusion flasks housed in a temperature-controlled Lucite box with a circulation fan. Lungs are ventilated by a positive pressure ventilation pump. The ventilation is arranged so that the lung can be ventilated with any desired gas composition with concomitant collection of expired gases. The perfusion medium is circulated at 10 ml/min with a peristaltic blood pump, and passes through a specially designed chamber to dampen pulmonary pressure and remove emboli. The perfusion medium presently used in our experiments consisted of washed bovine red blood cells resuspended to a 15% hematocrit with Krebs-Henseleit bicarbonate buffer containing 6% dialyzed Pentex bovine serum albumin. Circulating substrates include 6muM glucose and 0.4muM palmitate. The pH is adjusted to 7.4 with 0.8M Na carbonate. Lungs perfused for 1.5 hr with this apparatus maintain viability, show little edema, maintain blood gases, and show linear incorporation of labeled glucose into lung lipids. Perfused lungs made hypocapnic show a significant (p less than 0.05) rise in lactate and pyruvate, while perfused lungs made hypercapnia show a significant decrease in pyruvate with no change in lactate.
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PMID:Perfused lung preparation for studying altered gaseous environments. 1 88

Twenty-seven newborn Holstein bull calves were bottle-fed 2 litres of pooled colostrum which had been stored at -20 degrees C. Blood gas analysis before feeding showed a partially compensated respiratory acidosis in most of the calves, although they all appeared to be clinically normal. Mean venous blood pH was 7.346, carbon dioxide tension (PCO2) was 57.5 mmHg (7.6 kPa), bicarbonate was 30.6 mmol/l and base excess was 3.82 mmol/l. Mean serum IgG1 increased to 8.1 g/l after feeding colostrum. Several significant positive correlations were observed between post-absorptive serum protein, IgG1, IgM, gamma-glutamyltransferase (gamma GT) and D-xylose. Calves with either low serum albumin, high serum CK or low serum gamma GT before feeding tended to have less absorption of colostral protein. It was concluded that reduced absorption of IgG1 from colostrum is associated with hypercapnia in apparently healthy newborn calves.
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PMID:Relationships between acid-base balance, serum composition and colostrum absorption in newborn calves. 256 18

The decision to institute MV in patients with COPD and ARF is difficult because the risk of complications is high and the long-term prognosis is poor. We reviewed our experience with 95 COPD patients with ARF requiring MV. Fifty-five patients required MV for more than two weeks, 72 were weaned successfully, and 59 died within one year of follow-up. Survival was associated with premorbid level of activity (p less than .001), FEV1 (p less than .01), serum albumin level (p less than .05), and severity of dyspnea (p less than .01). Cor pulmonale on ECG, premorbid hypercarbia, and history of left ventricular failure were also more common among those who died. Weaning from MV was associated with premorbid level of activity (p less than .001), FEV1 (p less than .001), albumin level (p less than .05), and negative inspiratory pressure (p less than .001) and respiratory rate during T-piece trial (p less than .01). The duration of intubation was associated only with premorbid level of activity (p less than .01). Predictive models for the weaning success and the one-year survival were developed.
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PMID:Determinants of weaning and survival among patients with COPD who require mechanical ventilation for acute respiratory failure. 291 93

We analyzed the retroglenoid venous outflow (VOF) technique in the rat to document the validity of this method of measuring cerebral blood flow (CBF). Stereotypic changes in CBF were obtained with VOF during hypercarbia and hypotension. O2 content of retroglenoid venous blood did not differ significantly from O2 content of blood obtained from the sagittal sinus, suggesting minimal extracerebral contamination of the retroglenoid venous blood. This lack of extracerebral contamination was further analyzed using a double tracer technique (125I-labeled serum albumin, 22Na) that quantitated minimal extracerebral contamination in the retroglenoid vein. CBF measurements were made simultaneously using microsphere and VOF methods, and excellent correlation was found between the two techniques over a wide range of CBF during normoxia, hypoxia, and normoxic hypocarbia and hypercarbia. However, a decrease in the ratio of VOF to microsphere CBF was observed during severe normoxic hypotension (mean arterial pressure = 41 +/- 4 mmHg). VOF represented 18% of total CBF as measured by microsphere method. This study indicates that the retroglenoid outflow technique in rats is a valid method of measuring CBF.
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PMID:A venous outflow method for continuously monitoring cerebral blood flow in the rat. 308 Sep 2

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
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PMID:Hyperventilation with hypoproteinemia. 318 88

The purpose of this study was to examine effects of hypercapnia on susceptibility of the blood-brain barrier to disruption during acute hypertension. Two methods were used to test the hypothesis that cerebral vasodilatation during hypercapnia increases disruption of the blood-brain barrier. First, permeability of the blood-brain barrier was measured in anesthetized cats with 125I-labeled serum albumin. Severe hypertension markedly increased permeability of the blood-brain barrier during normocapnia, but not during hypercapnia. The protective effect of hypercapnia was not dependent on sympathetic nerves. Second, in anesthetized rats, permeability of the barrier was quantitated by clearance of fluorescent dextran. Disruption of the blood-brain barrier during hypertension was decreased by hypercapnia. Because disruption of the blood-brain barrier occurred primarily in pial venules, we also measured pial venular diameter and pressure (with a servo-null method). Acute hypertension increased pial venular pressure and diameter in normocapnic rats. Hypercapnia alone increased pial venular pressure and pial venular diameter, and acute hypertension during hypercapnia further increased venular pressure. The magnitude of increase in pial venular pressure during acute hypertension was significantly less in hypercapnic than in normocapnic rats. We conclude that hypercapnia protects the blood-brain barrier. Possible mechanisms of this effect include attenuation of the incremental increase in pial venular pressure by hypercapnia or a direct effect on the blood-brain barrier not related to venous pressure.
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PMID:Protection of the blood-brain barrier by hypercapnia during acute hypertension. 374 Feb 84

Spontaneous hypertensive rats (SHR) are less prone to develop a dysfunction of the blood-brain barrier (BBB) when exposed to an abrupt increase in blood pressure than normotensive rats (NR), probably as a result of vessel wall hypertrophy and increased vessel wall to lumen ratio. Hemodynamic studies have indicated that structural adaptation develops early as a response to the increased pressure load in renal hypertensive rats (RHR). In the present study RHR (one renal artery constricted and the contralateral kidney intact) were subjected to acute hypertension induced by bicuculline, a drug that induces an abrupt increase in blood pressure concomitant with pronounced cerebral vasodilatation. Protein leakage in the brain, as indicated by Evans blue-albumin and 125IHSA (human serum albumin) extravasation, was not reduced in RHR compared to NR. The cerebrovascular permeability was slightly but significantly (p < 0.01) increased in RHR even in the absence of further blood pressure manipulation. No neurological symptoms were observed in conscious RHR when the BBB dysfunction was aggravated by hypercapnia. The increased cerebrovascular permeability in RHR cold be due to a lower degree of structural adaptation in RHR compared to SHR and/or to some permeability-increasing humoral factor in renal hypertension.
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PMID:The blood brain barrier in renal hypertensive rats. 744 83

This study was undertaken to investigate the mechanisms of CBF increase as induced by hypercapnia. It was achieved in anesthetized rats by determining total cerebral blood volume (TCBV), parenchymal blood (CBV), plasma (CPV), erythrocyte (CEV) volumes and cerebral hematocrit (CHct) as well as CBF at about 40, 60, and 80 mm Hg PaCO2. TCBV was measured by a noninvasive blood dilution method using [99mTc]pertechnetate. CBV, CPV, and CEV were measured on isolated brain by 125I-serum albumin and 51Cr-erythrocytes. CBF was measured by both [131I/14C]iodoantipyrine and 57Co-microsphere extractions. The extraparenchymal blood volume (ECBV) was evaluated by subtracting CBV from TCBV. Under normocapnia, ECBV was 2.8 times larger than CBV. Under moderate hypercapnia, ECBV increased by 44%, CBV was not modified, and CBF increased by 52%. These results demonstrate that the main site of vasodilation is located in the extraparenchymal vasculature, which thus acts as a vascular reserve. By contrast, under severe hypercapnia, ECBV remained unchanged, whereas CBV then increased by 17%; CBF simultaneously showed an additional augmentation of either 52 or 309% when diffusible tracer or microspheres were used. This important increase in CBF cannot be explained either by capillary recruitment of closed capillaries or by active diameter lengthening of already open capillaries. The concomitant and great increase in capillary blood velocity was also shown to reduce cerebral flow efficiency, a situation consistent with a "luxury perfusion."
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PMID:Induced response to hypercapnia in the two-compartment total cerebral blood volume: influence on brain vascular reserve and flow efficiency. 759 45

The increase in local cerebral blood flow (LCBF) caused by hypercapnia may be mainly accomplished by raising the velocity of plasma and/or red blood cell (RBC) flow through the microvessels and not by perfusing more capillaries. This suggestion was tested in awake rats exposed to 8% CO2 and in control rats. LCBF was measured by the 14C-labeled iodoantipyrine method. The volume of blood in small parenchymal microvessels was estimated from the distribution spaces of 125I-labeled serum albumin (RISA) and 55Fe-labeled RBCs. Hypercapnia elevated LCBF 2.0- to 3.5-fold in the 40 brain areas studied, marginally raised the RBC spaces, and significantly increased the RISA and whole blood distribution spaces (approximately 25 and 19%, respectively). These changes in microvessel distribution volumes could be the result of perfusing a slightly larger fraction of capillaries (recruitment), increasing microvessel diameter somewhat, or both. With hypercapnia, the mean transit times fell to approximately 45% of control, which indicated that LCBF was mainly increased by raising the velocity of RBC and plasma flow through already perfused microvessels. Overall, few, if any, capillaries or other microvessels were recruited by hypercapnia.
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PMID:Hypercapnia slightly raises blood volume and sizably elevates flow velocity in brain microvessels. 849 49

The relationship between total bilirubin binding capacity (TBBC) and clinical status was investigated in order to assess the risk of bilirubin toxicity in 83 infants with jaundice in this study. Infants with respiratory distress, acidosis, hypoglycaemia, sepsis, asphyxia-anoxia and hypercarbia were accepted as ill and the remainders were well. Sephadex G-25 gel filtration method was used to determine TBBC. Serum albumin levels, TBBC and TBBC/albumin molar ratios were lower in ill premature and mature infants. Acidosis was the major risk factor for bilirubin toxicity in ill infants. Therefore, clinical status should be taken into consideration in the management of jaundiced infants.
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PMID:The influence of clinical status on total bilirubin binding capacity in newborn infants. 882 Jun 20


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