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

Cerebral air embolism can have hemodynamic effects such as increases in blood pressure and cerebral blood flow. It has been suggested that these factors play a role for the induction of the blood-brain barrier (BBB) dysfunction. In the present study, 5 microliters air was injected into the right internal carotid artery from a catheter in the external carotid artery after ligation of the extracerebral branches. No consistent change in blood pressure was observed with this small amount of air. Hypercapnia, which increases protein leakage in the brain under conditions of high intraluminal pressure, significantly reduced the extravasation in air embolism. Lidocaine and SITS (4 acetamido-4-isothiocyano-stilbene-2,2-disulfonic acid disodium), two drugs that effectively reduce the albumin leakage in acute hypertension, had no prophylactic effect in cerebral air embolism. Spontaneously hypertensive rats are less vulnerable than normotensive rats to pressure-induced BBB dysfunction but did not significantly differ from controls regarding albumin leakage in the present study. It is concluded that the increased cerebrovascular permeability in air embolism is not related to hemodynamic factors.
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PMID:Cerebral air embolism and the blood-brain barrier in the rat. 678 18

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

The serum anion gap is decreased in hyperchloremic (HCl) acidosis and increased in diuretic-induced alkalosis. These anion gap changes have been largely attributed to titration-induced variations in the net negative charge of the serum proteins, which are the predominant non-HCO3 buffers of serum. It has recently been shown, however, that albumin has all of the net protein charge, and titration-induced changes in charge are smaller than have been widely believed. Because the non-HCO3 buffers are also titrated in acute hypocapnia and hypercapnia, these disorders were induced in 16 anesthetized dogs for 10 min in order to assess the effect of acute changes in pH on the anion gap. Although the mean arterial pH varied from 7.04 to 7.65, the calculated mean albumin charge only varied from 6.8 to 9.0 mEq/L. When the anion gap was computed with HCO3 (AGHCO3 = Na + K - Cl - HCO3), the change in AGHCO3 per 0.1 change in pH (delta AGHCO3/ delta pH) was only 0.15 mEq/L per 0.1 pH. When the anion gap was computed with total CO2 content (AGTCO2 = Na + K - Cl - TCO2), delta AGTCO2/delta pH was larger (0.51 mEq/L per 0.1 pH) because of the effect of variable PCO2 levels on TCO2. In a review of 22 previous studies in humans and dogs, similar estimates of delta AG/delta pH were obtained (after adjusting for the lower albumin level in dogs). These results show that simple titration processes that occur within 10 min of a change in pH cause minimal changes in the anion gap. Titration of the known non-HCO3 buffers of serum does not explain the much larger anion gap changes of HCl acidosis and diuretic alkalosis.
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PMID:Effect of acute pH change on serum anion gap. 878 9

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

The interactions between the acid-base variables that contribute to exudate acidosis were studied in the subcutaneous air-pouch after carrageenan injection in rats. We studied the concurrent changes of exudate gases (PCO2 and PO2), main ions ([Na+], [K+], [Ca2+], [Mg2+], [Cl-] and [Lac-]), inorganic phosphate (P(i)) and albumin in acutely inflamed rats (4, 8, 12, 24 and 48 h of inflammation). A notable hypercapnia was found in the exudate after only 8 h (exudate PCO2 = 64.3 +/- 2.9 mm Hg) but this hypercapnia decreased after 48 h (32.9 +/- 12.7 mm Hg), coincident with the greatest increase in exudate cells. With respect to the metabolic acid-base variables, the most important changes found were a parallel decrease in the strong ion difference ([SID]) and exudate pH, as well as increases in the exudate weak acid buffers ([ATOT]) due to albumin and inorganic phosphate (P(i)) increases. However, after 12 h, the exudate acidosis was stable at around pH 7. A similar acid pH was obtained after 24 h of inflammation when the carrageenan solution injected was previously adjusted to a physiological pH (7.4). This pH, analogous to that of the exudate, was the result of compensation by the acid-base independent variables, a fact which suggests that acid pH may be a beneficial condition for cells taking part in inflammatory processes.
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PMID:Factors influencing the acid-base changes in the air-pouch exudate following carrageenan induced inflammation in rats. 887 14

Hypercapnic respiratory failure due to chronic obstructive pulmonary disease (COPD) is an indicator of poor prognosis compared to that for normocapnic patients. On the other hand, there exist particular patients who are hypercapnic during an acute exacerbation of COPD but revert to normocapnia after adequate therapy. The aims of this study were: 1) to document the admission characteristics of such patients in terms of clinical and laboratory findings; and 2) to analyse the long-term course and survival of chronic and reversible hypercapnic and normocapnic patients. Fifty-six consecutive patients, admitted with an acute exacerbation of COPD, were enrolled and divided into three groups according to arterial carbon dioxide tension (Pa,CO2) at first admission: 22 chronic hypercapnic (group 1), 15 reversible hypercapnic (group 2) and 19 normocapnic (group 3) patients. Age, sex, smoking history, white blood cell count, serum sodium, potassium, urea and albumin levels and pulmonary function tests at first admission were similar in the three groups. The haematocrit level was significantly higher in group 1 compared with the other groups. Groups 1 and 2 had lower pH, arterial oxygen tension (Pa,O2) and arterial oxygen saturation (Sa,O2) and a higher Pa,CO2 than group 3. The Pa,CO2 was also higher in group 1 than in group 2. The presence of cor pulmonale was significantly higher in group 1 compared with groups 2 and 3 (81.8 versus 60 and 10.5%, respectively). During the follow-up period, a significant increase was observed in airway obstruction associated with progressive hypercapnia and hypoxaemia in chronic hypercapnic patients, and 12 of 15 (80%) reversible hypercapnic patients progressed to a chronic hypercapnic status. The survival analyses after 10 yrs of follow-up revealed comparable survival durations in chronic and reversible hypercapnic patients (median of 8.86 versus 9.52 yrs, p > 0.05). In conclusion, despite careful monitoring of particular characteristics in chronic and reversible hypercapnic patients at the time of admission, no long-term predictivity of these features for either the course of the disease or survival could be found.
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PMID:Distinctive features and long-term survival of reversible and chronic hypercapnic patients with COPD. 1044 72

We investigated the hypothesis that lung blood flow distribution is modified in stage 1 chronic obstructive pulmonary disease (COPD). We compared patients with stage 1 COPD (n = 11) with restrictive patients with comparable blood gases (n = 7), to patients with low cardiac index with normal lungs (n = 11) and to control subjects (n = 11). Distribution of transit time (DTT) was computed by deconvolution from first pass radioactivity curves (albumin (99m)Tc) reconstructed from right and left ventricular regions of interest. Distribution descriptors, mean transit time (p < 0.05), standard deviation (p < 0.001), relative dispersion (p < 0.001), and kurtosis (p < 0.001) differed between groups (ANOVA). Cardiac index was the same in COPD and low CI groups but lower compared with normal subjects (p < 0.05). After normalization for cardiac output, the DTT of patients with COPD remained different from low CI and restrictive patients (p < 0.001). Therefore changes in DTT in patients with COPD compared with patients without COPD could not be explained on the basis of difference in cardiac output. Because P(O(2)), PC(O(2)), and pH were similar in COPD and restrictive groups, difference in distribution could not be explained either on the basis of blood gas data. We conclude that changes in DTT occurs in stage 1 COPD and cannot be explained by hypoxemia, hypercapnia, or acidosis alone but must relate to other structural or regulatory responses.
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PMID:Pulmonary blood flow distribution in stage 1 chronic obstructive pulmonary disease. 1111 17

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

Maintaining homogeneous perfusion in tissues undergoing remodeling and vascular expansion requires tight orchestration of the signals leading to endothelial sprouting and subsequent recruitment of perivascular contractile cells and vascular maturation. This regulation, however, is frequently disrupted in tumors. We previously demonstrated the role of tumor-associated myofibroblasts in vascularization and exit from dormancy of human ovarian carcinoma xenografts in nude mice. The aim of this work was to determine the contribution of stroma- and tumor cell-derived angiogenic growth factors to the heterogeneity of vascular permeability and maturation in MLS human ovarian carcinoma tumors. We show by RT-PCR and by in situ hybridization that VEGF was expressed by the tumor cells, while angiopoietin-1 and -2 were expressed only by the infiltrating host stroma cells. Vascular maturation was detected in vivo by vasoreactivity to hypercapnia, measured by BOLD contrast MRI and validated by immunostaining of histologic sections to alpha-smooth muscle actin. Vascular permeability was measured in vivo by dynamic contrast-enhanced MRI using albumin-based contrast material and validated in histologic sections by fluorescent staining of the biotinylated contrast material. MRI as well as histologic correlation maps between vascular maturation and vascular permeability revealed a wide range of vascular phenotypes, in which the distribution of vascular maturation and vasoreactivity did not overlap spatially with reduced permeability. The large heterogeneity in the degree of vascular maturation and permeability is consistent with the differential expression pattern of VEGF and angiopoietins during tumor angiogenesis.
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PMID:Functional and molecular mapping of uncoupling between vascular permeability and loss of vascular maturation in ovarian carcinoma xenografts: the role of stroma cells in tumor angiogenesis. 1588 Apr 97

Modified Hb solutions have been developed as O(2) carrier transfusion fluids, but of concern is the possibility that increased scavenging of nitric oxide (NO) within the plasma will alter vascular reactivity even if the Hb does not readily extravasate. The effect of decreasing hematocrit from approximately 30% to 18% by an exchange transfusion of a 6% sebacyl cross-linked tetrameric Hb solution on the diameter of pial arterioles possessing tight endothelial junctions was examined through a cranial window in anesthetized cats with and without a NO synthase (NOS) inhibitor. Superfusion of a NOS inhibitor decreased diameter, and subsequent Hb transfusion produced additional constriction that was not different from Hb transfusion alone but was different from the dilation observed by exchange transfusion of an albumin solution after NOS inhibition. In contrast, abluminal application of the cross-linked Hb produced constriction that was attenuated by the NOS inhibitor. Neither abluminal nor intraluminal cross-linked Hb interfered with pial arteriolar dilation to cromakalim, an activator of ATP-sensitive potassium channels. Pial vascular reactivity to hypocapnia and hypercapnia was unaffected by Hb transfusion. Microsphere-determined regional blood flow indicated selective decreases in perfusion after Hb transfusion in the kidney, small intestine, and neurohypophysis, which does not have tight endothelial junctions. Administration of a NOS inhibitor to reduce the basal level of NO available for scavenging before Hb transfusion prevented further decreases in blood flow to these regions compared with NOS inhibition alone. In contrast, blood flow to skeletal and left ventricular muscle increased, and cerebral blood flow was unchanged after Hb transfusion. This cross-linked Hb tetramer is known to appear in renal lymph but not in urine. We conclude that cell-free tetrameric Hb does not scavenge sufficient NO in the plasma space to significantly affect baseline tone in vascular beds with tight endothelial junctions but does produce substantial constriction in beds with porous endothelium. The data support increasing the molecular size of Hb by polymerization or conjugation to limit extravasation in all vascular beds to preserve normal vascular reactivity.
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PMID:Role of nitric oxide scavenging in vascular response to cell-free hemoglobin transfusion. 1589 76


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