Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The level of urinary excretion of hydroxyproline is considered as an index of the metabolic activity of the collagen. It increases in situations which include an increase in the osteoblastic activity or in the bone resorption. In respiratory insufficiency a series of conditions occur which are theoretically capable of modyfing this parameter. Twelve patients (9 males and 3 women) with chronic respiratory disease in a situation of respiratory insufficiency (hypoxemia and/or hypercapnia at rest) were studied. The urinary excretion of hydroxyproline in these patients was 15.30 +/- 8.16 mg/day/m2, significantly greater than that of a control group with similar characteristics which was 9.97 +/- 3.07 mg/day/m2 (p less than 0.05; Student's t test). The existence of a significant correlation between the urinary excretion of hydroxyproline and the degree of hypoxemia (r = 0.66; p less than 0.01) was likewise verified; in the same way, although to a lesser degree with the hypercapnia (r = 0.62; p less than 0.05). The different factors capable of influencing the bone metabolism in respiratory insufficiency are discussed, as well as the effects of the medications used by these patients. It is possible, on the other hand, that the increase of the urinary excretion of hydroxyproline does not depend only on alterations in the metabolic condition of the bone, but also on a reduction in the hepatic metabolism of the amino acid in relation with gasometric modifications.
 ...
PMID:[Urinary excretion of hydroxyproline in patients with chronic respiratory insufficiency (author's transl)]. 47 Apr 88

We examined the effects of ADP- and collagen-induced pulmonary platelet embolism in the rat. Homologous 51Chromium-labelled platelets were used to monitor extracorporally the distribution of platelets in the circulation. For that purpose, collimated iodide scintillation detectors were placed above thorax (C1) and abdomen (C2). A dose-dependent increase in thoracic radioactivity, paralleled by a decrease in the abdomen, was observed after intravenous injection of ADP and collagen. This resulted in a shift of C1/C2, so that the effect of collagen was more pronounced (maximal increase of C1/C2 = 134%) than ADP (maximal increase of C1/C2 = 79%). The increase in thoracic radioactivity was caused by the uptake of platelets in the lung as was shown after administration of collagen (6-fold enrichment of labelled platelets). Lung platelet sequestration resulted in a dose-dependent thrombocytopenia. The ADP -and collagen-induced pulmonary platelet embolism reversibly provoked cardiovascular symptoms of shock: hypotension and bradycardia. Impaired gas exchange during platelet accumulation manifested itself in a reversible arterial hypoxaemia and hypercapnia, followed by a weak acidosis. We were able to inhibit ADP-dependent thoracic platelet accumulation by ticlopidine in a dose-related manner as well as collagen-induced thoracic platelet accumulation by acetylsalicylic acid. The results indicate that behaviour of homologous labelled rat platelets in vivo can easily be monitored, thus offering the opportunity to investigate the effects of antiaggregatory drugs on platelets in their natural environment.
 ...
PMID:Evaluation of pulmonary accumulation of 51chromium-labelled rat platelets following intravenous application of ADP and collagen. 187 21

The influence of changes in pCO2, pH and pO2 on the aggregation of rabbit blood platelets was studied in vitro, with emphasis on hypercapnia, acidosis and hypoxia. Hypercapnia combined with acidosis caused a reduction in rabbit platelet aggregation, as induced by collagen, thrombin and ADP; the effect being most pronounced with collagen and smallest with ADP. Hypoxia reduced thrombin induced platelet aggregation, but had no effect on ADP and collagen induced aggregation. Synergistic activation of rabbit platelets, as induced by the addition of serotonin to platelet rich plasma together with collagen or ADP, seemed to be equally sensitive to changes in pCO2 and pH as activation by the individual agents, and insensitive to changes in pO2.
 ...
PMID:Influence of hypercapnia and hypoxia on rabbit platelet aggregation. 211 81

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
 ...
PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15

The antiaggregation ability of CO2 during ADP- and collagen-induced platelet aggregation has been discovered in cats under hypercapnia. The effect persisted after Pco2 normalization. The inhibition of cyclooxygenase by indomethacin suppressed the antiaggregation activity of CO2 in vivo but not in vitro. While estimating the regulatory role of CO2 in the metabolic control of cerebral circulation, it is also of importance to take into account the antiaggregation ability of CO2.
 ...
PMID:[Effect of CO2 on thrombocyte aggregation in the cat]. 642 43

The aim of the study was to find out the key manifestations of reorganization of lung aerohematic barrier (AB) components (cellular and tissue) in the process of a prolonged physical exercise, taking into account changes in the indices of blood acid-basic balance (ABB). The physical exercise (running in treadbane, 2 hours daily, rotation frequency -- 19 r/min) was reproduced in white laboratory rats, body weight 180.0-200.0 gr. Pulmonary tissue specimens were collected after 3, 7, 10-60 days. ABB was determinate in capillary blood samples with the apparatus "Microastrup". The materials were used for general histological, electronmicroscopic and morphometric examination. The digital findings were treated with MS Excel. The earliest informative sign of appearance of surfactant dependent atelectasis and alveolar epithelium is trombocytes stasis in interaalveolar capillary lumens with plasma insudation into the depth of aerohematic barrier that is negatively reflected on the processes of ventilation and gas exchange with the tendency of development of hypercapnia and metabolic acidosis to the end (50-60 days) of the experiment. The structural basis of this state is collagen formation in aerohematic barrier tissue component.
 ...
PMID:[Changes in ultrastructure of lung aerohematic barrier and blood gas indices in long term exercise]. 1614 80

The objective of the present study was to examine the impact of early stages of lung injury on ventilatory control by hypoxia and hypercapnia. Lung injury was induced with intratracheal instillation of bleomycin (BM; 1 unit) in adult, male Sprague-Dawley rats. Control animals underwent sham surgery with saline instillation. Five days after the injections, lung injury was present in BM-treated animals as evidenced by increased neutrophils and protein levels in bronchoalveolar lavage fluid, as well as by changes in lung histology and computed tomography images. There was no evidence of pulmonary fibrosis, as indicated by lung collagen content. Basal core body temperature, arterial Po(2), and arterial Pco(2) were comparable between both groups of animals. Ventilatory responses to hypoxia (12% O(2)) and hypercapnia (7% CO(2)) were measured by whole body plethysmography in unanesthetized animals. Baseline respiratory rate and the hypoxic ventilatory response were significantly higher in BM-injected compared with control animals (P = 0.003), whereas hypercapnic ventilatory response was not statistically different. In anesthetized, spontaneously breathing animals, response to brief hyperoxia (Dejours' test, an index of peripheral chemoreceptor sensitivity) and neural hypoxic ventilatory response were augmented in BM-exposed relative to control animals, as measured by diaphragmatic electromyelograms. The enhanced hypoxic sensitivity persisted following bilateral vagotomy, but was abolished by bilateral carotid sinus nerve transection. These data demonstrate that afferent sensory input from the carotid body contributes to a selective enhancement of hypoxic ventilatory drive in early lung injury in the absence of pulmonary fibrosis and arterial hypoxemia.
 ...
PMID:Acute lung injury augments hypoxic ventilatory response in the absence of systemic hypoxemia. 1688 52

The combination of long-term hypercapnia and hypoxia decreases pulmonary vascular remodeling and attenuation of right ventricular (RV) hypertrophy. However, there is limited information in the literature regarding the first stages of acclimatization to hypercapnia/hypoxia. The purpose of this study was to investigate the effect of four-day hypoxia (10% O2) and hypoxia/hypercapnia (10% O2 + 4.4% CO2) on the protein composition of rat myocardium. Expression of the cardiac collagen types and activities of matrix metalloproteinases (MMPs) and of their tissue inhibitor TIMP-1 were followed. The four-day hypoxia changed protein composition of the right ventricle only in the hypercapnic condition; remodeling was observed in the extracellular matrix (ECM) compartments. While the concentrations of pepsin-soluble collagenous proteins in the RV were elevated, the concentrations of pepsin-insoluble proteins were decreased. Furthermore, the four-day hypoxia/hypercapnia increased the synthesis of cardiac collagen due to newly synthesized forms; the amount of cross-linked particles was not affected. This type of hypoxia increased cardiac collagen type III mRNA, while cardiac collagen type I mRNA was decreased. MMP-2 activity was detected on the zymographic gel through appearance of two bands; no differences were observed in either group. mRNA levels for MMP-2 in the RV were significantly lower in both the hypoxic and hypoxic/hypercapnic animals. mRNA levels for TIMP-1 were reduced in the RV of both the hypoxic and hypoxic/hypercapnic animals. Hypoxia with hypercapnia increased the level of mRNA (6.5 times) for the atrial natriuretic peptide (ANP) predominantly in the RV. The role of this peptide in remodeling of cardiac ECM is discussed.
 ...
PMID:Protein remodeling of extracellular matrix in rat myocardium during four-day hypoxia: the effect of concurrent hypercapnia. 1766 May 88

Respiratory dysfunction is a common complication of obesity, conferring cardiovascular morbidity and increased mortality and often necessitating mechanical ventilatory support. While impaired lung expansion in the setting of increased adipose mass and reduced central response to hypercapnia have been implicated as pathophysiological drivers, the impact of obesity on respiratory muscles-in particular, the diaphragm-has not been investigated in detail. Here, we demonstrate that chronic high-fat diet (HFD) feeding impairs diaphragm muscle function, as assessed in vivo by ultrasonography and ex vivo by measurement of contractile force. During an HFD time course, progressive adipose tissue expansion and collagen deposition within the diaphragm parallel contractile deficits. Moreover, intradiaphragmatic fibro-adipogenic progenitors (FAPs) proliferate with long-term HFD feeding while giving rise to adipocytes and type I collagen-depositing fibroblasts. Thrombospondin 1 (THBS1), a circulating adipokine, increases with obesity and induces FAP proliferation. These findings suggest a novel role for FAP-mediated fibro-adipogenic diaphragm remodeling in obesity-associated respiratory dysfunction.
 ...
PMID:Fibro-Adipogenic Remodeling of the Diaphragm in Obesity-Associated Respiratory Dysfunction. 3057 76