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

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.
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PMID:Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue. 1065 46

Chronic hypercapnia is commonly found in patients with severe hypoxic lung disease and is associated with a greater elevation of pulmonary arterial pressure than that due to hypoxia alone. We hypothesized that hypercapnia worsens hypoxic pulmonary hypertension by augmenting pulmonary vascular remodeling and hypoxic pulmonary vasoconstriction (HPV). Rats were exposed to chronic hypoxia [inspiratory O(2) fraction (FI(O(2))) = 0.10], chronic hypercapnia (inspiratory CO(2) fraction = 0.10), hypoxia-hypercapnia (FI(O(2)) = 0.10, inspiratory CO(2) fraction = 0.10), or room air. After 1 and 3 wk of exposure, muscularization of resistance blood vessels and hypoxia-induced hematocrit elevation were significantly inhibited in hypoxia-hypercapnia compared with hypoxia alone (P < 0.001, ANOVA). Right ventricular hypertrophy was reduced in hypoxia-hypercapnia compared with hypoxia at 3 wk (P < 0.001, ANOVA). In isolated, ventilated, blood-perfused lungs, basal pulmonary arterial pressure after 1 wk of exposure to hypoxia (20.1 +/- 1.8 mmHg) was significantly (P < 0.01, ANOVA) elevated compared with control conditions (12.1 +/- 0.1 mmHg) but was not altered in hypoxia-hypercapnia (13.5 +/- 0.9 mmHg) or hypercapnia (11.8 +/- 1.3 mmHg). HPV (FI(O(2)) = 0.03) was attenuated in hypoxia, hypoxia-hypercapnia, and hypercapnia compared with control (P < 0.05, ANOVA). Addition of N(omega)-nitro-L-arginine methyl ester (10(-4) M), which augmented HPV in control, hypoxia, and hypercapnia, significantly reduced HPV in hypoxia-hypercapnia. Chronic hypoxia caused impaired endothelium-dependent relaxation in isolated pulmonary arteries, but coexistent hypercapnia partially protected against this effect. These findings suggest that coexistent hypercapnia inhibits hypoxia-induced pulmonary vascular remodeling and right ventricular hypertrophy, reduces HPV, and protects against hypoxia-induced impairment of endothelial function.
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PMID:Chronic hypercapnia inhibits hypoxic pulmonary vascular remodeling. 1066 61

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

Cor pulmonale is defined as "hypertophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, as congenital heart disease". Pulmonary hypertension is a frequent hemodynamic complication associated with a wide variety of respiratory systems disorders whose only common physiologic abnormalities are alveolar hypoxia and consequent arterial hypoxemia of longterm duration. The sustained elevation in pulmonary arterial hypertension is thought to be mediated through two pathophysiologic vascular mechanism: 1) persistent vasoconstriction and 2) vascular structural remodeling. The combination of these processes causes vascular luminal narrowing and vessel obliteration that reduce pulmonary vascular surface area to the critical degree necessary for the development of the pulmonary hypertension. Cor pulmonale may be difficult to diagnose, particularly early in its course, when they symptoms manifested may be interpreted as representing progression of an underlying pathophysiological state, such as chronic obstructive airways disease. The treatment of cor pulmonale is directed toward reversing the pathogenetic process that can be directly treated, while at the same time relieving the hypoxemia, hypercapnia or acidosis. At present long-term oxygen therapy is the best treatment for pulmonary hypertension. Heart failure in cor pulmonale is usually transient once the initiating mechanism is controlled. The usual therapeutic measures for heart failure apply: a low-salt regimen, and diuretics.
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PMID:[Chronic cor pulmonale]. 1114 67

Meconium Aspiration Syndrome (MAS) is a leading cause of respiratory distress in the newborn. Antenatal diagnosis of meconium stained amniotic fluid and fetal distress is important to reduce morbidity and mortality in the neonates. Amnioinfusion of saline and tracheal suctioning of meconium are preventive interventions. Babies with MAS who continue to have respiratory distress need to be put on conventional ventilators. Increasing hypoxia, hypercarbia and barotrauma warrants changing to high frequency oscillatory ventilation. Pulmonary hypertension is an important complication which should be promptly recognized. Nitric oxide therapy used with high frequency ventilation has improved the outcome of babies with severe MAS and pulmonary hypertension. Some of these babies who continue to worsen clinically need to be put on ECMO circuit. Surfactant infusion in babies with MAS has been shown to improve gas exchange, resolve pulmonary hypertension and decrease oxygenation index. Total and partial liquid ventilation with perflurocarbon improves oxygenation, increases lung expansion and increases pulmonary blood flow in model studies of animals with MAS. Surfactant infusion and liquid ventilation are newer promising modes of therapeutic interventions in babies with severe MAS.
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PMID:Advances in management of meconium aspiration syndrome. 1121 85

There are currently two surgical therapies aimed at crippling, end-stage emphysema: lung transplantation and lung volume reduction surgery (LVRS). Unfortunately, most emphysema patients are poor candidates for any surgical intervention. The authors favor a meticulous selection process in which indications and contraindications are considered and the best solution is devised for each patient. Patients with ideal circumstances for LVRS--hyperinflation, heterogeneous distribution of disease, FEV1 of more than 20%, and normal PCO2--are offered LVRS. Patients with diffuse disease, low FEV1, hypercapnia, and associated pulmonary hypertension are directed toward transplantation. LVRS has not been a satisfactory option for patients with a1-antitrypsin deficiency, and we prefer a transplant in most of these patients. With these considerations, we find that few patients are serious candidates for both procedures. Combinations of lung volume reduction and lung transplantation, simultaneously or sequentially, are possible but rarely necessary.
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PMID:Lung transplantation versus lung volume reduction as surgical therapy for emphysema. 1133 27

Sleep apnea (intermittent periods of hypoxia with or without hypercapnia) is associated with systemic hypertension and increased mortality from cardiovascular disease, but the relationship to pulmonary hypertension is uncertain. Previous studies on intermittent hypoxia (IH) in rats that demonstrated pulmonary hypertension utilized relatively long periods of hypoxia. Recent studies that utilized brief periods of hypoxia have conflicting reports of right ventricular (RV) hypertrophy. In addition, many studies have not measured pulmonary hemodynamics to asses the severity of pulmonary hypertension in vivo. Given the increasing availability of genetically engineered mice and the need to establish a rodent model of IH-induced pulmonary hypertension, we studied the effect of IH (2-min cycles of 10% and 21% O2, 8 h/day, 4 wk) on wild-type mice, correlating in vivo measurements of pulmonary hypertension with RV mass and pulmonary vascular remodeling. RV systolic pressure was increased after IH (36 +/- 0.9 mmHg) compared with normoxia (29.5 +/- 0.6) but was lower than continuous hypoxia (44.2 +/- 3.4). RV mass [RV-to-(left ventricle plus septum) ratio] correlated with pressure measurements (IH = 0.27 +/- 0.02, normoxia = 0.22 +/- 0.01, and continuous hypoxia = 0.34 +/- 0.01). Hematocrits were also elevated after IH and continuous hypoxia (56 +/- 1.6 and 54 +/- 1.1 vs. 44.3 +/- 0.5%). Evidence of neomuscularization of the distal pulmonary circulation was found after IH and continuous hypoxia. We conclude that mice develop pulmonary hypertension following IH, representing a possible animal model of pulmonary hypertension in response to the repetitive hypoxia-reoxygenation of sleep apnea.
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PMID:Selected Contribution: Pulmonary hypertension in mice following intermittent hypoxia. 1135 19

Hypoxic pulmonary vasoconstriction is a self-modulatory mechanism matching local blood flow to local alveolar ventilation. In pathological conditions, it may occur as an acute episode or as a sustained response with vascular remodeling and pulmonary hypertension. Chronic generalized alveolar hypoxia occurs in populations living at high altitude, in human disease states associated with decreased ventilation, or progressive lung destruction. Persistent hypoxic vasoconstriction and the associated vascular structural remodeling are the main mechanisms of the sustained pulmonary hypertension, although other factors, including secondary polycythemia, hypercapnia and increased airways resistance may be involved. Understanding of these mechanisms has increased rapidly and may result in the near future in specific treatment aimed at reversing the structural remodeling and matrix deposition in pulmonary arteries.
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PMID:[Chronic hypoxic pulmonary hypertension]. 1141 Nov 33

The authors present results of group of 13 neonates treated with high frequency positive pressure ventilation (HFPPV) with high positive end-expiratory pressure (PEEP) for severe respiratory failure. The ventilatory protocol was based on the following principles: a) higher mean airway pressure (MAP) to achieve adequate oxygenation, b) MAP titrated mainly with PEEP, c) fraction of inspired oxygen (FiO2) below 0.6, d) small tidal volumes 3-6 ml/kg, e) ventilatory rates to achieve normocapnia in newborns with persistent pulmonary hypertension and to allow permissive hypercapnia in others. During HFPPV, the maximum values for respiratory rate, PEEP, MAP and peak inspiratory pressures (PIP), the incidence of airleak and the need for inotropic support were recorded. The values for arterial partial pressure of oxygen (paO2), FiO2, paO2/FiO2 and MAP during conventional ventilation and 30 minutes after initiation of HFPPV were statistically analyzed. paO2 increased from 8.0 kPa (3.3-10.4) to 11.8 kPa (7.3-16.2, p < 0.001) and paO2 (torr)/FiO2 increased from 62.2 (24.7-101.2) to 157.5 (62.2-275.2, p < 0.001) 30 minutes after institution of HFPPV when MAP was increased from 11.8 cmH2O (9-13.8,) to 17.2 H2O (14.8-22.2) p < 0.001. This allowed turning down FiO2 from 1 (0.6-1) to 0.6 (0.4-1 p < 0.001). Maximal ventilatory rates used were in average 60/min (50-105), PEEP 8 cmH2O (6-10), PIP 30 cmH2O (26-45), MAP 18.8 cmH2O (14.8-22.2). Air leak did not occur in any patient. Catecholamines were used in 8 patients. The duration of ventilatory support lasted in average 6 days (2-18). All patients were successfully extubated. 5 of them required nasal continuous positive airway pressure (14 hours--7 days). (Tab. 3, Fig. 3, Ref. 19.)
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PMID:[High-frequency pressure ventilation with high positive end-expiratory pressure in the treatment of respiratory failure in neonates]. 1143 1

Because sensitivity of equine pulmonary vasculature to endogenous as well as exogenous nitric oxide (NO) has been demonstrated, we examined whether endogenous NO production plays a role in exercise-induced arterial hypoxemia. We hypothesized that inhibition of NO synthase may alter the distribution of ventilation-perfusion mismatching, which may affect the exercise-induced arterial hypoxemia. Arterial blood-gas variables were examined in seven healthy, sound Thoroughbred horses at rest and during incremental exercise protocol leading to galloping at maximal heart rate without (control; placebo = saline) and with N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (20 mg/kg iv). The experiments were carried out in random order, 7 days apart. At rest, L-NAME administration caused systemic hypertension, pulmonary hypertension, and bradycardia. During 120 s of galloping at maximal heart rate, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, hyperthermia, and acidosis occurred in the control as well as in NO synthase inhibition experiments. However, statistically significant differences between the treatments were not found. In both treatments, exercise caused a significant rise in hemoglobin concentration, but the increment was significantly attenuated in the NO synthase inhibition experiments, and, therefore, arterial O(2) content (Ca(O(2))) increased to significantly lower values. These data suggest that, whereas L-NAME administration does not affect pulmonary gas exchange in exercising horses, it may affect splenic contraction, which via an attenuation of the rise in hemoglobin concentration and Ca(O(2)) may limit performance at higher workloads.
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PMID:Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses. 1150 5


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