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

Retinopathy of prematurity (ROP) is a bilateral retinal disease found in premature infants born at less than 36 weeks gestation or weighing less than 1,600 g. Several recent studies have suggested a multifactorial basis for ROP development. Risk factors include apnea treated by mask or bag ventilation, repeated blood transfusions, prolonged parenteral nutrition, hypoxemia, hypercarbia, hypocarbia, and supplemental oxygen administration. Disease stages are: stage 1--demarcation line; stage 2--intraretinal ridge; stage 3--ridge plus extraretinal fibrovascular proliferation; and stage 5--total retinal detachment.
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PMID:Retinopathy of prematurity. 189 44

A high incidence of retinopathy of prematurity (ROP) was found in the very low-birth-weight infants discharged from the neonatal intensive care unit during the years 1977 to 1980, in spite of frequent monitoring of oxygen use. Although the yearly incidence of ROP in infants weighing less than 1,500 g varied between 35% to 36%, none were blind. The medical records of 65 infants with a birth weight between 501 and 1,250 g; surviving in 1979 to 1980, were reviewed in order to find risk factors for ROP. There were no significant differences between the 34 infants with ROP and the 31 infants who did not have ROP in mean birth weight or mean gestational age. Of 32 possible risk factors examined, the factors significantly associated with ROP were: apnea with mask and bag ventilation; prolonged parenteral nutrition; number of blood transfusions; and episodes of hypoxemia, hypercarbia, and hypocarbia. A highly significant association between hypocarbia and the development of severe ROP was found.
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PMID:Retinopathy of prematurity: incidence and risk factors. 640 96

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

Retinopathy of prematurity (ROP) usually occurs after a prolonged exposure to normobaric hyperoxia in newborn mammals and infants. We hypothesized that experimental ROP also could develop after acute exposures to hyperbaric oxygenation (HBO), providing that a severe and maintained retinal vasoconstriction occurred during HBO exposure. Five- to seven-day-old, Long Evans Sprague-Dawley rats were exposed for 5 h either to 5 atm abs oxygen or to 5 atm abs O2 with 190 mmHg inspired PCO2 (hypercapnia). Control rats breathed air at atmospheric pressure. Two months after exposures, rats were anesthetized, perfused intraventricularly with India ink, and retinal images were obtained. Retinal vascular density (RVD) in each image was calculated as the number of pixels in the retinal vessel area divided by the total number of pixels in the image (retinal tissue and vessels). The RVD was significantly increased from 0.0112 +/- 0.004 in the air-exposed controls to 0.0417 +/- 0.029 in the HBO-exposed rats (mean +/- SD; n = 4 in each group). HBO with hypercapnia produced a nonsignificant increase in RVD (0.0255 +/- 0.007; n = 4), reducing the HBO-induced increase in RVD by 39%. These results are consistent with the hypothesis that a sustained HBO-induced retinal vasoconstriction in newborn rats, followed by a hypoxic-ischemic injury, might result in vascular proliferation, thereby initiating ROP development on return to air. Hypercapnia does not completely prevent HBO-induced retinal vasoproliferation, probably because possible vasodilation, induced by hypercapnia, can greatly elevate retinal tissue PO2 and promote oxidative damage.
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PMID:Experimental retinopathy by hyperbaric oxygenation. 774 8

In the recent years it has been recognized that nitric oxide is an important regulator of ocular blood flow. Nitric oxide is involved in the control of basal blood flow in the choroid, optic nerve and the retina. In addition, nitric oxide mediates a number of vasodilator responses in ocular vessels to agonists such as acetylcholine, bradykinin, histamine, substance P and insulin. Nitric oxide also plays a role in hypercapnia-induced vasodilation in the choroid and is a modulator of pressure autoregulation in this vascular bed. Abnormalities of the L-arginine/nitric oxide system have been observed in a variety of ocular diseases including glaucoma, diabetic retinopathy and retinopathy of prematurity. This makes the L-arginine/nitric oxide pathway an attractive target for therapeutic interventions. Additional research is required, particularly in characterizing the role of the three nitric oxide synthase isoforms in the control of ocular perfusion, to implement this concept into the clinical management of ocular diseases.
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PMID:Role of nitric oxide in the control of ocular blood flow. 1158 19

High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence suggests a significant role for high carbon dioxide (CO(2)) tension as well. Along these lines, although ischemia is often considered to be synonymous with an oxygen deficit, it is also associated with a concomitant local elevation of CO(2) that can lead to impaired developmental and ischemic neovascularization. The mechanisms by which hypercapnia induces retinal microvascular degeneration, a critical step which precedes the subsequent proliferative preretinal neovascularization, are not known. Nitrative stress has an important role in microvascular degeneration leading to ischemia in conditions such as ROP. Hypercapnia is a facilitator of nitration in vitro. We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularization through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects. Moreover, we demonstrate that an in vivo nitrative stress associated with retinal vasoobliteration results in nitration of arachidonic acids into trans-arachidonic acids (TAAs), which can act as mediators of nitrative stress by causing microvascular degeneration by inducing expression of the antiangiogenic factor thrombospondin-1. These recent findings establish a previously unexplored means by which hypercapnia hinders efficient neovascularization and provide new insight into the molecular mechanisms of nitrative stress on microvascular injury involving TAA, and suggest new therapeutic avenues in the management of nitrative stress disorders such as in ischemic retinopathies (of prematurity and of diabetes) and encephalopathies.
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PMID:Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity. 1681 71

High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence also suggest a significant role for high levels of carbon dioxide (CO(2)). Hypercapnia is a facilitator of nitration in vitro, and nitrative stress is known to have an important role in microvascular degeneration leading to ischemia in conditions such as ROP. We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularisation through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects. Moreover, in a model of oxygen-induced retinopathy, we demonstrate that an in vivo nitrative stress associated with retinal vasoobliteration results in nitration of cis-arachidonic acids into trans-arachidonic acids (TAAs). TAAs act in turn as mediators of nitrative stress by causing microvascular degeneration by inducing expression of the anti-angiogenic factor thrombospondin-1. These recent findings establish a previously unexplored means by which hypercapnia hinders efficient neovascularisation and provide new insight into the molecular mechanisms of nitrative stress on microvascular injury involving TAA, therefore opening new therapeutic avenues in the management of nitrative stress disorders such as in ischemic retinopathies (of prematurity and of diabetes) and encephalopathies.
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PMID:[Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity]. 1802 4

Chronic neonatal lung disease (CNLD) is defined as a supplemental oxygen requirement beyond 36 weeks' postmenstrual age, with more severely affected infants requiring oxygen beyond a full-term-equivalent age. Low-flow supplemental oxygen facilitates discharge from hospital of infants with CNLD who develop hypoxia in air. There is a lack of data on the most appropriate minimum mean target oxygen saturation (Spo(2)) level. Reflecting a variety of clinical practices and infant comorbidities (frequency of oxygen desaturation, presence of pulmonary hypertension, retinopathy of prematurity, and adequacy of growth), the minimum mean target range for Spo(2) during overnight oximetry should be 93%-95%. The effect of supplemental oxygen on carbon dioxide retention should be considered before deciding on an oxygen flow. Most infants with CNLD are not ready for discharge until their supplemental oxygen requirement is < or = 0.5 litres per minute delivered through a nasal cannula. The safety of short-term disconnection from supplemental oxygen should be assessed before discharge. Assessment of oxygenation during sleep with continuous overnight oximetry or polysomnography is recommended when weaning infants from supplemental oxygen. Discontinuation of oxygen therapy is based on clinical assessments and documentation of adequate oxygenation in room air. There is limited objective evidence on which to base recommendations.
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PMID:Infants with chronic neonatal lung disease: recommendations for the use of home oxygen therapy. 1901 58

Retinopathy of prematurity (ROP) is a complex disease of the developing retinal vasculature in premature infants. Clinical manifestations range from mild, usually transient changes of the peripheral retina to severe progressive vasoproliferation, and potentally blinding retinal detachment. With better standards in premature units and with increased survival rate of low gestational age and low birth weight infants the incidence of ROP also increased. The incidence of ROP has been decreasing in developed countries over the past decade, and ROP has become potentially confined to immature neonates with birth weights less than 1000 grams in these countries. Prematurity and retinal immaturity are the major risk factors. Oxygenation, respiratory distress, apnea, bradycardia, hearth disease, infection, hypercarbia, acidosis, anemia, and the need for transfusion are thought by some to be contributory factors. All of the preterm babies with a birth weight under 1500 grams and a gestational age under 32 weeks should be followed for ROP.
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PMID:[Retinopathy of prematurity]. 1940 50