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)

Restriction of both oxygen influx to the cornea and carbon dioxide efflux from the cornea by contact lenses results in adverse tissue changes. We measured the extent of hypoxia and hypercapnia at the corneal surface of 10 human volunteers during static, dynamic (blinking), and closed-eye wear of hydrogel and nonhydrogel contact lenses of different gas transmissibilities. During open-eye wear, hypoxia and hypercapnia are lower beneath lenses of higher oxygen and carbon dioxide transmissibilities, respectively (p less than 0.001). Blinking plays a significant role in alleviating corneal hypoxia (p less than 0.05), but not hypercapnia, during lens wear. In the absence of lenses, the gaseous tensions at the anterior corneal surface during eye closure were: pO2 = 37.4 +/- 20.9 mm Hg and pCO2 = 39.3 +/- 3.1 mm Hg. Closed-eye lens wear resulted in greater levels of hypoxia and hypercapnia that were directly correlated with lens transmissibility (p less than 0.001). These data form the basis of models for predicting adverse tissue changes during contact lens wear and suggest prophylactic and therapeutic clinical strategies for alleviating lens-induced hypoxia and hypercapnia.
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PMID:Corneal hypoxia and hypercapnia during contact lens wear. 211 89

Contact lens wear induces a wide spectrum of changes in the appearance and function of the cornea. The most salient effect of lens wear is the hypoxically induced reduction in the rate of metabolic activity of the corneal epithelium and its sequellae. Other important alterations to corneal health associated with contact lens wear may be caused by antigenic and toxic stimuli, mechanical forces, osmotic effects and carbon dioxide retention. Perhaps the most important task facing the contact lens clinician is to distinguish between an acceptable state of physiological modification and an anomalous or pathological state of hypofunction. In this article, we review the assortment of corneal changes primarily on the basis of the causative agents and time scale with reference to the physical and chemical processes leading to the observed signs or symptoms. This procedure allows a strong foundation for understanding the etiology and management principles for the variety of effects that contact lenses may have on the cornea.
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PMID:Corneal pathophysiology with contact lens wear. 220 28

Thick, 0.34 mm, 38% water hydrogel lenses were fitted, under a pressure patch, to one eye of 18 type I diabetic patients (aged 18-40 years) to assess the acute response to hypoxia and hypercapnia; the response was compared with that in 18 healthy, aged-matched non-diabetic subjects; the closed-eye lens wear was started mid-morning. Pre-lens wear assessments were made of acuity, intraocular pressure (IOP), central corneal thickness (CCT) and corneal appearance by biomicroscopy. The mean duration of the diabetes was 13 +/- 7 years and the average fasting blood glucose was 8.7 +/- 3.3 mMl-1. Baseline CCT values were marginally greater in diabetic patients (600 +/- 33 microns) compared with a group of non-diabetic control subjects (584 +/- 26 microns; P > 0.5). A 7.7 +/- 2.1% increase in CCT was measured after 3 h lens wear in the diabetic patients while an average 10.6 +/- 2.4% increase in CCT was measured in the control subjects (P < 0.05). The recovery of corneal thickness to baseline values in diabetic patients was slower (at 44.8 +/- 2.0% per hour) than the control subjects (53.9 +/- 2.1 per hour; P < 0.05) although recovery of corneal thickness occurred in both groups within 2.5-3h. IOP values (non-contact tonometry) were higher in the diabetic patients than in the controls (14.5 +/- 2.9 vs 12.4 +/- 1.7 mmHg; P < 0.01). Overall, those corneas with greater baseline CCT values tended to swell less than those with lower baseline CCT values (r = 0.582). Positive correlations were also found between corneal thickness and IOP and blood glucose. The diabetic patients thus tended to have slightly thicker corneas (but this could be related to blood glucose or IOP rather than true corneal disease) and also had corneas that tended to swell less with a contact lens stress test (but this could be constitutively due to the slight oedema already present). The different corneal response in diabetic patients may thus be the result of physical determinants such as initial oedema and IOP and not the result of a disease of the cornea itself.
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PMID:Corneal swelling and recovery following wear of thick hydrogel contact lenses in insulin-dependent diabetics. 766 21

It has been assumed that contact lens wear (CLW) may induce stromal acidosis, which is a result of corneal hypoxia and the accumulation of CO2 (hypercapnia) at the tear-lens interface. However, it has not been directly shown whether hypoxia and hypercapnia are the only causes of CL-Induced corneal acidification. In this study, we provide preliminary data about the relative contributions of hypercapnia and hypoxia to CL-induced stromal acidification by monitoring pH while the cornea was exposed to a hyperbaric oxygen atmosphere. This paradigm minimized if not eliminated the pH effects of lens-induced hypoxia on all but one subject without altering the pH effect of hypercapnia. Seven subjects were fitted with hydrogel lenses; 5 with low O2 transmissibility (Dk/LO2 = 14.0 x 10(-9) (cm/s) (ml O2/[ml x mm Hg)]), and 2 with medium O2 transmissibility (Dk/LO2 = 17.2 x 10(-9) (cm/s) (ml O2/[ml x mm Hg])) lenses. After lens insertion, modified goggles were fitted to control the corneal environment by exposing 1 eye to 20%O2 and 80%N2 (air), and the contralateral eye to 80%O2 and 20%N2 (hyperbaric O2). Corneal thickness (CT) was measured before CL insertion and over 120 min of wear. We assumed that corneal hypoxia was present if CT increased during the test period. Stromal pH was measured using a slitlamp fluorophotometer before lens insertion and at 20-min intervals for a total of 80 min. After 80 min of wearing the low Dk/L lens under hyperbaric exposure, 4 of 5 subjects showed reduced pH (mean delta pH = 0.23 +/- 0.05) and no increase in CT, suggesting that only hypercapnia was contributing to acidosis. For the same lens, but with exposure to air, 4 of 5 subjects showed a larger drop in pH (mean delta pH = 0.62 +/- 0.48) compared to hyperbaric exposure and an increase in CT, indicating that both hypoxia and hypercapnia reduced pH. Subjects wearing the medium Dk/L lens showed a small but equal drop in pH under both air and hyperbaric conditions without changes in CT, suggesting that only hypercapnia was contributing to acidosis. These preliminary results suggest that both mechanisms contribute to the pH shift accompanying CLW and that the contribution of hypercapnia is approximately 30%. Finally, the effects of hypercapnia and hypoxia are dependent on individual metabolic requirements and the transmissibility of the lens to O2 and CO2.
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PMID:Effects of hypoxia and hypercapnia on contact lens-induced corneal acidosis. 872 19

The literature is reviewed concerning the pathophysiologic effects of contact-lens wear, the microbiology of contact-lens wear, the change in microflora with contact-lens wear, the contamination of contact lenses and contact-lens products, patient compliance, and corneal interaction with the contact lens. Hypoxia and hypercapnia are the most significant changes in the cornea as a result of contact-lens wear. Changes take place in the conjunctival flora in patients with contact lenses. Compliance of patients and contamination of contact lenses and contact-lens products are significant risk factors. The corneal interaction with the contact lens can overwhelm the protective mechanisms of the cornea, increasing the ability of microbes to adhere to the cornea and progress to microbial keratitis. Some of the factors associated with microbial keratitis are modifiable and should stimulate the contact-lens industry to develop better contact lenses and contact lens products and also permit ophthalmologists to obtain better informed consent from their patients.
Cornea 1997 May
PMID:Contact lens-related microbial keratitis: Part II: Pathophysiology. 914 96

Contact lenses can induce changes in the epithelium, stroma and endothelium of the cornea, all of which can be observed clinically using the slit-lamp biomicroscope. These complications include epithelial microcysts, vacuoles and staining, stromal oedema and vascularization, and endothelial polymegethism and blebs. Each complication can be attributed to one or more aetiological factors such as hypoxia, hypercapnia, tissue acidosis, trauma, hypersensitivity and toxicity. This review outlines the way in which these complications manifest clinically, and consideration is given to management strategies and likely prognoses. Early detection of these conditions and appropriate action can usually prevent more serious ocular complications.
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PMID:Non-inflammatory corneal complications of contact lens wear. 1630 57

Laser speckle contrast imaging (LSCI) offers a cost-effective means to image blood flow in vivo. However, it is not commonly used to image rodent retinas because of the challenges associated with imaging through the curved cornea and delivering light through the highly scattering lens. A solution to overcome these problems by using LSCI in conjunction with an endoscope to obtain high spatiotemporal blood flow images is described. Its utility is demonstrated by imaging blood flow changes in rat retinas using hyperoxic, hypercapnic, and visual (flicker) stimulations. Hypercapnia increases blood flow, hyperoxia decreases blood flow, and visual stimulation increases blood flow in the retina relative to basal conditions. The time-to-peak of the LSCI response to visual stimulation is also measured. This approach may prove useful to investigate dysregulation in blood flow-evoked responses in retinal diseases and to evaluate treatment strategies in rodents.
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PMID:Laser speckle contrast imaging of blood flow in rat retinas using an endoscope. 2406 47