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)

A bolus injection of almitrine bismesylate (0.5 mg.kg-1 i.v.) in anaesthetised artificially ventilated cats caused a significantly greater increase in carotid chemosensory discharge in animals with sectioned ipsilateral ganglioglomerular sympathetic nerves in comparison with a group in which these nerves were intact. Plasma levels of almitrine were similar in both groups. Responses to hypoxia and hypercapnia post-almitrine were also bigger if the ganglioglomerular nerves were cut. Domperidone (10-50 micrograms.kg-1 i.a), a dopamine D2 receptor antagonist, greatly increaed the responsiveness of chemoreceptors to almitrine in ganglioglomerular nerve-intact preparations. Almitrine-induced chemosensory activity was unaffected by illuminating the carotid bifurcation with light from a fibre optic lamp, regardless of whether or not the ganglioglomerular nerves were cut. It is concluded that almitrine may directly or indirectly activate an efferent pathway in the ganglioglomerular nerves to cause depression of chemoreceptor activity, possibly by releasing dopamine to act at D2 dopamine receptors in the carotid body.
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PMID:Ganglioglomerular nerves influence responsiveness of cat carotid body chemoreceptors to almitrine. 252 5

Cerebral vasodilation in response to hypercapnia involves prostanoids in newborn pigs. This study examines the hypothesis that endothelial injury in vivo inhibits cerebral vasodilation and prostacyclin synthesis in response to hypercapnia, thus suggesting prostacyclin is a primary endothelium-derived vasodilating factor in newborn pig cerebral circulation. Anesthetized piglets with closed cranial windows were studied before and after injury caused by light/dye or before and after dye-only sham control. Light/dye injury was produced by injecting sodium fluorescein intravenously and passing filtered light from a mercury arc lamp through the cranial window. Ultrastructural changes to endothelium of pial vessels were produced that were characterized by surface pits, vacuolar cytoplasmic inclusions, and mitochondrial injury. After the light/dye injury, dilation to hypercapnia was absent while dilations to iloprost, isoproterenol, and sodium nitroprusside and constrictions to norepinephrine and acetylcholine were retained. Before light/dye treatment, hypercapnia increased cortical periarachnoid 6-keto prostaglandin F1 alpha concentration approximately threefold. However, after treatment, 6-keto-prostaglandin F1 alpha was not increased significantly in response to hypercapnia. These findings are consistent with the hypothesis that endothelial prostacyclin synthesis induced by hypercapnia participates in dilation of adjacent smooth muscle.
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PMID:Light/dye microvascular injury selectively eliminates hypercapnia-induced pial arteriolar dilation in newborn pigs. 751 49

Using a closed cranial window system and intravital microscopy/videometry, we studied the rat pial arteriolar (30-60 microns) responses to CO2 before and following a light/dye (L/D) endothelial injury or topical application of the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine (L-NA) or its inactive form, D-NA. L/D treatment consisted of intravenous injection of sodium fluorescein and the illumination (for 90 s) of arteriolar discrete segments on the cortical surface with light from a mercury lamp. Functional changes in pial arteriolar endothelium were characterized by evaluating responses to topical application of acetylcholine (Ach, 5 x 10(-4) M) and to intravenous (i.v.) oxotremorine (OXO, a stable blood-brain barrier permeant muscarinic agonist, 1 microgram kg-1 min-1). After the L/D injury, dilation to Ach was absent whereas dilations to the NO donor, S-nitrosoacetyl-penicillamine (SNAP, 10(-5) M) and to CO2 (5%) were unchanged (PaCO2 = 70 mm Hg). Loss of Ach response but intact SNAP response confirmed functional endothelial injury and intact smooth-muscle function. The global endothelium-dependent vasodilation induced by i.v. OXO was markedly attenuated when expanding the L/D injury field from 300 microns to 6 mm in diameter. However, the global vasodilation induced by inhalation of CO2 was still unaffected by this increase in the area of light exposure. This provides evidence that the expanded exposure was capable of impairing global vasodilation resulting from endothelium-dependent stimuli but not from inhalation of CO2. The intact CO2 response despite an endothelial dysfunction suggests that the reported NO dependence of hypercapnia-induced cerebral hyperemia in rats cannot be attributed to an endothelial NO source.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of endothelium and nitric oxide in rat pial arteriolar dilatory responses to CO2 in vivo. 792 57

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

Ocular circulation is regulated to maintain the homeostasis of retinal function in response to physiological stimulus. It is important to understand the mechanism of the regulation of ocular circulation under physiological conditions because the impairment of ocular circulation should cause severe retinal disorders. We previously investigated the physiological mechanism of ocular circulation in response to hypoxia, hypercapnia, and acute increased systemic blood pressure. In addition, it was reported that transpupillary thermotherapy might change ocular blood flow in patients with age-related macular degeneration. However, it still remains unclear whether the increased ocular tissue temperature may be associated with alteration of the ocular blood flow. Therefore, we examined the effect of ocular warming on retinal blood flow (RBF) and subfoveal choroidal blood flow (CBF) in humans. Ocular warming was induced in 10 healthy volunteers using an ocular warming lamp for 10 minutes. The RBF in the retinal artery and vein and the CBF in the foveal region were examined with a retinal laser Doppler velocimetry system and a laser Doppler flowmeter, respectively. Ocular warming increased RBF in the retinal artery and vein but decreased CBF in the foveal region. The CBF in the foveal region may contribute to maintaining a constant retinal temperature in response to ocular warming.
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PMID:[Physiological mechanism for the regulation of ocular circulation]. 1713 35