Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0595921 (intraocular pressure)
 11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of topical application of neutral formaldehyde (1%) and intracameral administration of calcitonin gene-related peptide (CGRP, 0.5- or 2.0 micrograms) on the intraocular pressure (IOP), blood-aqueous barrier, pupil size, blood pressure and cyclic AMP (cAMP) content in the aqueous humour of a rabbit were studied. Topical chemical irritation with 1% formaldehyde caused a typical irritative response in the eye with a rise in the IOP, breakdown of the blood-aqueous barrier and miosis. The cAMP content in the aqueous humour was also increased (88.5 +/- 35.0 pmol ml-1, P less than 0.05) when compared with the control group (16.3 +/- 3.6 pmol ml-1). Intracameral administration of CGRP caused a rise in the IOP, breakdown of the blood-aqueous barrier and also systemic hypotension. Miosis was not observed after intracameral CGRP but an increase in the cAMP content in the aqueous humour was seen (130.5 +/- 30.3- and 158.7 +/- 48.1 pmol ml-1, both P less than 0.01, after 0.5 or 2.0 micrograms, respectively). The cAMP concentration in the aqueous humour after topical chemical irritation and intracameral CGRP correlated with the intensity of the breakdown of the blood-aqueous barrier. CGRP seems to cause most, but not all, of the ocular changes after sensory nerve stimulation elicited by topical neutral formaldehyde. Of these CGRP-induced changes, only the breakdown of the blood-aqueous barrier is related to an increase in the cAMP content in the aqueous humour. Contralateral responses after sensory nerve stimulation were similar to contralateral responses to intracameral CGRP.
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PMID:CGRP in relation to neurogenic inflammation and cAMP in the rabbit eye. 284 78

The effect of alpha-adrenergic and serotonergic (5-HT) blockers on the acute irritative response in the rabbit eye elicited by topical, neutral formaldehyde (1%), was studied. In the control animals, the peak rise in the intraocular pressure (delta IOP) after irritation was 29.5 +/- 5.7 mm Hg, and the perfusion pressure of the eye at 1 min after irritation was 50.1 +/- 2.8 mm Hg. The peak rise in the IOP was inhibited by phentolamine (alpha- and 5-HT-antagonist, delta IOP = 6.6 +/- 2.1 mm Hg, P less than 0.01), methysergide (5-HT-antagonist, delta IOP = 10.6 +/- 4.4 mm Hg, P less than 0.05), and prazosin (alpha 1-antagonist, delta IOP = 12.8 +/- 3.7 mm Hg, P less than 0.05). Perfusion pressures of the eyes were decreased after pretreatment with phentolamine or prazosin, and were 35.2 +/- 4.8 mm Hg (P less than 0.05) and 25.7 +/- 3.7 mm Hg (P less than 0.01), respectively. Perfusion pressure in the methysergide group remained unchanged (75.4 +/- 14.2 mm Hg). Yohimbine (alpha 2-antagonist) and ketanserin (5-HT2-antagonist) did not inhibit the IOP response. None of the antagonists could inhibit the miosis or disruption of the blood-aqueous barrier induced by topical neutral formaldehyde. In the contralateral eyes, the changes in the IOP, in the integrity of the blood-aqueous barrier, and also in the pupil size, were enhanced by ketanserin. The present study demonstrates the inhibitory actions of methysergide, phentolamine, and prazosin on the neurally mediated, acute irritative response in the rabbit eye. Methysergide seems to inhibit the response, probably acting via the 5-HT1-receptors. A part of the effect of phentolamine might be explained by an inhibitory action via 5-HT1-receptors. The effect of phentolamine and prazosin on the alpha 1-receptors seems to create an inhibitory action on the irritative response by lowering the perfusion pressure of the eye.
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PMID:Effect of alpha-adrenergic and serotonergic blockers on the acute irritative response in the rabbit eye. 289 93

The effects of somatostatin, cyclo(D-Trp-Lys-Thr-Phe-Pro-Phe) acetate, a somatostatin analog, neurotensin, and met-enkephalin were studied in the rabbit eye by measuring the intraocular pressure (IOP), aqueous humor protein concentration, ocular blood flow and the pupil diameter. Somatostatin or the analog injected intracamerally (10 micrograms/eye) and infused intra-arterially (0.6-4 micrograms/min) had no significant effect on the parameters studied in normal eyes. However, somatostatin and, particularly, the analog attenuated the miotic response to a standard nociceptive stimulus consisting of topical application of 1% neutral formaldehyde. The other component parts of the irritative response were not attenuated. Intracameral injection of 1-2 micrograms neurotensin caused vasodilation in the anterior segment of the eye, a slight increase in aqueous humor protein concentration, and some decrease in IOP. Intracameral injection of 1-50 micrograms met-enkephalin had no effect on the blood-aqueous barrier, IOP or the pupil diameter. Neither did this dose of met-enkephalin attenuate the miotic response to exogenous substance P. It seems likely that somatostatin and the somatostatin analog attenuate the miotic response to nociceptive stimuli by preventing the release of a substance, presumably substance P, from sensory nerves.
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PMID:Effects of somatostatin, a somatostatin analog, neurotensin and met-enkephalin in the eye with special reference to the irritative response. 290 80

The effects of sensory nerve stimulation (topical neutral formaldehyde, 1%) and intracameral injection of calcitonin gene-related peptide (CGRP) on regional ocular blood flow, intraocular pressure (IOP), the blood-aqueous barrier, pupil size, and blood pressure were studied in the rabbit. Sensory nerve stimulation elicited a typical irritative response in the rabbit eye, with vasodilation in the ciliary body (from 128 +/- 31 to 363 +/- 105 mg/min, p less than 0.05) accompanied with a breakdown of the blood-aqueous barrier, rise in the IOP, and miosis. CGRP caused similar, but not identical, changes in the eye: vasodilation in the ciliary body (from 60 +/- 14 to 258 +/- 75 mg/min, p less than 0.05), breakdown of the blood-aqueous barrier and rise in the IOP, accompanied with systemic hypotension. Miosis was not observed after CGRP. In the present study, the vasodilatory action of CGRP on the rabbit eye has been shown. This makes our understanding of the mechanism of the ocular irritative response after sensory nerve stimulation more complete. Thus, CGRP through vasodilation disrupts the blood-aqueous barrier and raises the IOP. The more intense increase in the IOP after sensory nerve stimulation than after CGRP is probably caused by a CGRP-induced vasodilation and breakdown of the blood-aqueous barrier, enhanced by a miosis-induced pupillary block.
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PMID:Effect of neurogenic irritation and calcitonin gene-related peptide (CGRP) on ocular blood flow in the rabbit. 326 39

An acute irritative response in the rabbit eye, taking the form of a rise in the intraocular pressure (IOP), miosis, and breakdown of the blood-aqueous barrier, was elicited by topical application of 1% neutral formaldehyde. The peak rise in IOP was 22.1 +/- 2.5 mmHg and occurred within 14.2 +/- 1.9 min, after which IOP returned to normal values in 45.4 +/- 5.2 min. An increased amount of i.v.-injected Evans Blue was found in the aqueous humour when injected 15 min after the irritation (119.0 +/- 21.2 micrograms/ml, compared with 2.1 +/- 1.4 micrograms/ml in intact eyes; P less than 0.001), and the protein concentration in the aqueous humour was also increased, to 11.3 +/- 1.4 mg/ml (P less than 0.001). When Evans Blue was injected 60 min after the irritation, no statistically significant difference was found from normal in the amounts (13.7 +/- 7.8 micrograms/ml) in the aqueous humour, although the protein concentration in the aqueous humour was again found to be elevated (7.9 +/- 1.6 mg/ml, P less than 0.01). Histologically, the Evans Blue was shown to leak through both the ciliary and the iris barriers at 15 min. At 60 min only occasional Evans Blue leakage was demonstrated between the nonpigmented epithelial cells and only minor fluorescence was seen in iris stroma. The histological findings were in good agreement with Evans Blue analyses in the aqueous humour. The miosis lasted over 60 min in the formaldehyde-treated eyes. After sympathectomy the rise in IOP was more rapid at the beginning of the response, suggesting greater sensitivity of the sympathectomized eyes to the irritative stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery of the blood-aqueous barrier after topical chemical irritation in the rabbit eye. 365 21

Topical chemical irritants induce an acute reaction in the eye, consisting of an increased intraocular pressure (IOP), breakdown of the blood-aqueous barrier, anterior uveal vasodilation and miosis. In the present study these effects were studied in the rabbit eye after topical application of neutral formaldehyde by measuring IOP continuously using electromanometrical equipment. The protein content of the aqueous humour was measured and miosis as well as anterior hyperemia were analyzed. Intravenously injected sodium fluorescein was used to visualize the site of the disruption of the blood-aqueous barrier in freeze-dried specimens. Iridectomies were performed to study the mechanisms of hypertension and disruption of the blood-aqueous barrier. In iridectomized rabbits the acute irritative response was very similar to that of normal eyes. Breakdown of the blood-aqueous barrier, miosis and anterior hyperemia occurred. However, the increase in IOP was only partially reduced. This indicates that a pupillary block due to the intense miosis plays a minor role in the hypertensive reaction or in the breakdown of the barrier. The effect of three autonomic receptor blocking agents: phentolamine (alpha-adrenergic antagonist), timolol (beta-adrenergic antagonist) and biperiden (cholinergic antagonist) on the irritative ocular response caused by formaldehyde was studied. Phentolamine proved to be an efficient inhibitor of the hypertensive reaction. It also effectively prevented the breakdown of the blood-aqueous barrier. Biperiden inhibited only slightly the increase in IOP caused by formaldehyde. Timolol had no significant effect. None of these three antagonists was able to prevent the miosis or hyperemia. The present findings indicate that a part of the irritative response is mediated by a phentolamine-sensitive neuronal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of autonomic receptor blockers on the ocular response to topical chemical irritation. 674 78

Evidence for the biosynthesis and release of prostaglandins and related substances in pathophysiological states of ocular tissues is reviewed and their participation in ocular injury and acute inflammation discussed. Ocular tissues are capable of generating prostaglandins from the endogenous or exogenous precursor, arachidonic acid. Prostaglandins are released into the aqueous humour in response to paracentesis, mechanical or laser injury to the iris, and in experimental immunogenic and non-immunogenic ocular inflammation. Antidromic stimulation of the trigeminal nerve, formaldehyde or nitrogen mustard-induced irritation of the eye do not cause the release of prostaglandins, nor are the responses to these stimuli inhibited by prostaglandin synthetase inhibitors. Prostaglandins in small doses administered topically or intraocularly produce some of the responses of injury and inflammation, such as hyperaemia, miosis, breakdown of the blood-aqueous barrier and rise in intraocular pressure. Also, E-type prostaglandins administered topically together with histamine (but not the individual components) cause cellular infiltration and produce oedema in conjunctival tissues. Non-steroidal aspirin-like drugs at concentrations which inhibit prostaglandin biosynthesis markedly block injury responses but have only a moderate inhibitory effect on acute inflammatory reactions of the eye. The present evidence suggests that prostaglandins are involved in some of the injury and inflammatory responses. However, recent studies indicate that the intermediates of arachidonic acid metabolism, especially hydroxy fatty acids, may play a greater role in inflammatory responses.
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PMID:Prostaglandins and inflammatory reactions in the eye. 680 89

Angiotensin converting enzyme (ACE) -inhibitors inhibit degradation of inflammatory mediators substance P (SP) and bradykinin, which may further stimulate the synthesis of prostaglandins. The resulting increase in inflammatory mediators in tissues is suggested to be the reason for the dry cough, involving sensory C-fiber activation, among patients receiving ACE-inhibitor therapy. In the present study, the effect of an ACE-inhibitor, captopril, on ocular irritative responses was studied in the rabbit. Intravenous captopril decreased markedly the blood pressure and the intraocular pressure (IOP) modestly. Topical neutral formaldehyde elicits an irritative response in the eye mediated through sensory neuropeptides SP and calcitonin gene-related peptide (CGRP). Following topical neutral formaldehyde, the increase in IOP and breakdown of the blood-aqueous barrier were inhibited by captopril, while miosis was not affected. Cyclic AMP (cAMP) content in the aqueous humour was increased by captopril, and this increase was inhibited by indomethacin. Following YAG-laser anterior capsulotomy, captopril inhibited the increase in IOP, breakdown of the blood-aqueous barrier and miosis. The present study demonstrates that use of short-term administration of captopril prior to sensory nerve stimulation or YAG laser anterior capsulotomy does not enhance the ocular responses to these stimuli in the rabbit. In the present study, captopril inhibited these responses, at least partly by decreasing the blood pressure.
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PMID:Effect of captopril on ocular irritative response to topical neutral formaldehyde and YAG-laser capsulotomy in the rabbit. 859 Feb 56

We have previously shown the presence and localization of mast cells and the intraocular effects of compound 48/80 in the rabbit eye. In the present study we have evaluated the mechanism of action of compound 48/80 using ruthenium red as a blocker of sensory axon reflexes in the rabbit eye and by measuring the intraocular pressure (IOP), the pupil size, the blood pressure, the protein and cAMP content in the aqueous humour. Topical neutral formaldehyde was used as a topical inducer of neuronally mediated response in a separate series of experiment. Intracamerally-injected ruthenium red suppressed the compound 48/80-induced elevation intraocular pressure and prevented miosis, while having little if any effect on the breakdown of the blood-aqueous barrier and on the increase in the cAMP concentration in aqueous humour. Ruthenium red also inhibited the irritative response in eyes treated with topical 1% formaldehyde. As the blood-aqueous barrier in the rabbit is an extremely sensitive system higher doses of ruthenium red causes damage of the barrier in the ruthenium red treated eyes. The results demonstrate that compound 48/80 not only has a mast cell degranulating effect but also a sensory nerve- stimulating effect.
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PMID:Intraocular effects of ruthenium red in responses to compound 48/80 and topical formaldehyde in rabbit. 892 1