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At least 883 records · Page 49Linked to original sources
PubMed1975

Comparative pharmacologic effects of pilocarpine administered to normal subjects by eyedrops or by ocular therapeutic systems.

Normal volunteers used 1, 2, and 4% pilocarpine eyedrops, three times daily, or ocular therapeutic systems placed in the conjunctival cul-de-sac to control intraocular pressure. The systems continuously release 20 and 40 mug/hour of pilocarpine for one week. Although the amount of drug delivered to the eye from the ocular therapeutic system was one fifth that obtained from the eyedrops, the decrease of intraocular pressure was comparable. The ocular therapeutic systems produced small, constant effects on visual acuity, refractive error, and miosis that did not cause visual handicaps or require correction. The effects of eyedrops on these visual factors were large and varied and produced marked visual handicaps that were not correctable with spectacles. Despite its comparable hypotensive effect in normal subjects, continuous delivery of pilocarpine by means of an ocular therapeutic system elicits less severe side effects than pilocarpine eyedrops.

Adult↗
PubMed1984

Arecoline miosis.

Explore the source record for details and available documents.

Arecoline↗
PubMed1982

Pupillographic analysis of morphine action in the rabbit: role to the autonomic nervous system.

Pupillary response of albino rabbits were recorded using an infrared video pupillometer. The transient response to an i.v. injection of morphine (1-12 mg/kg) consists of three phases. Phase 1 is a brief mydriasis of 20 s duration. Phase 2 is a miosis that reaches a maximum within 2-4 min and is the only dose-related endpoint observed. Time-averaged pupil size is not decreased by morphine in a dose-related manner when measured 5 min after injection. Phase 3 is large amplitude fluctuation that reaches peak amplitude within 20 min and may last for several hours. Thus, dynamic pupillography reveals that the terms "miosis' and "mydriasis' may be insufficient to fully describe opiate-induced pupillary effects. All three phases are blocked by naloxone (0.1 mg/kg i.v.) and by topical pretreatment with scopolamine. These results are consistent with the theory that morphine alters pupil size by interaction with opiate receptors that are involved in the control of parasympathetic output to the iris.

Animals↗
PubMed1995

Opposite modulation by tachykinin (NK1) and CGRP receptors of sympathetic control of mouse vas deferens motility.

Electrical field stimulation of isolated mouse vas deferens elicited sympathetic twitch whose amplitude was transiently enhanced by the selective tachykinin NK1 receptor agonist, [Sar9,Met(O2)11]substance P (0.3-30 nM), but not by selective NK2 and NK3 receptor agonists. Potentiation by [Sar9,Met(O2)11]substance P was antagonized by (+/-)-CP 96,345 [(2S,3S)-cis-2-(diphenylmethyl)-N- [(2-methoxyphenyl)-methyl]-1-azabicyclo[2.2.2]octan-3-amine] (IC50 = 0.1 microM). On the other hand, electrical field stimulation-induced contractions were inhibited by calcitonin gene-related peptide, CGRP (0.1-30 nM), and this action was reduced by its antagonist, human CGRP-(8-37) (3 microM). [Sar9,Met(O2)11]substance P (3 nM) did not affect either high-K+ or noradrenaline-induced contraction, while CGRP (3 nM) significantly reduced the noradrenaline-induced motor response. Capsaicin (1 microM) inhibited sympathetic twitches, and this effect was partially antagonized by human CGRP-(8-37). In the presence of this antagonist, capsaicin induced a short-living and (+/-)-CP 96,345-sensitive twitch enhancement. These data suggest that the sympathetic control of mouse vas deferens motility can be modulated in an opposite manner by tachykinin NK1 (prejunctionally located) and by CGRP (pre- and/or postjunctionally located) receptors.

Animals↗
PubMed1995

Histamine-induced edema in the rat paw--effect of capsaicin denervation and a CGRP receptor antagonist.

Histamine is known to cause edema and excitation of small-diameter primary afferent neurons. In the present study we wanted to investigate to which extent afferent neurons participate in histamine-induced edema and, subsequently, determine possible inhibitory effects of a tachykinin NK1 receptor and CGRP receptor antagonist on the histamine response. Intraplantar injection of histamine (0.5 mumol) into the rat hind paw caused a 34% increase of paw volume. In capsaicin-denervated rats, this effect of histamine was nearly abolished. The calcitonin gene-related peptide (CGRP) receptor antagonist CGRP-(8-37), but not the tachykinin NK1 receptor antagonist SR140333, caused significant inhibition of the edema response. Further indication that CGRP can promote the histamine action was obtained in capsaicin-denervated rats, where co-injection of CGRP (0.3 pmol) increased the edema response to intraplantar histamine. In additional experiments, plasma protein extravasation in the paw skin was evaluated after close arterial infusion of histamine. Also in these experiments CGRP-(8-37), but not SR140333, significantly reduced the histamine effect. The observation that in the rat hind paw a CGRP receptor antagonist, but not a tachykinin NK1 receptor antagonist, attenuates histamine-induced vascular leakage raises the possibility that in some tissues CGRP receptor antagonists may be superior to tachykinin NK1 receptor antagonists in reducing histamine-induced neurogenic inflammatory responses.

Animals↗
PubMedDate not supplied

The "no treatment" approach to ocular hypertension.

Should patients with ocular hypertension be treated to prevent glaucomatous visual field loss? Three considerations suggest that for most patients the answer is no. First, the average risk of visual field loss in untreated ocular hypertension is small. Population surveys and prospective studies indicate that no more than about one of every nine persons with intraocular pressures higher than 20 mm Hg will develop a visual field defect. Secondly, treatment of ocular hypertension to lower intraocular pressure is unproven efficacy in preventing visual field defects. Thirdly, adverse reactions to glaucoma therapy occur frequently and are sometimes serious. Although pressure reduction may be indicated for some patients who possess certain risk factors which make them especially susceptible to glaucomatous damage, for most patients "no treatment" is the best management. Untreated patients must be observed carefully with periodic visual field and optic disc examinations.

Adult↗