Synaptic organization in the oculomotor nucleus.
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Animals↗
Biomedical subjects
T Gherezghiher
Publications and source records attributed to T Gherezghiher.
Histologic study of a neodymium-YAG laser sclerostomy.
A glaucoma filtering procedure was performed with the YAG laser in an eye to be enucleated for malignant melanoma. Scanning electron microscopic examination shows the extent and position of the incision and the effects of the procedure on the cornea. To our knowledge, this article represents the first report of complete perforation of the sclera in a living human eye with the use of a laser alone.
Cornea↗
Neodymium-YAG laser sclerostomy in primates.
A one-stage sclerostomy procedure was performed "noninvasively" in four cynomolgus monkeys solely with the neodymium-YAG laser. The neodymium (Nd)-YAG laser was focused, for the most part, a few diopters behind the focus of the helium-neon aiming beam. This enabled optical breakdown to occur entirely within the sclera to produce a perforating micropuncture of the scleral tissue. Two monkeys were treated with higher energy (23 and 24 joules) and two were treated at lower energy levels (12 and 14 joules). An immediate reduction of intraocular pressure in the treated eye was associated with a significant increase in outflow facility. The sclerostomy remained patent for more than 180 days, as determined by tonography and histologic examination. Scanning electron microscopic examination of the cornea revealed no significant damage to the central cornea or to tissue adjacent to the visual axis in any of the treated eyes. However, there was some endothelial cell loss at the site of the laser treatment at the peripheral cornea and in the area immediately posterior to the incision; there was also a focal break in Descemet's membrane.
Animals↗
Studies on the mechanism of clonidine-induced mydriasis in the rat.
Intravenous administration of clonidine hydrochloride (3-100 micrograms/kg) produced a dose-dependent pupillary dilation in anaesthetized rats. All experiments were carried out in rats in which vagosympathetic nerve trunks were sectioned bilaterally at the cervical level. Clonidine-induced mydriasis was present only in those preparations having intact parasympathetic neural tone to the iris. Depletion of CNS monoamines by more than 95% with reserpine (5 mg/kg) and alpha-methyl-para-tyrosine (2 X 300 mg/kg) failed to alter the dose-response relation to clonidine. Pretreatment with the alpha-2-adrenoceptor antagonist, yohimbine hydrochloride (1.5 mg/kg), produced about a 10-fold shift to the right in the pupillary dose-response curve to clonidine. Yohimbine administered after the highest dose of clonidine also antagonized the mydriatic response. The above results suggest that clonidine acts on CNS post-synaptic alpha-2-adrenoceptors to produce mydriasis by withdrawal of parasympathetic neural tone to the iris. In an attempt to assess the physiological substrate(s) involved, mydriatic responses, due to parasympatho-inhibition, were evoked by electrical stimulation of ascending (sciatic nerve and medullary) and descending (hypothalamic) pathways. Yohimbine (0.3 and 1.0 mg/kg) produced a dose-dependent inhibition of the pupillary dilation evoked by stimulation of the sciatic nerve and medullary loci, whereas these doses of yohimbine failed to alter the dilation in response to hypothalamic stimulation. Similarly, monoamine depletion greatly antagonized the pupillary dilation elicited by sciatic nerve and medullary stimulation without significantly affecting mydriasis due to hypothalamic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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Ocular effects of adrenergic stereoisomers in the rabbit.
Because of the need to develop ocular hypotensive agents with low incidence of side effects, the dextrorotatory enantiomers of adrenergic agents have prompted some attention. In the present study, the relative potency and efficacy of various adrenergic stereoisomers with respect to their ocular hypotensive and mydriatic effects have been determined after topical administration to conscious rabbits. The relative order of potency was found to be, iris: 1-epinephrine much greater than d-epinephrine congruent to 1-norepinephrine congruent to dl-alpha-methyl-norepinephrine greater than dl-alpha-methyl-epinephrine greater than d-norepinephrine; intraocular pressure (IOP): l-epinephrine greater than dl-alpha-methyl-epinephrine greater than d-epinephrine greater than dl-alpha-methyl-norepinephrine greater than d-norepinephrine congruent to 1-norepinephrine. The pupil and the initial ocular hypertensive responses clearly demonstrated the phenomenon of stereoselectivity of adrenergic stimulants, in that the 1-form was relatively more potent than the d-form. However, such order of potency does not seem to hold for IOP. The apparent discrepancy and reversal of order of potency for IOP responses may be related to the hypothesis that the net ocular hypotensive effect of adrenergic agents is the summation of the initial hypertension and the delayed hypotension produced by these agents. It is anticipated that the results of the present study may improve our understanding of ocular pharmacology of adrenergic stereoisomers. The ability to separate the dose-response profiles of pupillary and IOP effects of these agents may have potential therapeutic significance and thus warrants further investigation in other species.
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Quantitative assessment of ocular norepinephrine concentration in the rabbit using liquid chromatography with electrochemical detection.
An assay technique that utilizes liquid chromatography with electrochemical detection to determine the norepinephrine (NE) concentration of the rabbit aqueous humor (AH) and iris-ciliary body (ICB) is discussed. NE concentration was monitored in control preparations as well as in experiments involving stimulation of the cervical sympathetic nerve (CSN) or 24 h following extirpation of the superior cervical ganglion. In 15 control rabbits, the baseline AH NE concentration was determined to be 7.2 and 7.8 ng/ml in the left and right eyes, respectively. Prolonged unilateral electrical stimulation of the CSN increased the AH NE concentration to 59.0 +/- 1.2 ng/ml on the stimulated side. Pretreatment with cocaine (12.5 mg/kg) and subsequent stimulation of the CSN increased the NE in the AH to 93.7 +/- 1.3 ng/ml on the stimulated side, and raised the baseline AH NE of the control (non-stimulated) side to 25.9 +/- 5.0 ng/ml. The baseline concentration of NE in the ICB was 5.4 +/- 0.8 micrograms/g. 24 h after a unilateral removal of the superior cervical ganglion, the NE content of the ICB was depleted by more than 90% in the ganglionectomized eye with no apparent change in the level of NE in the AH. The accurate analysis of catecholamines in the AH, ICB and other parts of the eye may be useful in providing information as to the extent of innervation and the possible role of sympathetic nerve supply in the overall control of AH dynamics.(ABSTRACT TRUNCATED AT 250 WORDS)
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Design of new contact lens for YAG laser filtering procedures.
A contact goniolens has been developed specifically for YAG laser filtering procedures both for use in unblocking failed surgical filtering procedures and for performing two-stage or one-stage YAG filtering procedures. The design concentrates the YAG energy and maintains a constant small angle with the cornea.
Contact Lenses↗
Acute intraocular pressure elevation produced by argon laser trabeculoplasty in the cynomolgus monkey.
The short-term effect of argon laser trabeculoplasty (ALT) was studied in a nonhuman primate model. The ALT treatment produced a consistent intraocular pressure elevation in the treated eye for eight hours. A statistically significant indomethacin-resistant increase in aqueous humor protein concentration was also observed. Morphologic observations using light microscopy and scanning and transmission electron microscopy revealed evidence of a fibrinous material covering the trabecular openings four hours after ALT. Cells and tissue debris appeared to be trapped in this fibrinlike net and may be the cause of the acute rise in IOP. Twenty-eight hours after ALT, the fibrin net was shown to be discontinuous, with fewer cells and less debris present. These acute morphologic alterations were not seen in control eyes or the laser-treated eyes observed later.
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Experimental YAG laser sclerostomy.
A Q-switched neodymium-YAG laser was used to produce a corneoscleral perforation in human cadaver eyes. A through-and-through incision could be created solely with the YAG-laser at peak pulse energies of 16 millijoules (mJ). The minimal total energy required for perforation was 3,312 mJ. However, "optimal" perforation, producing splitting along natural scleral cleavage planes, required 26,676 mJ. Scanning electron microscopy showed the perforations to be clean holes with little debris.
Cornea↗
Ultrastructural and pharmacologic studies on laser-induced glaucoma in primates and rabbits.
Sustained high intraocular pressure resulting in optic nerve cupping and loss of ganglion cells was produced in five rhesus monkeys and eight pigmented rabbits by applying argon laser energy to the trabecular meshwork. In addition, the rabbits manifested buphthalmus. Flow of carbon particles subsequently injected into the anterior chamber was obstructed at the trabecular meshwork by a wound-healing response that closed the intratrabecular spaces. Besides this sustained high intraocular pressure as a result of late scarring, an acute hypertensive response was seen in all rabbits which may correspond to the acute hypertension seen after laser trabeculoplasty in humans. The acute hypertensive response could be only partially blocked by prostaglandin inhibitors and we believe that prostaglandins are not primarily responsible for this effect. Medications known to lower intraocular pressure were systematically tested in both glaucoma models.
Animals↗
CNS adrenergic inhibition of parasympathetic oculomotor tone.
Inhibition of parasympathetic neural tone to the iris was produced by electrical stimulation of the afferent sciatic nerve, medullary reticular formation, and posterior hypothalamus in anesthetized cats in which only the parasympathetic nerves to the eye were intact. Stimulation of all 3 sites of activation produced a graded pupillary dilation and reduction of tonic nerve activity in the short ciliary nerves. Intravenous administration of the alpha-2-adrenoceptor antagonist, yohimbine hydrochloride, (0.03-1.0 mg/kg) produced a dose-dependent antagonism of the mydriasis elicited by activation of the ascending (sciatic nerve and medullary) mechanisms but did not block the pupillary dilation evoked by stimulation of the system descending from the hypothalamus. This differential action of yohimbine was confirmed directly by means of nerve recordings taken from the parasympathetic nerve to the eye. Depletion of CNS monoamines with reserpine and alpha-m-p-tyrosine reduced the norepinephrine concentration of the medulla and midbrain by 95% and 97%, respectively. In these depleted preparations, stimulation of the hypothalamus still produced the characteristic mydriasis and inhibition of parasympathetic tonic activity whereas activation of ascending mechanisms (sciatic or medullary) were no longer effective in producing these effects. Taken together, these results suggest that ascending parasympatho -inhibition is mediated by a monoamine (probably norepinephrine) and that inhibition descending from the hypothalamus is mediated by a non-monoaminergic mechanism.
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Alpha-methyl-DOPA induced mydriasis in the cat. Relationship between pupillary response and the oculomotor perfusate concentration of methyldopa and its metabolites.
In pentobarbital anaesthetized cats, intravenous administration of 30 mg/kg, alpha-methyl-DOPA produced mydriasis that reached a maximum plateau in 2--2.5 h. The oculomotor nucleus was perfused with saline using a push-pull cannula system chronically implanted over the nucleus. Perfusate samples were collected and subsequently analyzed by liquid chromatography with electrochemical detection (LC-EC). Alpha-methyl-DOPA administration resulted in a gradual build up of alpha-methyl-noradrenaline to approximately 32 mumoles over the 3 h sampling period. In contrast, the concentration of alpha-methyl-dopamine was below the detection level for the first 90 min with peak levels of less than 6 mumoles after 3 h. A linear regression analysis demonstrated a negative correlation (R = 0.90) between the pupil size and the perfusate concentration of alpha-methyl-DOPA and a positive correlation for both alpha-methyl-dopamine and alpha-methyl-noradrenaline (R = 0.88 and 0.94 respectively). Pretreatment with the DOPA-decarboxylate inhibitor, 3-hydroxy-benzyl-hydrazine (NSD-1015; 25 mg/kg, i.p.) completely blocked the mydriatic response to alpha-methyl-DOPA, with neither alpha-methyl-dopamine nor alpha-methyl-noradrenaline reaching detectable levels in the oculomotor perfusate. After treatment with the dopamine-beta-hydroxylase inhibitor, bis (4-methyl-homopiperazinyl thiocarbonyl) disulfide (FLA-63; 2.5 mg/kg, i.p.) there was a significant accumulation of alpha-methyl-dopamine when compared to that obtained in the alpha-methyl-DOPA controls but with no apparent alpha-methyl-dopamine related pupillary dilation. However, the correlation between alpha-methyl-noradrenaline concentration and the increase in the diameter of the pupil was maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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Effects of corticosteroid pretreatment on argon laser trabeculoplasty.
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Animals↗
RO 15-1788 selectively reverses antagonism of pentylenetetrazol-induced discriminative stimuli by benzodiazepines but not by barbiturates.
The specificity of ethyl 8-fluro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo (1,5-a) (1,4) benzodiazepine-3-carboxylate (RO 15-1788) in reversing the effectiveness of diazepam and des-methylclobazam, but not of pentobarbital, in antagonizing discriminative stimuli produced by pentylenetetrazol is described. Male hooded rats were trained to discriminate pentylenetetrazol-induced interoceptive discriminative-stimuli (IDS) in a two-lever choice paradigm on an FR10 schedule of food reinforcement. These IDS pharmacologically model verbal report of anxiogenic activity in humans. Diazepam (1,4 benzodiazepine), des-methylclobazam (1,5 benzo-diazepine), and pentobarbital antagonized pentylenetetrazol-IDS. RO 15-1788 neither generalized to nor antagonized pentylenetetrazol-IDS. It also did not cause convulsions in pentylenetetrazol sensitized rats at doses up to 40 mg/kg. It did, however, antagonize the action of diazepam (10 mg/kg) as well as that of des-methylclobazam (160 mg/kg) but not that of pentobarbital. These data suggest that RO 15-1788 is not an anxiomimetic, anxiolytic or a convulsant drug, but it is a specific and effective antagonist of anxiolytic action of benzodiazepines.
Animals↗
Studies on the mechanism of methyl-dopa-induced mydriasis in the cat.
Alpha-methyl-Dopa (10-100 mg/kg, i.v.) produced a dose-dependent mydriasis in cats anaesthetized with pentobarbital (30 mg/kg, i.p.). The onset was gradual, reaching a maximum plateau in 2-2.5 h. Intracerebroventricular administration of 1 or 3 mg of alpha-methyl Dopa (MD) also produced pupillary dilation with a similar time course. These dosages were without effect when given intravenously. Pretreatment with the alpha 2-adrenoceptor antagonist, yohimbine (0.5 mg/kg i.v.), blocked the pupillary response to MD. The alpha 1-adrenoceptor antagonist, prazosin (1.0 mg/kg. i.p.), was ineffective. Selective enzymatic blockade with 3-hydroxy-benzyl-hydrazine (NSD-1015; 25 mg/kg, i.p.), a Dopa-decarboxylase enzyme inhibitor, as well as with bis (4-methyl-homopiperazinyl-thiocarbonyl) disulfide (FLA-63; 2.5 mg/kg, i.p.), a dopamine-beta-hydroxylase blocker, prevented the mydriatic effect of MD. These results support the hypothesis that MD produces a clonidine-like, CNS mediated mydriasis in the cat, primarily by action of its metabolite alpha-methyl-noradrenaline acting on alpha 2-adrenoceptors.
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Clonidine mydriasis in the rat.
Pupillary responses to clonidine (3--100 micrograms/kg, i.v.) and epinephrine (1--30 micrograms/kg, i.v.) were observed in anesthetized rats. Clonidine caused a dose-dependent mydriasis which was effectively antagonized by pretreatment with yohimbine (1.5 mg/kg, i.v.). Pretreatment with phentolamine (5 mg/kg, i.v.) was less effective in antagonizing this clonidine-induced mydriasis. Phenoxybenzamine (2 mg/kg, i.v.) was almost without effect. In contrast, both phentolamine and phenoxybenzamine blocked the pupillary dilation produced by epinephrine while yohimbine pretreatment resulted in no antagonism of epinephrine-induced mydriasis. These results suggest that clonidine-induced mydriasis in the rat is mediated by a central adrenergic inhibitory mechanism.
Adrenergic alpha-Antagonists↗