PubMed Health⌕ Search

Biomedical subjects

M C Koss

Publications and source records attributed to M C Koss.

At least 55 records · Page 3Linked to original sources

Characterization of adrenergic receptors of the cat iris and nictitating membrane.

Graded pupillary dilations and nictitating membrane (NM) contractions were elicited in anesthetized cats by electrical stimulation of the preganglionic sympathetic nerve or by i.a. administration of norepinephrine (NE) or phenylephrine into the carotid artery. Pupil and NM responses were measured simultaneously from the same side. Alpha-adrenoceptor antagonists were administered intravenously. All of the alpha 1-adrenoceptor blockers tested produced a dose-related reduction of NM responses to both neural and agonist activation; the potency rank order was prazosin greater than WB-4101 greater than phentolamine greater than phenoxybenzamine (PBZ). In contrast, responses of the iris dilator were antagonized only by WB-4101 and PBZ. The iris was almost totally refractory to doses of prazosin and phentolamine that blocked NM responses by more than 75% of control. Neither alpha 2- nor beta-adrenoceptor antagonism produced significant inhibition of neural or agonist activation of either organ (with the exception of high doses of yohimbine on the NM). These results suggest that the postjunctional adrenoceptors of the NM are exclusively of the alpha 1-adrenoceptor subtype. In contrast, those of the iris dilator muscle cannot be easily classified pharmacologically as either alpha 1 or alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗

Long posterior ciliary arterial blood flow and systemic blood pressure.

The purpose of the current study was to investigate the relationship between systemic blood pressure (BP) and long posterior ciliary arterial (LPCA) blood flow (BF) in response to autonomic drugs, and to determine the types of receptors involved. LPCA BF was measured in anesthetized rabbits at the retrobulbar region using laser Doppler flowmetry. The observation that most of the short posterior ciliary arteries diverge from two LPCAs in rabbits was confirmed using a vascular casting technique. Therefore, the LPCA BF at the retrobulbar region should be representative of total uveal BF. Norepinephrine (IV) increased systemic BP and decreased LPCA BF. These responses were suppressed only slightly by yohimbine, but were inhibited markedly by prazosin and by the combination of yohimbine and prazosin. B-HT 920 (IV), a selective alpha-2 adrenoceptor agonist, increased systemic BP and decreased LPCA BF. B-HT 920 (IA) also decreased LPCA BF, with all effects of B-HT 920 antagonized by yohimbine. Methacholine (IV) decreased systemic BP and increased LPCA BF whether administered IV or IA. These effects were blocked uniformly by atropine. The current results suggest that LPCA BF is controlled both by systemic BP and local ocular vascular tone. There are vasoconstrictive alpha-1 and alpha-2 adrenoceptors and vasodilative muscarinic receptors in the rabbit ocular vascular tree.

Adrenergic alpha-Agonists↗

Characterization of adrenoceptor subtypes in cat cutaneous vasculature.

Experiments were undertaken to characterize the relative contribution of adrenoceptor subtypes in mediating vasoconstriction to exogenous agonists in the digital cutaneous vascular bed of the anesthetized cat using laser-Doppler flowmetry. Intra-arterial administration of (-)-epinephrine and (-)-norepinephrine into the brachial artery caused a dose-related vasoconstriction (decreased flow) with ED50 values of 7 and 21 ng, respectively. Blockade of beta adrenoceptors with propranolol did not alter the response to (-)-epinephrine nor did i.a. isoproterenol produce a significant vasodilation. Vasoconstrictor responses elicited by (-)-epinephrine and (-)-norepinephrine were antagonized by treatment with phentolamine (2.5 mg/kg i.v.) and by yohimbine (0.5 mg/kg i.v.) but were only marginally blocked by prazosin (0.1 mg/kg i.v.). A dose-related depression of cutaneous blood flow was also caused by clonidine at doses virtually identical to those of (-)-norepinephrine. Clonidine-induced vasoconstriction was antagonized by rauwolscine (0.5 mg/kg i.v.) but not by prazosin (0.1 mg/kg i.v.). Dose-response curves to a variety of additional adrenoceptor stimulants were constructed with the potency rank order for all agonists being: (-)-epinephrine greater than B-HT 920 = (-)-norepinephrine = clonidine much greater than (-)-phenylephrine much greater than B-HT 933 greater than methoxamine. Treatment with prazosin (0.1 mg/kg i.v.) antagonized methoxamine induced cutaneous vasoconstriction but not the decreased blood flow caused by B-HT 933. In contrast, rauwolscine (0.5 mg/kg i.v.) blocked the responses to B-HT 933 but not methoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Argon laser-induced ocular hypertension: animal model of ocular inflammation.

There is substantial evidence that prostaglandins (PG's) mediate acute elevations of intraocular pressure (IOP) due to laser irradiation of the iris. In the present study, we determined the optimal laser parameters needed to produce the maximal rise in IOP in anesthetized rabbits. Application of argon laser (0.75 watts, 0.5 sec. duration, and 8 spots of 500 micron size) to the iris of pigmented rabbits elicited an acute rise in IOP and miosis accompanied by an increase in aqueous protein concentration. This response was followed by a delayed ocular hypotension that lasted for more than 3 days and returned to baseline by day 5. The onset of ocular hypertension occurred within 15 min. and remained elevated for at least 90 min. The laser induced rise in IOP was related more to the number of laser spots applied to the iris than to the intensity of the total laser energy utilized. Pretreatment with either indomethacin or flurbiprofen produced a dose dependent inhibition of ocular hypertensive response and significantly reduced aqueous protein concentration. Indomethacin (0.01-30 mg/kg) was administered intraperitonially 1 hr. before laser treatment and flurbiprofen (0.03-0.3%) was administered topically 45 and 15 min. prior to laser application. The hypertensive response was reduced by more than 90% of control after both drugs, whereas the delayed hypotension was significantly antagonized only at the highest dose of indomethacin. Neither indomethacin nor flurbiprofen altered the maximum miotic response to laser irradiation of the iris. However, 0.3% flurbiprofen and 30 mg/kg indomethacin significantly increased the recovery rate of the miotic pupil. The results of this study support the contention that argon laser induced ocular hypertension may provide a quantitative assessment of inhibition of prostaglandin mediated responses.

Animals↗

Topical application of CO2 increases skin blood flow.

The topical application of carbon dioxide water to the rat hindpaw produced a concentration-dependent increase of skin blood flow as measured by a laser Doppler flowmeter. About a 100% increase of skin blood flow occurred in response to CO2 when the bath temperature was at 23 degrees C or 34 degrees C, but there was no significant effect of CO2 at 41 degrees C. Carbon dioxide exposure also produced about the same increase of skin blood flow in the acutely or chronically denervated paw as in the control. These findings give experimental support for the clinical use of CO2 bathing in the treatment of disturbances of skin circulation as well as skin ulcers and wounds.

Administration, Topical↗

Mechanism of dexamphetamine-induced mydriasis in the anaesthetized rat.

1. The effect of intravenous administration of dexamphetamine [+)-Amp) on rat pupil diameter was investigated. In all experiments, the vagosympathetic trunks were sectioned bilaterally at the cervical level. 2. In rats anaesthetized with urethane, (+)-Amp (0.1-0.3 mg kg-1, i.v.) produced a dose-related increase in pupil size. The mydriatic effects of (+)-Amp were evident immediately after administration. 3. Pretreatment with the alpha 2-adrenoceptor antagonists yohimbine (1.5 mg kg-1 i.v.) or idazoxan (0.5 mg kg-1, i.v.) blocked the pupillary response to (+)-Amp. Yohimbine caused about a 30 fold shift to the right in the dose-response curve whereas idazoxan almost completely abolished the mydriatic response to (+)-Amp. 4. In contrast, pretreatment with the alpha 1-adrenoceptor antagonist phenoxybenzamine (2 mg kg-1, i.v.), failed to alter significantly the pupillary response to (+)-Amp. 5. Depletion of central nervous system (CNS) monoamines with reserpine (5 mg kg-1, i.p.) and alpha-methyl-p-tyrosine (2 x 300 mg kg-1, i.p.) prevented the pupillary response to (+)-Amp. 6. The mydriatic effect of (+)-Amp was present only in preparations that had intact parasympathetic neural tone to the iris. Central preganglionic denervation of the oculomotor nerve abolished the mydriatic response of (+)-Amp. 7. These results indicate the (+)-Amp acts in the CNS to produce mydriasis in the anaesthetized rat by stimulating CNS postsynaptic alpha 2-adrenoceptors, findings that are consistent with the hypothesis that (+)-Amp acts predominantly as an indirect sympathomimetic agent to release endogenous stores of a monoaminergic neurotransmitter (perhaps noradrenaline).

Adrenergic alpha-Antagonists↗

Studies on the mechanism of prazosin induced sympatho-inhibition.

Intravenous administration of the alpha 1-adrenoceptor antagonist, prazosin (3-300 micrograms/kg), produced a depression of sympathetic-cholinergic electrodermal responses evoked by electrical stimulation of the posterior hypothalamus in pentobarbital anesthetized cats. Pretreatment with the alpha 2-adrenoceptor antagonists yohimbine (0.5 mg/kg) or idazoxan (0.1 mg/kg) significantly blocked the depressant effects of prazosin but had no effect on hypothalamic evoked electrodermal responses when given alone. Electrodermal responses were readily elicited in animals depleted of CNS monoamines. Monoamine depletion, however, totally abolished prazosin's depression of centrally evoked electrodermal responses. Prazosin also depressed the amplitude of electrodermal responses evoked by electrical stimulation of the cervical spinal cord in spinalized cats. In contrast to hypothalamic stimulation, yohimbine when given alone potentiated spinally evoked electrodermal responses which suggests that both excitatory and inhibitory mechanisms were being activated. Taken together these results suggest that prazosin produces its CNS sympatholytic effect by enhancing inhibition mediated by alpha 2-adrenoceptor mechanisms and not directly by blockade of excitatory alpha 1-adrenergic receptors in the central nervous system. A spinal cord site of action for prazosin is also implicated.

Adrenergic Fibers↗

Clonidine inhibits electrodermal responses by an action on the spinal cord.

Experiments were designed to determine the neural site of action for clonidine inhibition of sympathetic-cholinergic electrodermal responses (EDR) in anesthetized cats. Administration of clonidine (0.3-3.0 micrograms i.a.) directly to the stellate ganglion did not significantly decrease the amplitude of responses evoked by submaximal hypothalamic stimulation but did inhibit hypothalamic-evoked EDR when administered intrathecally at the C6 to T2 spinal levels. Administration of clonidine to the ganglion, however, did depress EDR evoked by the ganglionic stimulant, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP, 10 micrograms i.a.). Intravenous clonidine (1-30 micrograms) also reduced EDR amplitude evoked by single pulse stimulation of both the pre- and postganglionic sympathetic nerves with responses elicited from both sites depressed to an equal extent. Yohimbine (0.5 mg/kg i.v.) uniformly antagonized clonidine's depression of EDR regardless of the site or mode of activation. These results indicate that clonidine depresses centrally evoked sudomotor responses by activation of alpha 2-adrenoceptors in the spinal cord and to a limited extent by direct action at the neuroeffector junction. Although a possible DMPP-clonidine interaction appears to take place at the level of the sympathetic ganglion, it is unlikely that ganglionic blockade contributes significantly to clonidine inhibition of EDR evoked by electrical activation of the nervous system.

Animals↗

Pharmacological characterization of alpha-adrenoceptors involved in nictitating membrane and pupillary responses to sympathetic nerve stimulation in cats.

Electrical stimulation of the preganglionic cervical sympathetic nerve produced frequency-related contraction of the nictitating membrane (NM) and dilation of the pupil in anesthetized cats. Observations of the effects of alpha-adrenoceptor blockade on these effectors were made simultaneously from the same preparations. All of the alpha 1-adrenoceptor antagonists tested produced a dose-related blockade of the NM with the relative potencies being prazosin greater than WB-4101 greater than phentolamine greater than phenoxybenzamine. In contrast, the iris dilator response was blocked by WB-4101 and phenoxybenzamine but was almost totally refractory to antagonism by doses of prazosin and phentolamine that reduced the evoked NM responses by more than 75% in these same preparations. Neither alpha 2-adrenoceptor (yohimbine or rauwolscine) nor beta-adrenoceptor (propranolol) antagonism produced significant inhibition of the activation of either organ. These results suggest that: 1) neural activation of the nictitating membrane is solely due to stimulation of alpha 1-adrenoceptors; 2) neither beta- nor alpha 2-adrenoceptors contribute significantly to nerve activation of either the nictitating membrane or iris dilator muscle in vivo; 3) the alpha-adrenoceptors on the dilator muscle that are activated neurally can not be classified pharmacologically as either alpha 1 or alpha 2 receptors.

Adrenergic alpha-Antagonists↗

Inhibition of a peripheral sympathetic-cholinergic system by presynaptic alpha 2-adrenoceptors.

Intravenous administration of catecholamines produced dose-related inhibition of electrodermal responses (EDRs) evoked by electrical stimulation of the post-ganglionic sciatic nerve in anaesthetized rats, with relative potencies being (-)-adrenaline greater than (+/-)-adrenaline greater than (-)-noradrenaline = (+)-adrenaline. The suppression of EDRs by (+/-)-adrenaline and (-)-noradrenaline was blocked by pretreatment with yohimbine (0.75 mg/kg i.v.) but not by prazosin (0.3 mg/kg i.v.). The selective alpha 2-adrenoceptor agonist B-HT 920 also inhibited neurally evoked skin potential responses. This effect of B-HT 920 was antagonized by the selective alpha 2-adrenoceptor antagonist idazoxan (0.1 mg/kg i.v.) but was insensitive to prazosin. Idazoxan was more potent than yohimbine in blocking (+/-)-adrenaline-induced suppression of EDRs. Methacholine administered into the femoral artery evoked EDRs by an atropine-sensitive mechanism. Methacholine-induced EDRs were not suppressed by intravenous administration of (-)-adrenaline (1 microgram/kg or 3 micrograms/kg) whereas EDRs evoked by the sciatic nerve stimulation on the other hindpaw were inhibited. Increase in the endogenous catecholamines by asphyxia strongly inhibited EDRs by a mechanism which was also sensitive to yohimbine but not to prazosin. These results suggest that peripheral presynaptic alpha 2-adrenergic mechanisms are involved in inhibition of transmitter release in this sympathetic-cholinergic system.

Adrenergic alpha-Antagonists↗

Alpha-adrenoceptor activation of nictitating membrane and iris in cats.

Intra-arterial administration of (+)- and (-)-isomers of adrenaline and noradrenaline produced dose-related contraction of the nictitating membrane (NM) and dilation of the pupil in anesthetized cats. The relative potencies were (-)-adrenaline greater than (+)-adrenaline = (-)-noradrenaline greater than (+)-noradrenaline. Observations of the effects of alpha-adrenoceptor antagonists on (-)-noradrenaline activation of these two effectors were made simultaneously. All of the alpha 1-adrenoceptor antagonists tested produced a dose-related blockade of the NM with the relative potencies being prazosin greater than WB-4101 greater than phentolamine greater than phenoxybenzamine. In contrast, the iris dilator was blocked by WB-4101 and phenoxybenzamine but was refractory to antagonism by doses of prazosin and phentolamine that reduced the (-)-noradrenaline evoked NM response by 75-80% in the same animals. The alpha 2-adrenoceptor antagonist, yohimbine, produced significant inhibition of the NM only at high dose (1 mg/kg) but even at this level had no effect on pupil diameter. These results suggest that activation of the NM by exogenous noradrenaline is due solely to stimulation of alpha 1-adrenoceptors. alpha 2-adrenoceptors do not seem to significantly contribute to noradrenaline induced activation of either the NM or iris dilator muscle in vivo. In contrast, the alpha-adrenoceptors on the iris dilator muscle that are stimulated by exogenous noradrenaline can not easily be classified pharmacologically as either alpha 1- or alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗

Systemic blood pressure and intraocular pressure relationship.

The relationship between intraocular pressure (IOP) and arterial blood pressure (BP) was analyzed in response to two pressor agents (norepinephrine and angiotensin II) and two depressor agents (methacholine and isoproterenol) in pentobarbital anesthetized cats. Both IOP and BP were measured manometrically in the same animals. Intravenous norepinephrine and angiotensin II produced dose-dependent increases, whereas intravenous methacholine and isoproterenol produced dose-dependent decreases of both BP and IOP. The IOP response to methacholine was biphasic, with an initial decrease followed by an increase above the pre-drug level. In some experiments a cannula loop was inserted into a carotid artery in order to separate the direct ocular effect of drugs on IOP from that contributed by the changes in systemic BP. Intravenous administration of norepinephrine and angiotensin II produced a larger increase in IOP on the side where drugs were delayed by the loop. Conversely, methacholine produced a larger fall in IOP on the cannulated side while the effect of isoproterenol was essentially unchanged. In other experiments injections were made directly into the ocular arterial blood supply. Norepinephrine and angiotensin II produced a decrease in IOP, methacholine produced a rise of IOP and isoproterenol was not active by this route. The present findings indicate that IOP is largely influenced by arterial BP changes in the acute phase and that the IOP response to drugs is the algebraic sum of effects on systemic BP and their direct ocular effects.

Angiotensin II↗

Atypical alpha-adrenoceptor mediates phenylephrine-induced mydriasis in anesthetized cats.

Pupillary dilation and nictitating membrane (NM) contraction were elicited by pharmacological activation of alpha-adrenoceptors in vivo in anesthetized cats. A constant intravenous infusion of the alpha 1-adrenoceptor selective agonist phenylephrine (150 micrograms/min) was administered to produce a near maximal activation of both organs. Steady-state responses were attained about 15 minutes after starting the phenylephrine infusion. Administration of the alpha 1-adrenoceptor selective antagonist prazosin produced a dose-dependent blockade of NM contractions without altering phenylephrine-induced mydriasis when given as pretreatment (1.0 mg/kg i.v.) or post-treatment (0.01-1.0 mg/kg i.v.). In contrast, post-treatment with the alpha 1-adrenoceptor selective antagonist WB-4101 (0.1-1.0 mg/kg i.v.) or pretreatment with phenoxybenzamine (3.0 mg/kg i.v.) blocked both the NM and pupillary responses. These results suggest that the in vivo pupillary response to phenylephrine is mediated by an atypical alpha-adrenoceptor that cannot be readily classified as an alpha 1- or alpha 2-adrenoceptor. In contrast, the alpha-adrenoceptors of the NM appear to be of the classical alpha 1 subtype.

Adrenergic alpha-Antagonists↗

Alpha 1- and alpha 2-adrenoreceptor antagonists produce opposing mydriatic effects by a central action.

1. In anaesthetized rats, intravenous administration of alpha 2-adrenoreceptor antagonists yohimbine (0.3-3.0 mg kg-1), idazoxan (0.03-0.3 mg kg-1) and raulwolscine (0.3-3.0 mg kg-1) produced a dose-related inhibition of sciatic nerve-(ScN) mediated reflex pupillary dilation (parasympatho-inhibition). The rank order of potency was idazoxan greater than yohimbine greater than rauwolscine. 2. Under similar experimental conditions, intravenous administration of alpha 1-adrenoreceptor antagonists prazosin (0.03-1.0 mg kg-1), phenoxybenzamine (0.3-3.0 mg kg-1) and corynanthine (0.03-1.0 mg kg-1) produced a dose-dependent potentiation of the reflex mydriasis with the potency order being prazosin greater than corynanthine greater than phenoxybenzamine. Intravenous yohimbine (1.5 mg kg-1) reversed the potentiation caused by the alpha 1-adrenoreceptor antagonists and blocked the reflex mydriasis. 3. Parasympatho-inhibition and mydriasis elicited by hypothalamic stimulation was not affected by the alpha 2-adrenoreceptor antagonists yohimbine (0.3-3.0 mg kg-1), idazoxan (0.03-0.3 mg kg-1) or the alpha 1-adrenoreceptor antagonist prazosin (0.3-1.0 mg kg-1). 4. Microinjection of prazosin (3-30 ng) into the oculomotor nuclear complex (IIIn), produced a dose-related potentiation, whereas microinjection of yohimbine (0.3-3.0 micrograms) produced a dose-related blockade of reflex mydriasis. 5. The above findings support the hypothesis that ascending mechanisms (e.g. afferent ScN) produce inhibition of parasympathetic oculomotor tone to the iris by activation of central postsynaptic alpha 2-adrenoreceptors. Furthermore, these studies demonstrate that alpha 2-adrenoreceptor antagonists block and alpha 1-adrenoreceptor antagonists potentiate the reflex mydriasis. These actions appear to be localized within the pupilloconstrictor regions of the brain (oculomotor nuclear complex).

Adrenergic alpha-Antagonists↗

alpha-Methyldopa produces mydriasis in the rat by stimulation of CNS alpha 2-adrenoceptors.

1. The effects of i.v. administration of alpha-methyldopa (MD) on rat pupil diameter were investigated. All experiments were carried out in rats in which vagosympathetic nerve trunks were sectioned bilaterally at the cervical level. 2. In anaesthetized rats MD produced a marked dose-related increase in pupil diameter. The onset of pupillary response to MD was gradual and reached maximal levels 2-3 h after administration. 3. Pretreatment with alpha 2-adrenoceptor antagonists yohimbine (1.5 mg kg-1, i.v.) or idazoxan (0.5 mg kg-1, i.v.) blocked the pupillary response to MD. In contrast, the alpha 1-antagonists prazosin (1.0 mg kg-1, i.v.) and phenoxybenzamine (1.5 mg kg-1, i.v.) did not significantly alter the pupillary effects of MD. 4. Selective enzymatic blockade with 3-hydroxy-benzyl-hydrazine (NSD-1015; 25 mg kg-1, i.p.), a dopa-decarboxylase inhibitor, as well as bis (4-methyl-homopiperazinyl-thiocarbonyl) disulphide (FLA-63, 5.0 mg kg-1, i.p.), a dopamine-beta-hydroxylase inhibitor, prevented the mydriatic effect of MD. 5. The above findings support the hypothesis that MD produces a clonidine-like CNS mydriasis in the rat. This effect appears to be mediated primarily by the MD metabolite, alpha-methylnoradrenaline. 6. These results indicate that MD produces mydriasis in the rat by a CNS action. The mydriatic action of MD appears to be produced by its metabolite alpha-methylnoradrenaline which in turn stimulates CNS postsynaptic alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗

Opposing central autonomic actions of alpha 1- and alpha 2-adrenoceptor antagonists on oculomotor tone.

Electrical stimulation of the afferent sciatic nerve produces reflex mydriasis in anesthetized rats. The alpha 2-antagonist idazoxan (10-100 micrograms/kg i.v.) inhibited this reflex in a dose-dependent fashion. In contrast, the alpha 1-antagonist prazosin (30-300 micrograms/kg i.v.), produced a dose-related enhancement of the reflex. Single dose administration of the alpha 2-antagonists yohimbine (3.0 mg/kg i.v.), rauwolscine (3.0 mg/kg i.v.) and idazoxan (1.0 mg/kg) also blocked the reflex, whereas the alpha 1-antagonists phenoxybenzamine (3.0 mg/kg i.v.), corynanthine (1.0 mg/kg i.v.) and prazosin (1.0 mg/kg i.v.) potentiated this response. These studies demonstrate that alpha 2-antagonists block and alpha 1-adrenoceptor antagonists potentiate alpha 2-adrenoceptor-mediated inhibition of oculomotor tone.

Adrenergic alpha-Antagonists↗

Rapid and sensitive method for measurement of hyaluronic acid and isomeric chondroitin sulfates using high-performance liquid chromatography.

A high-performance liquid chromatographic method for the separation and analysis of the unsaturated tetrasaccharide and hexasaccharide from Streptomyces hyaluronidase (S.HAase) enzyme digestion products of hyaluronic acid (HA) and standard unsaturated disaccharides 2-acetamido-2-deoxy-3-O-(beta-D-gluco-4-enepyranosyluronic acid)-D-galactose (delta Di-0S), 2-acetamido-2-deoxy-3-O-(beta-D-gluco-4-enepyranosyluronic acid)-4-O-sulfo-D-galactose (delta Di-4S) and 2-acetamido-2-deoxy-3-O-(beta-D-gluco-4-enepyranosyluronic acid)-6-O-sulfo-D-galactose (delta Di-6S) is described. An amino phase chemically bonded to silica with a particle diameter of 6 micron was used as the column. The composition and the pH of the mobile phase were systematically varied to determine the optimal chromatographic conditions for separation and analysis of the compounds. For HA, a complete separation was accomplished in less than 12 min with a practical detection limit of 100 ng. Separation of the disaccharides also required less than 15 min with detection limits of 10 ng for delta Di-0S and 25 ng each for delta Di-4S and delta Di-6S. This chromatographic method represents a significant improvement over existing methods. It allows the simultaneous separation and analysis of HA and chondroitin sulfate isomers (after digestion of the latter with chondroitinase) at a higher speed, and with more sensitivity and efficiency.

Chondroitin↗

Safety of high-energy neodymium:YAG laser pulses in YAG sclerostomy.

YAG sclerostomy was performed in 15 eyes of nine cynomolgus monkeys. Individual pulse energies ranged between 10 and 135 millijoules. Total pulse energy ranged between 2,000 and 36,000 millijoules in order to test the extreme range of energy that might be required. Both acute effects and chronic effects were studied in the corneal endothelium, the lens capsule, the iris, the ciliary body, the retina, and the sclera. Techniques included flat preparations of the corneal endothelium, paraffin sections for light microscopy, and scanning and transmission electron microscopy. Our conclusion is that individual pulse energies of up to 135 millijoules with a total of up to 36 joules of energy are safe in monkey eyes when performing YAG sclerostomy.

Animals↗