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Biomedical subjects

A Bill

Publications and source records attributed to A Bill.

At least 55 records · Page 3Linked to original sources
PubMed1986

The blood-aqueous barrier.

This paper reviews studies on the permeability of the blood-aqueous barrier to substances that are not transported by cellular mechanisms. The intercellular movement of small molecules and ions from the ciliary processes into the posterior chamber is restricted by tight junctions between the nonpigmented epithelial cells. For plasma proteins the endothelial cells of the capillaries constitute an additional barrier. The number of tight junctional strands and the electrical conductance of the epithelium is such that it can be classified as a border case between leaky and tight epithelia. The iris vessels seem to constitute a more efficient barrier in primates than in rabbits and cats most probably due to the presence of more complete junctional strands between the endothelial cells in primates. Although there is no anatomical barrier there is an efficient functional barrier between the stroma of the ciliary processes and the anterior chamber. The flow of aqueous humour most probably plays a role in the process of control of the barrier function in the routes between Schlemm's canal and the anterior chamber.

Animals↗
PubMed1985

Blood flow and glucose consumption in the optic nerve, retina and brain: effects of high intraocular pressure.

Glucose consumption and regional blood flow were determined using the [14C]-2-deoxyglucose (2-DG) method and microspheres in the optic nerve, the retina and different parts of the brain in monkeys. The relationship between the 2-DG accumulation and blood flow in the optic nerve head region was similar to that in grey matter of the brain under pentobarbital anaesthesia as well as under urethan anaesthesia. Pentobarbital anaesthesia resulted in lower values for blood flow and glucose metabolism in most regions. In the optic nerve the highest values were observed in the distal part; there was a fall in blood flow and metabolism along the nerve. There was a corresponding increase in myelin content. Artificial increments in intraocular pressure resulting in a perfusion pressure (mean arterial pressure minus intraocular pressure) of 40 cm H2O had no appreciable effect on the 2-DG accumulation. At a perfusion pressure of 20 cm H2O 2-DG accumulation in the retina and prelaminar part of the optic nerve was markedly increased indicating partial ischemia resulting in anaerobic glycolysis. At intraocular pressures higher than the systolic arterial blood pressure there was still some accumulation of 2-DG in the intraocular tissues, but no blood flow, which indicates that glucose could diffuse into the eye through the sclera. Behind the lamina cribrosa there was no indication of a reduction in blood flow or a metabolic disturbance. The results indicate that the blood flow and metabolism of the retina and prelaminar part of the optic nerve is disturbed only at very high intraocular pressures, and that even at extreme pressures there is no disturbance behind the lamina cribrosa in acute experiments. The 2-DG method will be useful in further studies on the nutritional status of the optic nerve head since it can detect abnormal glycolysis even in very discrete regions due to its high spatial resolution.

Animals↗
PubMed1985

Characteristics of uveal vasodilation produced by facial nerve stimulation in monkeys, cats and rabbits.

The effect of electrical stimulation of the facial nerve on ocular blood flow and intraocular pressure (IOP) was studied in monkeys, cats and rabbits. Ocular blood flow was determined with radioactive microspheres or by direct measurement of uveal blood flow from a cannulated vortex vein in rabbits. Frequency-response relationships were determined in monkeys (intraocular pressure) and rabbits (uveal blood flow). Stimulation of the facial nerve produced a marked increase (greater than 100%) in choroidal blood flow in all three species. The effect in the anterior uvea appeared the same, but less pronounced. Retinal blood flow was not affected by the stimulation in any of the species. In cats, local blood flow in the optic nerve was significantly increased by the stimulation. As there was no significant change in mean arterial blood pressure, the increase in blood flow must have been due to decreased vascular resistance. The uveal vasodilation was resistant to muscarinic blockade in all three species, excluding acetylcholine as the principal peripheral transmitter. Stimulation of the facial nerve also caused a moderate increase in IOP (range 1-11 cmH2O), only investigated in monkeys. This increase in IOP seems to be secondary to the intraocular vasodilation. The maximal increase in intraocular pressure, in monkeys, and vasodilation, in rabbits, was obtained at 15-20 Hz. At these frequencies, the vasodilation was always abolished by ganglionic blockade. In rabbits, stimulation at high frequencies (greater than 40 Hz) sometimes produced uveal vasodilation even after ganglionic blockade. This vasodilation was always less pronounced than before the ganglionic blockade and could be abolished by muscarinic blockade. The increase in uveal blood flow, in rabbits, was not affected by administration of indomethacin, indicating that prostaglandins are not critically involved in the vasodilation produced by facial nerve stimulation. The vasodilatory nerve fibers in the facial nerve are likely to be involved in regulation of choroidal blood flow to control the environmental temperature for the retina. The present study establishes the existence of efferent vasodilatory nerve fibers of facial nerve origin to the uvea. The peripheral transmitter causing the vasodilation is suggested to be vasoactive intestinal polypeptide (VIP).

Animals↗
PubMed1985

Control of ocular blood flow.

The eye has a dual vascular supply. The uveal vessels are distributed within the choroid, the ciliary body, and the iris; and the retinal vessels within the inner parts of the retina. The vascularization of the uvea is very rich and the blood flow is high, which stabilizes the temperature of the eye. The vascularization of the retina is relatively sparse, which is an obvious advantage for the optics. The perfusion pressure in the eye can be defined as the local arterial blood pressure minus the intraocular pressure. Reductions in perfusion pressure, caused by increments in intraocular pressure, or reductions in mean arterial pressure reduce the blood flow in the choroid. In the retina, there are efficient autoregulatory mechanisms that prevent changes in flow within a wide range of perfusion pressures. Stimulation of the cervical sympathetic chain causes vasoconstriction in the uvea, with near-maximal effects as 10 Hz. The sympathetic nerves are not activated during moderate hemorrhage. They apparently prevent overperfusion and breakdown of intraocular barriers under conditions of acute elevation of the arterial blood pressure. Electrical stimulation of the oculomotor nerve causes cholinergic vasoconstriction in the anterior uvea. Near-maximal vasoconstriction is obtained between 10 and 20 Hz. In conscious animals, muscarinic blockade causes vasodilatation in the iris, indicating that there is a basal traffic in the vasomotor fibers of the oculomotor nerve. Electrical stimulation of the facial nerve causes vasodilatation in the uvea that cannot be prevented by muscarinic blockade: near-maximal vasodilatation is obtained between 10 and 20 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A method for near-continuous determination of aqueous humor flow; effects of anaesthetics, temperature and indomethacin.

A method is described for near-continuous determination of aqueous humor flow. The anterior chamber is perfused with push-pull coupled syringes at a low rate with a fluid containing labelled albumin. An external circuit is used to determine continuously the anterior chamber concentration of the labelled protein. The dilution data are analysed on-line by a minicomputer which permits rapid calculation of the anterior chamber volume and the rate of flow of aqueous humor. The technique and some experiments of technical interest are reported. Experiments in monkeys with different anaesthetics resulted in flow values of 0.99 +/- 0.02, 1.47 +/- 0.09 and 0.99 +/- 0.04 microliter min-1 for pentobarbital, urethane and ketamine anaesthesia, respectively. By using 125I-labelled albumin in one eye and 131I-labelled albumin in the other, it was possible to determine flow in both eyes. Highly significant correlation coefficients between the two sides were found for the rate of aqueous flow, intraocular pressure and anterior chamber volume. Rapid changes in inflow into the anterior chamber from the posterior chamber were produced by elevating and then lowering the intraocular pressure; the delay inherent in the method was about 6 min. Indomethacin, 3 mg kg-1 body wt., had no effect on aqueous humor flow in eyes cannulated with a minimum of trauma. In eyes with problematic cannulation indomethacin at this dose tended to delay an irritation response. Changes in temperature of the fluid perfused through the anterior chamber had no clear effect on the rate of aqueous flow. Warming the animals about 3-4 degrees C above the normal temperature tended to increase the rate of aqueous flow. Cooling by 3-4 degrees C had no clear effect. Cooling after an initial warming also had no clear effect. The rate of flow of aqueous humor from the anterior chamber to the general circulation was calculated from data for the accumulation of labelled albumin in the general circulation. The difference between the rate of aqueous flow determined from the dilution data and the flow into blood was assumed to represent uveoscleral flow. In 14 animals with an aqueous flow of 1.19 +/- 0.08 microliters min-1 the flow to the general circulation was 0.57 +/- 0.055 and uveoscleral flow 0.61 +/- 0.09 microliters min-1. The procedure and mathematical treatment will be applicable to flow determinations with other large molecules and in other systems.

Anesthetics↗
PubMed1984

[Effect of acute hemorrhaging in rabbits on blood circulation in the eye and various other tissues. The role of the sympathetic nerves].

The labeled microsphere method was used to determine the blood flow in the eyes and some other tissues in conscious rabbits with unilateral section of the cervical sympathetic chain. Flow measurements were made before and after a hemorrhage corresponding to 17.3 +/- 1.6 ml/kg body weight. The mean arterial blood pressure fell from 90 +/- 3 mmHg to 53 +/- 2 mmHg. Before bleeding, the blood flow in the iris, ciliary body and choroid was similar on the two sides. After the hemorrhage there was little change in the blood flow in the brain and adrenals. The flow in heart muscle and kidney cortex was 70 and 48% of that before the bleeding, respectively. In the stomach wall, the spleen and the skin the corresponding figure was 10%. In the iris, ciliary body and choroid the flow on the intact side was 37, 26 and 38%, respectively, of that before the bleeding. On the other side the flow was slightly higher. The results indicate that there was little sympathetic tone to the blood vessels of the uvea either before or after the hemorrhage and that circulating vasoconstrictor substances had only a slight to moderate effect on the uveal blood vessels.

Acute Disease↗
PubMed1984

Effects of the substance P antagonist, (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP on the miotic response to substance P, antidromic trigeminal nerve stimulation, capsaicin, prostaglandin E1, compound 48/80 and histamine.

The effects of the substance P analogue (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP on the ocular inflammatory responses (miosis, vasodilation, protein leakage into the aqueous humour and eye pressure rise) to antidromic trigeminal nerve stimulation (trigeminal stimulation), intracameral injections of substance P (SP), capsaicin, prostaglandin E1 (PGE1), compound 48/80 and histamine were investigated in albino rabbits. The effects of nerve blockade with tetrodotoxin and blockade of histamine receptors on the responses to compound 48/80 and histamine were also investigated. Histamine H1 receptors were blocked with clemastin and H2 receptors with cimetidin. Formation of endogenous prostaglandins was prevented with indomethacin. The pupil size and the eye pressure were measured. The aqueous humour was collected immediately after the animal was killed, and analyzed for protein concentration. (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP had no significant miotic effect, but tended to cause a break-down of the blood-aqueous barrier. Miosis caused by SP, trigeminal stimulation, capsaicin, PGE1, compound 48/80 or histamine was blocked by (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP. Histamine miosis was significantly reduced by blockade of nerve conduction or histamine receptors, while miosis caused by compound 48/80 was not. Nerve blockade abolished the rise in intraocular pressure caused by compound 48/80. Our results indicate that (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP is a specific SP blocker in the sphincter pupillae muscle. They are strong evidence for the hypothesis that trigeminal stimulation and capsaicin cause miosis by release of SP or a related substance (SPLI), and it seems likely that the miosis caused by PGE1 and compound 48/80 is also caused by SPLI release. Histamine miosis is probably mediated both by SP receptors and histamine receptors in the pupillary sphincter muscle.

Alprostadil↗
PubMed1984

Hypertonic KCI, NaCl and capsaicin intracamerally causes release of substance P-like immunoreactive material into the aqueous humor in rabbits.

We have investigated release of substance P-like immunoreactivity (SPLI) into the anterior chamber of the rabbit eye evoked by stimuli which cause non-cholinergic miosis. In a recent study such miosis was reported to be blocked by the substance P analogue (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP. Mechanical intracranial antidromic trigeminal nerve stimulation caused marked SPLI release presumably from primary sensory nerve endings in the anterior part of the eye. Intermittent stimulation for 20 min was not more effective than stimulation for 10 min. Intracameral injection of either 20 microliters 4.65 M KCI, 20 microliters 4.65 M NaCl or 100 micrograms capsaicin also caused SPLI release. Intracameral injection of 70 microliters 150 mM KCI, 28 micrograms prostaglandin E1 or 200 micrograms of compound 48/80 did not cause detectable SPLI release.

Alprostadil↗
PubMed1984

Vasoactive intestinal polypeptide (VIP): effects in the eye and on regional blood flows.

The effect of vasoactive intestinal polypeptide (VIP) on regional blood flows was studied with labeled microspheres in albino rabbits. Intravenous injection of 500 ng VIP/kg b.w. during 100 s did not change the arterial blood pressure significantly, but caused a rise in intraocular pressure (IOP) and an increase in the choroidal blood flow by 35%, while the blood flow through the anterior uvea was unaffected. The most pronounced vasodilation was observed in the pancreas, the thyroid gland and the parotid gland. In these tissues local blood flow increased by more than 100%. Other tissues, in which this dose of VIP produced vasodilation, were the submandibular gland, the eyelids, the nictitating membrane, the choroid plexus and the heart muscle. Ganglionic or muscarinic blockade had little or no effect on the VIP-induced vasodilation in most of the tissues. Intracameral injection of VIP (1 microgram) produced vasodilation in the iris and the ciliary body, but did not affect IOP. VIP had no apparent effect on the pupil size or the blood-aqueous barrier. In experiments with direct blood flow determination from an opened vortex vein intravenous infusion of VIP, 100 ng X kg-1 X min-1 b.w., during five minutes reduced the uveal vascular resistance by about 50%. This study shows that VIP is a potent vasodilator in many tissues at doses hardly affecting the arterial blood pressure and supports the suggestion, that VIP is responsible for the non-cholinergic vasodilation in the eye caused by facial nerve stimulation.

Animals↗
PubMed1984

Thyrotropin-releasing hormone (TRH) causes sympathetic activation and cerebral vasodilation in the rabbit.

The effects of TRH on regional blood flow were studied in rabbits under urethane anesthesia. Four types of experiments were performed with the following results. (1) I.v. injection of 2 mg/kg b.w. TRH in animals with unilateral cervical sympathotomy caused a rise in mean arterial blood pressure from 10.0 +/- 0.5 to 13.3 +/- 0.5 kPa. Total cerebral blood flow, measured with labeled microspheres, increased from 75 +/- 5 to 126 +/- 16 g/min/100 g tissue on the intact side. There was a similar increase on the side with sympathotomy. The greatest increase, about 70%, was observed in cortical gray matter, caudate nucleus and thalamic region. There were marked reductions in blood flows in the spleen, gastric mucosa, skin and skeletal muscle. Mydriasis occurred on the side with an intact sympathetic supply. (2) I.v. infusion of 0.06 mg/kg b.w. per min TRH in animals with unilateral cervical sympathotomy and stabilized blood pressure increased total cerebral blood flow from 84 +/- 10 to 139 +/- 7 g/min/100 g. Blood flows to the masseter muscle, submandibular gland and facial skin but not to the eye or tongue were markedly reduced on the side with an intact sympathetic supply while little or no effect was observed on the side with sympathotomy. (3) Unilateral peripheral stimulation of the sympathetic chain at 1 Hz after bilateral sympathotomy caused a reduction in blood flows in the tongue, masseter muscle, submandibular gland and facial skin in animals with stabilized blood pressure. No potentiation of the stimulation effect was observed during TRH infusion. (4) The arteriovenous difference in oxygen saturation in the brain decreased from 39.1 +/- 2.8 to 26.4 +/- 3.7% after i.v. injection of 2 mg/kg b.w. TRH. The results indicate that TRH caused cerebral vasodilation in excess of that required by possible changes in cerebral metabolism. The vasoconstriction in the head region and the mydriasis was caused mainly by an increase in the activity of the cervical sympathetic nerves.

Acid-Base Equilibrium↗
PubMed1984

The drainage routes for aqueous humor in monkeys as revealed by scanning electron microscopy of corrosion casts.

The outflow routes for aqueous humor from the anterior chamber in cynomolgus monkeys were studied. The routes were filled with a mixture of Mercox CL2R and methyl methacrylate, 4:6, which had a low viscosity. Polymerization was delayed by cooling. Some experiments were performed after fixation with glutaraldehyde. Scanning electron microscopy was used to study the casts after dissolution of the tissue. The casts indicate inflow into the first intertrabecular space through a limited number of 10-100 microns openings. The first space is an irregular circular plexus. Subsequent uveal intertrabecular spaces also constitute complex channels. In the ciliary muscle the plastic entering from the uveal intertrabecular spaces could pass through narrow spaces into the supraciliary and suprachoroidal spaces. The intertrabecular spaces in the corneoscleral meshwork were thinner than those in the uveal meshwork. The outermost layer which tended to fill incompletely especially in fixed preparations communicated with the spaces of the juxtacanalicular tissue. In this tissue there was very limited filling even in unfixed preparations. On the casts of the canal of Schlemm there were remnants of communications with the juxtacanalicular tissue. These remnants indicated that only pores with diameters of 2-3 microns or more had been large enough to drain plastic into the canal. The collector channels formed a deep scleral plexus at many places. This plexus and direct collector channels drained into superior and inferior episcleral veins. Apparently the casting technique permitted visualization of most of the uveal and corneoscleral intertrabecular spaces and of preferential channels through the juxtacanalicular tissue and the inner wall of Schlemm's canal. The number of such channels was about 10-20/mm2 of inner wall.

Animals↗
PubMed1983

Physiology of the choroidal vascular bed.

The choroidal vascular bed has many interesting features such as relatively wide but flat capillaries, fenestrated capillary walls and an enormous blood flow. The high flow rate results in a high oxygen tension in the tissue and is also of importance in the temperature control of the eye. The capillary wall is permeable to plasma proteins which is probably of great importance for the supply of vitamin A to the pigment epithelium. The permeability to low molecular weight substances is very high which results in a tissue fluid similar to plasma with respect to small molecules. It is not clear whether the choriocapillaris is normally reabsorbing fluid transported into the choroid from the retina and from the anterior chamber or if there is a net filtration from the choriocapillaris. Fluid can pass from the choroid through the suprachoroid into the episcleral tissues via the scleral substance and spaces around the blood vessels and nerves.

Animals↗
PubMed1983

In the eye (D-Pro2, D-Trp7,9)-SP is a substance P agonist, which modifies the responses to substance P, prostaglandin E1 and antidromic trigeminal nerve stimulation.

A substance P analogue, (D-Pro2, D-Trp7,9)-SP, has been described to have SP antagonistic and SP agonistic effects in different tissues. We have investigated the effects of (D-Pro2, D-Trp7,9)-SP on the sphincter pupillae muscle, the blood aqueous barrier (BAB) and the intraocular pressure (IOP) in the albino rabbit eye. We also investigated the modifying effects of (D-Pro2, D-Trp7,9)-SP on miosis, BAB damage and IOP rise caused by SP, prostaglandin E1 (PGE1), capsaicin and on the miosis caused by electrical intracranial antidromic trigeminal nerve stimulation (NV stim). Endogenous PG synthesis was inhibited by systemic indomethacin i.v., cholinergic influence on the pupil size was inhibited with biperiden, i.v., adrenergic nerve influence by cervical sympathectomy just prior to the expts. Tubocurarine chloride was used to cause relaxation of striated muscles in the expts with NV stim. We found 100 micrograms (D-Pro2, D-Trp7,9)-SP to cause miosis, breakdown of the BAB with heavy leakage of Evans blue into the ciliary processes and aqueous humor, and a rise in IOP. At 10 micrograms (D-Pro2, D-Trp7,9)-SP caused slight miosis and did not inhibit the miosis caused by SP or capsaicin, but caused a significant reduction of the miotic response caused by PGE1 and NV stim. The rise in protein concentration in the aqueous humor caused by SP or PGE1 was slightly but significantly lower after pretreatment with (D-Pro2, D-Trp7,9)-SP. Thus (D-Pro2, D-Trp7,9)-SP was found to act as a SP agonist on the sphincter pupillae muscle, on the BAB and IOP. However, (D-Pro2, D-Trp7,9)-SP seemed to have some SP antagonistic effects on mechanisms that require sensory nerve conduction e.g. miosis caused by PGE1 and NV stim. The antagonistic mechanism is not clear. The SP analogue may have an unspecific membrane stabilizing effect or a toxic effect or block SP receptors on the sensory nerve fibers. Such effects of (D-Pro2, D-Trp7,9)-SP may explain also why the rise in protein concentration in the aqueous humor caused by SP and PGE1 was lower in eyes pretreated with (D-Pro2, D-Trp7,9)-SP.

Alprostadil↗
PubMed1983

Regional cerebral, ocular and peripheral vascular effects of naloxone and morphine in unanesthetized rabbits.

Effects of morphine and naloxone were investigated on cerebral, ocular and peripheral blood flow in unanesthetized rabbits. Blood flow measurements were performed with the labelled microsphere method. Cervical sympathotomy was performed on one side the day before the flow determination. Naloxone 2 mg/kg b.w. i.v. had no consistent effect on cerebral, ocular or peripheral blood flow or on mean arterial blood pressure. Morphine 2 mg/kg b.w. i.v. caused a rise in PaCO2 of 0.9 kPa and tended to increase cerebral blood flow in all parts investigated. In the hippocampal region, caudate nucleus and collicles the increase in flow was about 30% which is more than expected from the rise in PaCO2. Blood flow in the retina increased while the other parts of the eye showed no consistent changes in blood flow. Morphine reduced the blood flow in the duodenum by 60%. Mean arterial blood pressure did not change after morphine. No effect of the cervical sympathotomy was detected on cerebral or ocular blood flow before or after morphine or naloxone. Thus, we found no evidence for a tonically operating opioid system controlling cerebral, ocular or peripheral blood flow. However, exogenously administrated opiate can influence blood flows in these areas.

Animals↗
PubMed1981

Effects of vitrectomy and phakectomy on the drainage of the vitreous compartment.

Plastic microspheres (7-10 micrometers in diameter), 51Cr-labeled autologous red blood cells (RBC), and 125I-tagged homologous albumin were injected into the vitreous space of vitrectomized phakic and aphakic rabbits. The drainage into the aqueous compartments and blood circulation was assessed. In phakic eyes, there was practically no movement of microspheres and RBC into the anterior chamber over a period of 19 days. In aphakia, vitreous clearance improved but only 1%-3% of labeled RBC appeared in the blood circulation during the first 3-4 days. About 40%-70% of the 125I-albumin injected left the eye within 24 h, as compared to 15%-25% in phakic rabbits. Thus, a vitrectomy in phakic eyes does not lead to anterior drainage of intact RBC and even after combined vitrectomy and phakectomy, the drainage of RBC is not complete; the elimination of albumin is greatly enhanced after vitrectomy.

Animals↗
PubMed1981

Cerebral circulation in acute arterial hypertension--protective effects of sympathetic nervous activity.

The cervical sympathetic chain was stimulated electrically at 6 or 3 Hz on one side in anesthetized cats. Acute arterial hypertension was induced by ligation of the aorta. Evans blue was given as tracer for protein leakage. The regional blood flow in the brain was determined by using labelled microspheres. At high blood pressures there was a multifocal breakdown of the blood-brain barrier. The regions with breakdown had 10-20 times the normal flow rates. With a maintained hypertension regions which were overperfused at 5 min were still overperfused at 10 min, but there was little addition of new overperfused areas. Normalization of the pressure resulted in almost twice the normal flow rates in previously overperfused regions. The breakdown of the blood-brain barrier was restricted to the non-stimulated side, or more marked on that side. The protective effect of the sympathetic stimulation lasted more than 10 min. The results indicate that acute arterial hypertension tends to cause forced and long-lasting vasodilation in some areas in the brain but regions which are resistant to the acute rise have an increase in the vascular tone. Sympathetic activity helps in developing this tone. Normalization of the blood pressure results in partial recovery of the vascular tone in previously overperfused regions and normalization in other areas.

Acute Disease↗
PubMed1981

Ocular responses to antidromic trigeminal stimulation, intracameral prostaglandin E1 and E2, capsaicin and substance P.

The role of nerve conduction was studied in acute experimental uveitis caused by antidromic trigeminal nerve stimulation, prostaglandin E1 and E2 (PGE1 and PGE2), capsaicin and substance P (SP). Systemic indomethacin was used to prevent formation of endogenous prostaglandins, and intracameral injection of tetrodotoxin (TTX) was used to block nerve conduction. 10 micrograms TTX prevented the miosis and reduced the rise in intraocular pressure (IOP) usually caused by antidromic trigeminal nerve stimulation. At a low dose of PGE1 the IOP rise was blocked by TTX. At higher doses of PGE1 and PGE2 the pressure effect was not blocked by TTX; the miotic effect was markedly diminished. Capsaicin caused a rise in IOP that was almost totally blocked by TTX, while the miosis at high doses seemed unaffected. At low doses, capsaicin-induced miosis could be abolished by TTX. SP caused miosis in TTX treated eyes similar to that in untreated eyes; the IOP rise was delayed by TTX. The results indicate that nerve conduction plays a role in the IOP reaction caused by low doses of PGE1 and by capsaicin and SP. The mechanism suggested is an axon reflex, elicited in the anterior uvea and resulting in transmitter release in the ciliary processes. Nerve conduction with release of SP or a similar substance in the iris seems to be required for the miotic effects of PGE1 and PGE2. SP and capsaicin are similar in not requiring nerve conduction to cause miosis, but the capsaicin effect probably requires presence of nerves, since denervated eyes--which respond to SP--have been reported no to respond to capsaicin does similar to those used here.

Animals↗