Risk of homelessness after discharge from psychiatric wards in Denmark: a nationwide register-based cohort study.

OBJECTIVE: To examine the absolute and relative risk of homelessness following discharge from psychiatric wards in Denmark. METHODS: A nationwide, register-based, cohort study including people aged 18+ years discharged from psychiatric wards in Denmark between 1 January 2001 and 31 December 2015. We analysed associations between psychiatric diagnoses and risk of homelessness using survival analysis. RESULTS: A total of 126 848 psychiatric in-patients were included accounting for 94 835 person-years. The incidence of homelessness one year following discharge was 28.18 (95% CI 26.69-29.75) and 9.27 (95% CI 8.45-10.16) per 1000 person-years at risk in men and women respectively. The one-year cumulative probability of first homelessness after discharge from psychiatric wards was 1.58% (95% CI 1.48-1.68) in males and 0.55% (95% CI 0.50-0.61) in females. Substance use disorders increased the risk of homelessness after discharge with adjusted incidence rate ratios of 6.60 (95% CI 5.19-8.40) (men) and 13.06 (95% CI 9.31-18.33) (women), compared with depressive disorders. Prior history of homelessness was an important predictor for homelessness following discharge. CONCLUSIONS: The first year following discharge from psychiatric wards is a high-risk period of homelessness, especially when having a substance use disorder or a prior history of homeless shelter contact. Improved efforts to prevent homelessness are needed.

Nitric oxide as a mediator of parasympathetic vasodilation in ocular and extraocular tissues in the rabbit.

PURPOSE: The aim of this study was to investigate in rabbits the relationship between nitric oxide and the noncholinergic vasodilation caused by facial nerve stimulation in the eye and some extraocular tissues. METHODS: Uveal vascular resistance was determined by measuring simultaneously the flow from a cannulated vortex vein with intraocular pressure and arterial blood pressure recordings. The local blood flow in different parts of the eye (iris, ciliary body, choroid, and retina), eyelids, nictitating membrane, Harderian gland, and lacrimal gland was determined using radioactive microspheres. The effects of facial nerve stimulation, at different frequencies, were examined before and after the administration of nitric oxide synthase (NOS) inhibitors. RESULTS: In the experiments with direct determination of uveal blood flow, stimulation of the facial nerve caused a frequency-dependent decrease in uveal vascular resistance, indicating vasodilation. This effect was reduced or abolished by NOS inhibition at low frequencies but was unaffected at high frequencies. Determination of regional blood flow, with radioactive microspheres, showed that the stimulation increased local blood flow in all parts of the uvea. Compared to the nonstimulated control side, stimulation at 2 Hz increased choroidal blood flow by 89% +/- 12% before NOS inhibition and by 45% +/- 10% after NOS inhibition, a difference of 44% +/- 77% (n = 9; P < or = 0.05). Iris and ciliary body vasodilation appeared to be equally reduced. In eyelids, Harderian gland, and lacrimal gland, the vasodilation elicited by stimulation at 2 Hz was abolished almost completely by NOS inhibition. The vasodilation in most of the extraocular tissues was reduced significantly by NOS inhibition at 5 Hz, with only a slight reduction in the choroid, iris, and ciliary body. Retinal blood flow also was significantly increased by facial nerve stimulation at 2 Hz and 5 Hz. The increase in retinal blood flow appeared to be more sensitive to NOS inhibition than the increase in uveal blood flow. CONCLUSIONS: These results suggest that the formation of nitric oxide plays an important role in the uveal, retinal, and extraocular vasodilation brought about by facial nerve stimulation at low frequencies. At high frequencies, other neurotransmitters also seem to be involved.

Ocular blood flow and retinal metabolism in abyssinian cats with hereditary retinal degeneration.

PURPOSE: To investigate if retinal blood flow decreases with progression of the disease in Abyssinian cats with progressive retinal atrophy (PRA), to examine if the choroidal blood flow was affected by the disease, and to determine the uptake of glucose and formation of lactate in the outer retina. METHODS: Local blood flow in different parts of the eye was determined with radioactive microspheres, in 9 normal cats and in 10 cats at different stages of PRA. Three blood flow determinations were made in each animal, during control conditions, after IV administration of indomethacin and after subsequent administration of N(omega)-nitro-L-arginine (L-NA). Blood samples from a choroidal vein and a femoral artery were collected to determine the retinal formation of lactate and uptake of glucose. RESULTS: In Abyssinian cats with PRA (n = 10), the retinal blood flow was significantly (P < or = 0.01) lower than in normal cats (n = 9) during control conditions, 6.4 +/- 1.7 compared with 14.1 +/- 1.9 g min(-1) x (100 g)(-1). The vascular resistance in the iris and ciliary body was significantly higher in the cats at a late stage of PRA, both compared with normal cats and to cats at an early stage of the disease, whereas the choroidal vascular resistance was not significantly affected. Indomethacin had no effect on ocular blood flows in normal cats, but in cats with PRA, iridal blood flow was more than doubled after indomethacin. The retinal formation of lactate was significantly (P < or = 0.001) lower in cats with PRA than in normal cats, 0.111 +/- 0.035 (n = 8) compared with 0.318 +/- 0.024 (n = 8) micromol x min(-1). The uptake of glucose was not significantly different in cats with PRA. CONCLUSIONS: Retinal blood flow is severely decreased in Abyssinian cats at a late stage of retinal degeneration, whereas the choroidal microcirculation is not significantly affected by the disease. At a late stage of retinal degeneration, vascular resistance in the iris is significantly increased, which at least in part could be caused by cyxlooxygenase products.

PACAP-27 and PACAP-38: vascular effects in the eye and some other tissues in the rabbit.

The effects of pituitary adenylate cyclase activating polypeptide (PACAP) on regional blood flow in the eye and other tissues were investigated in albino rabbits. Direct determination of the flow from a cannulated vortex vein, in animals pretreated with a vasopressin receptor antagonist, showed that i.v. infusion of either PACAP-27 or PACAP-38 caused a dose-dependent (0.08-0.64 pmol/kg per min) decrease in the uveal vascular resistance. Regional blood flow was determined, with radioactive microspheres, during i.v. infusion of PACAP-27 or PACAP-38 (0.64 pmol/kg per min) in rabbits pretreated with hexamethonium and a vasopressin receptor antagonist. In these experiments, both PACAP-27 and PACAP-38 increased choroidal blood flow by about 50%, whereas there was no effect in the anterior uvea. Nor was there any major effect on blood flow in the anterior uvea after intracameral injection of PACAP-27 or PACAP-38 (3 pmol). The largest blood flow increases, caused by i.v. infusion of PACAP-27 or PACAP-38, were observed in the parotid gland, submandibular gland, eyelids and nictitating membrane. Local blood flow in the choroid plexus, pineal gland, posterior pituitary gland, stomach, kidney and adrenal gland was also significantly increased during the i.v. infusion of PACAP-27. The results of the present investigation indicate that PACAP-27 and PACAP-38 are about 100 times more potent than vasoactive intestinal polypeptide and peptide histidine isoleucine as vasodilators in the rabbit choroid and, possibly, also in many other tissues of the rabbit.

Non-adrenergic sympathetic vasoconstriction in the eye and some other facial tissues in the rabbit.

The effects of unilateral sympathetic nerve stimulation (SNS) on regional blood flow in the rabbit were studied with radioactive microspheres. SNS at 10 or 4 Hz caused an approximately 60% reduction in choroidal blood flow, which was partly resistant to alpha-adrenoceptor blockade with phenoxybenzamine. The vasoconstriction evoked by SNS at 2 Hz was completely abolished by alpha-adrenoceptor blockade. A similar response was seen in the iris, ciliary body, masseter muscle and lacrimal gland. In the harderian gland, however, SNS (2 Hz) after alpha-adrenoceptor blockade caused a significant reduction in blood flow. In the salivary glands, combined beta- and alpha-adrenoceptor blockade with propranolol and phenoxybenzamine revealed a slight non-adrenergic vasoconstriction during SNS at 10 Hz; however, the blood flow was significantly increased during SNS at 4 and 2 Hz following alpha-adrenoceptor blockade. These results indicate that there is a frequency-dependent, non-adrenergic component in the sympathetic vasoconstriction of the eye and several facial tissues. In the salivary glands, beta-adrenoceptor-mediated vasodilatation tends to mask a non-adrenergic vasoconstriction.

Suppression of VIP- and terbutaline stimulated aqueous humor flow by increased intraocular pressure in the cynomolgus monkey.

The effect of increased intraocular pressure (IOP) on stimulated aqueous humor flow (AHF) was studied in cynomolgus monkeys. Two experimental series were performed, one with unilateral VIP-treatment (60 micrograms intracamerally) and one with unilateral terbutaline-treatment (10 micrograms.ml-1 perfusion fluid). The AHF was determined with a labelled albumin dilution method, and an artificial increase in IOP was produced by clamping the outlet of the perfusion system, thus causing a net inflow of perfusion fluid. The initial AHF was significantly higher in the VIP-treated eye than in the control eye - 1.568 +/- 0.095 as compared to 1.112 +/- 0.103 microliters.min-1 (P less than or equal to 0.01). The spontaneous IOP was 5.8 +/- 0.4 mmHg (P less than or equal to 0.001) higher in the VIP-treated eye. There was no difference in pseudofacility between the VIP-treated eye (0.063 +/- 0.016 microliter.min-1.mmHg-1) and the control eye (0.065 +/- 0.022 microliter.min-1.mmHg-1), but the total and true outflow facilities were higher in the VIP-treated eye. In the experiments with terbutaline, the initial AHF was 1.729 +/- 0.114 for the experimental eye and 1.262 +/- 0.104 microliters.min-1 for the control eye (P less than or equal to 0.01). The pseudofacility tended to be higher in the terbutaline-treated eye (0.072 +/- 0.026 microliters.min-1.mmHg-1) than in the control eye (0.048 +/- 0.012 microliters.min-1.mmHg-1), but the difference was not statistically significant. There was no difference in total and true outflow facility between the experimental and control eye. The results indicate that the pressure sensitivity of the AHF is independent of the initial level of the AHF. VIP increases true outflow facility, possibly via a direct effect on the trabecular meshwork. VIP also appears to rise the IOP due to an increase in episcleral venous pressure, which could be secondary to vasodilatation in the anterior segment.

Effects of timolol on terbutaline- and VIP-stimulated aqueous humor flow in the cynomolgus monkey.

The effects of timolol on terbutaline- and VIP-stimulated aqueous humor flow were investigated in cynomolgus monkeys, with a labeled albumin dilution method. The maximal increase in aqueous humor flow caused by intracameral (100 micrograms/ml) or intravenous (0.4 micrograms/kg/min) administration of terbutaline was about 100%. The effect of intravenously infused terbutaline was completely abolished by intracameral administration of timolol, 0.1 mg/ml. The same dose of timolol also abolished the effect of intravenously infused VIP, 50 ng/kg/min. Intravenous administration of timolol, 0.2 mg/kg, had no effect on VIP-stimulated aqueous humor flow, when VIP (90 micrograms) was given intracamerally, but abolished completely the effect of intracameral terbutaline, 100 micrograms/ml. The results suggest that the effect of intravenously infused VIP on aqueous humor flow is secondary to activation of the sympathetic nervous system, while the effect of intracameral administration of VIP is a direct effect on the ciliary epithelium. The maximal aqueous humor flow achieved with terbutaline is comparable to that in conscious cynomolgus monkeys.

Pituitary adenylate cyclase-activating polypeptide- and VIP-induced activation of adenylate cyclase in the porcine non-pigmented ciliary epithelium: effects of antagonists.

Vasoactive intestinal polypeptide (VIP) and two pituitary adenylate cyclase-activating polypeptides (PACAP-38 and PACAP-27) were investigated for their ability to activate the adenylate cyclase system in membrane preparations from the porcine non-pigmented ciliary epithelium (NPE). The NPE was dissociated from the adjacent pigmented ciliary epithelium of the iris-ciliary body (ICB) by incubation in low Ca2+ Ringer's solution. All three peptides caused a dose-dependent increase in cAMP formation in the NPE and the remaining part of the ICB. A VIP antagonist had a small effect on the dose-response curve for VIP, while the two PACAP fragments, PACAP(6-38) and PACAP(6-3 1), caused a rightward shift of the concentration response curves for PACAP-38, PACAP-27 and VIP. The results of the present study indicate that the non-pigmented ciliary epithelium of the porcine eye contain receptors for PACAP- and VIP-coupled to adenylate cyclase activation.

The retinol-binding protein.

Vitamin A is transported from its storage site in the liver to the epithelial tissues by a carrier protein, the Retinol-binding protein (RBP). In plasma RBP forms a complex with thyroxine-binding prealbumin. The present article reviews available data on the RBP system. The complete primary structure of RBP has been determined. The plasma concentration of RBP is regulated by the vitamin A status so that in vitamin A deficiency RBP molecules are not secreted from the liver. RBP molecules interact with a cell membrane receptor, probably a protein component present on epithelial cells. Vitamin A is thereby delivered to the cells. The uptake of vitamin A by the cells causes a reduction of the affinity of RBP for prealbumin. The RBP molecules which no longer are able to interact efficiently with prealbumin are excreted through the kidney glomerulus and degraded.

The uveoscleral outflow routes.

As there is no epithelial barrier between the anterior chamber and the ciliary muscle, aqueous humour may freely pass between the ciliary muscle bundles into the supraciliary and suprachoroidal spaces, from which it is drained through the sclera. This uveoscleral outflow of aqueous humour accounts for 40-60% of the total outflow in monkeys, whereas it is considerably less in (3-8%) in cats and rabbits. Direct measurements in human eyes have suggested that less than 15% is drained by the uveoscleral routes. However, indirect calculations have given a value of about 35% in young adults and 3% in elderly persons (> 60 years). Under normal conditions, in monkeys, the uveoscleral outflow is insensitive to changes in the intraocular pressure, but cyclodialysis and experimental uveitis increase the uveoscleral outflow and make it more pressure sensitive. The uveoscleral outflow is decreased by contraction (pilocarpine) and increased by relaxation (atropine) of the ciliary muscle. Thus, changing the tone of the ciliary muscle may redistribute aqueous humour between the conventional and uveoscleral outflow routes. Prostaglandins decrease the intraocular pressure by increasing the uveoscleral outflow. Two mechanisms seem to contribute to this effect: relaxation of the ciliary muscle and changes in extracellular matrix, causing decreased resistance in the uveoscleral outflow routes.

Neuropeptide Y (NPY): a vasoconstrictor in the eye, brain and other tissues in the rabbit.

The effect of neuropeptide Y (NPY) on uveal vascular resistance was studied in rabbits by direct determination of uveal blood flow from a cannulated vortex vein. Regional blood flows, in the eye, the brain and several other tissues, were measured, with radioactive microspheres, during neuropeptide Y-infusion in rabbits with and without alpha-adrenoceptor blockade. Intravenous infusion of increasing doses of neuropeptide Y caused a dose-dependent increase in the total uveal vascular resistance. Maximal effect, a 70% increase, was achieved with 120 pmol kg-1 min-1. In the microsphere experiments, this dose rate was given i.v. over 10 minutes and blood flow determinations were made before and at 2 and 10 minutes after the start of the infusion. After 2 minutes of neuropeptide Y, there were marked blood flow reductions in the spleen, kidneys, adrenal glands, gastro-intestinal tract, choroid plexus and pineal and pituitary gland. The effect in the eye was small at 2 minutes, but at 10 minutes local blood flows in the choroid and the ciliary body were decreased by 50% and the iridal blood flow by 30%. Retinal blood flow was not affected by neuropeptide Y. At 10 minutes there were also significant blood flow reductions in the brain, tongue, masseter muscle and several glandular tissues. The effects of neuropeptide Y on local blood flow in rabbits that had been subjected to alpha-adrenoceptor blockade were very similar to the effects in the animals without alpha-adrenoceptor blockade. The results show that, in the rabbit, neuropeptide Y has marked effects on local blood flows in several tissues, including the eye, and suggest that neuropeptide Y may significantly contribute to the uveal vasoconstriction during sympathetic nerve stimulation.

The significance of nitric oxide for parasympathetic vasodilation in the eye and other orbital tissues in the cat.

The role of nitric oxide formation in the vasodilation in the eye and other orbital tissues caused by pre-ganglionic stimulation of the facial nerve was studied in cats under alpha-chloralose anaesthesia. Regional blood flows were determined with radioactive microspheres during unilateral stimulation of the facial nerve before and after inhibition of nitric oxide synthase (NOS), alone or in combination with muscarinic blockade.N(omega)-nitro-L-arginine (L-NA), a non-selective NOS-inhibitor, caused a significant increase in mean arterial blood pressure (MABP) and a decrease in cardiac output (CO). Concomitantly, local blood flows on the non-stimulated control side were reduced in most of the investigated tissues, indicating marked vasoconstriction. An inhibitor selective for neuronal NOS, 7-nitro-indazole (7-NI), had no significant effect on MABP, CO or local blood flows. During facial nerve stimulation at 5 Hz (n =6), choroidal blood flow on the stimulated side was 108+/-41% (P

Comparison of the vasodilatory effects of vasoactive intestinal polypeptide (VIP) and peptide-HI (PHI) in the rabbit and the cat.

In rabbits, intravenous infusion of increasing doses of peptide-HI (PHI), with direct measurement of the uveal blood flow from a cannulated vortex vein, caused a dose-dependent decrease in the uveal vascular resistance. The maximal effect, a 50% decrease, was achieved with about 60 pmol kg-1 min-1. This is similar to what has previously been reported for vasoactive intestinal polypeptide (VIP). Determination of local blood flows, with radioactive microspheres, showed that i.v. infusion of VIP or PHI (60 pmol kg-1 min-1) caused about the same increase in the choroidal blood flow, while the local blood flow in the anterior uvea was unaffected by both peptides. The most marked effect of VIP was observed in glandular tissues, such as the pancreas, submandibular, parotid and thyroid glands. The pancreas was the only one of these tissues in which PHI caused an increased blood flow. In cats, i.v. infusion of VIP (30 pmol kg-1 min-1) during 5-7 min caused a markedly increased blood flow in several tissues. The vasodilation in glandular tissues was even more marked than in rabbits; 3-15 times the normal compared with two to five times the normal in rabbits. The choroidal blood flow was however significantly decreased and the local flow in the anterior uvea tended also to be reduced. Intravenous infusion of either a higher dose of VIP (60 pmol kg-1 min-1) or of PHI (1800 pmol kg-1 min-1) during 2 min had no effect on the uveal vascular resistance. This dose of PHI had only minor effects on local blood flows in other tissues. The results of the present study indicate that porcine VIP is a more potent vasodilator than porcine PHI in most tissues of both the cat and the rabbit, but that there may be exceptions such as the rabbit uvea. The difference in potency may also vary considerably between the species.

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)

Effects of cervical sympathetic nerve stimulation and neuropeptide Y (NPY) on cranial blood flow in the cat.

Effects of cervical sympathetic nerve stimulation (SNS) at 10 Hz and intravenous infusion of neuropeptide Y (NPY), 10 and 100 pmol x kg body wt-1 x min-1 for 5 min, on regional blood flow in the cat were investigated with radioactive microspheres. Sympathetic nerve stimulation caused significant reductions in blood flows in the facial tissues including the eye. Alpha-adrenoceptor blockade with phenoxybenzamine and combined beta- and alpha-adrenoceptor blockade with propranolol and phenoxybenzamine abolished the effects of sympathetic nerve stimulation in most facial tissues except in the tongue, upper eyelid and masseter muscle. In most cranial tissues, neuropeptide Y reduced regional blood flow and increased vascular resistance. No effect of neuropeptide Y on vascular resistance was observed in the choroid. In the present study, evidence for a non-adrenergic component in sympathetic vasoconstriction was found in the tongue, upper eyelid and masseter muscle but not in the majority of feline facial tissues. Neuropeptide Y was a potent vasoconstrictor in many cranial tissues, while in parts of the uvea, the effects of neuropeptide Y were less pronounced.

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.

Studies on thyroid hormone-binding proteins. I. The subunit structure of human thyroxine-binding globulin and its interaction with ligands.

Thyroxine-binding globulin was isolated from human plasma by ammonium sulfate fractionation, chromatographic separations on diethylaminoethyl-Sephadex, gel chromatography, and two different electrophoretic procedures. The highly purified was homogeneous when subjected to polyacrylamide gel electrophoresis, ultracentrifugation analyses, and immunochemical determinations. The weight average molecular weight as determined by sedimentation equilibrium ultracentrifugations was 54,000 and by sedimentation diffusion data 55,000. Amino acid analyses indicated a minimum of 110 amino acid residues per molecule. By determination of the minimum in the curve for the fraction of maximum deviation from the amino acid analyses it was found that the minimum molecular weight for the polypeptide was 12,200. Carbohydrate analyses demonstrated the presence f equimolar amounts of amnnose, galactose, and glucosamine, and the carbohydrate portion constituted 7.5% of the total weight. The amino acid analyses suggested that thyroxine-binding globulin is composed of 4 subunits. Molecular weight determinations by gel chromatography in 6 M guanidine hydrochloride indicated the presence of three species of globulin with apparent molecular weights 52,000, 25,000, and 13,500, respectively. Prolonged storage in guanidine hydrochloride promoted a more than 60% yield of the monomeric species. Moreover, a half-molecule of thyroxine-binding globulin was isolated and shown to consist of two polypeptide chains of similar molecular weight...

Isolation and identification of the major concanavalin A binding glycoproteins from murine-lymphocytes.

The major glycoproteins which bind concanavalin A have been isolated and identified from murine spleen cells, thymocytes,and purified thymus-derived (T) lymphocytes, and from the spleen cells of congenitally athymic (nude) mice. The cells were radiolabeled by lactoperoxidase catalyzed 125I iodination or by culturing the cells in media containing [3H]leucine or [3H]fucose. The cell membrane was solubilized with Nonidet P-40 and the concanavalin A binding proteins were isolated by affinity chromatography and analyzed according to their mobility on polyacrylamide gel electrophoresis in sodium dodecyl sulfate. The major proteins from various lymphocyte preparations were identified by immunoprecipitation with specific antisera. The molecules coded by the histocompatibility-2 complex acted as concanavalin A binding proteins H-2K and H-2D were isolated from T lymphocytes, thymocytes, and bone marrow derived (B) lymphocytes. The Ia antigens were identified from B lymphocytes and tentatively identified from T lymphocytes. In addition to these H-2 complex proteins, immunoglobulin M and D on B lymphocytes also bound concanavalin A binding. All these glycoproteins have previously been identified as cell surface molecules. The presence of certain minor unidentified concanavalin A binding proteins on lymphoid cells is indicated.

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).