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Biomedical subjects

L Thörig

Publications and source records attributed to L Thörig.

At least 19 recordsLinked to original sources
PubMed1989

Cholinergic receptors in the extraocular rectus muscle of the rabbit.

The cholinergic receptors in rabbit isolated rectus muscle preparations were characterized by means of cholinergic agonists and antagonists. The concentration-dependent contraction induced by acetylcholine, carbachol or oxotremorine remained uninfluenced by atropine (10(-5) M), whereas the nicotinic receptor antagonist hexamethonium caused a parallel shift of the concentration-response curve. The agonists pilocarpine, methacholine and aceclidine, which are selective muscarinic receptor stimulants, did not cause contraction of the muscle preparation. However, the nicotinic receptor stimulant 1,1-dimethyl-4-phenylpiperazine iodide (DMPP) caused contraction similar to that induced by acetylcholine. DMPP-induced contractions were inhibited by hexamethonium, causing a parallel rightward shift of the concentration-response curve. This shift could be quantified by means of a Schild plot, indicating competitive antagonism with a PA2 value of 4.63 for hexamethonium. Atropine when applied together with hexamethonium did not cause a further shift of the concentration-response curve. The present results clearly indicate that the cholinergic receptors which mediate contraction in the rabbit isolated extraocular muscle preparation belong to the nicotinic subtype.

Acetylcholine↗
PubMed1986

Effects of B-HT 920 in the eye and on regional blood flows in anaesthetized and conscious rabbits.

The influence of unilateral ocular instillation of B-HT 920 (50 micrograms) on regional ocular, cerebral and peripheral blood flows was investigated with the labelled microsphere method in conscious and anaesthetized albino rabbits. In urethane-anaesthetized rabbits the intraocular pressure (IOP) fell during 1 hr following topical B-HT 920 whereas no changes in regional blood flows were observed. Only in conscious rabbits was a decrease in regional blood flows found. B-HT 920 caused a short-term reduction in choroidal blood flow by about 20%. Transient vasoconstrictor effects, due to systemic absorption, were also seen in some extraocular tissues. Concomitantly, B-HT 920 reduced the total cerebral blood flow (CBF) by 23%. In the grey matter and hypothalamic region the decrease in flow was about 20%, while in the hippocampal region, thalamic region, collicles and pons-mesencephalon it was about 10%. In experiments with direct blood flow determination from an opened vortex vein, there was no consistent change of uveal vascular resistance, while IOP and mean arterial pressure (MAP) fell dose-dependently following cumulative intravenously administered bolus doses (10 and 50 micrograms/kg) of B-HT 920. Unilateral loss of the mediated sympathetic tone seemed to increase the ocular responses to B-HT 920, unmasking a vasoconstrictor effect. Additional systemic pretreatment with the selective blocking agents rauwolscine and sulpiride suggests that B-HT 920 produces its ocular hypotensive effect, predominantly by acting on dopamine (DA2) receptors in the eye rather than on alpha 2-adrenoceptors, and its ocular vasoconstrictor effects via both receptor types.

Anesthesia↗
PubMed1986

Topical prostaglandins inhibit trauma-induced inflammation in the rabbit eye.

Topical administration of prostaglandin E1 (PGE1) and prostaglandin F2 alpha (PGF2 alpha) prior to ocular trauma can reduce the ocular inflammatory response in rabbits. In the present study, the ocular trauma consisted of puncture of the cornea, without aspiration of aqueous. Corneal puncture, which causes and inflammatory response, a breakdown of the blood-aqueous barrier, and a biphasic response of the intraocular pressure (IOP), yields a valid model of a mild inflammatory response. Pretreatment with PGE1 and PGF2 alpha led to a lower rise in the aqueous prostaglandin E2 (PGE2) concentration and a reduced inflammatory response after corneal puncture; in addition, the increase in the aqueous protein concentration was smaller and the aqueous ascorbate level was higher. The lower increase in the aqueous PGE2 concentration after pretreatment with PGs correlated with the reduced changes in IOP. It is suggested that PGE1 and PGF2 alpha reduced the trauma-induced inflammatory response by decreasing the formation of endogenous prostaglandins, as reflected by their concentration in aqueous. This study also indicates that the results of studies that require perforation of the cornea or cannulation of the anterior chamber may be affected by profound changes in the levels of cyclo-oxygenase products in the tissues surrounding the aqueous.

Administration, Topical↗
PubMed1985

Effect of acetazolamide (Diamox) on tear secretion.

The side effects of acetazolamide (Diamox) on lacrimation were measured in rats by means of the cotton-thread tear test. After a daily oral 1-mg dose (administered for five days), comparable to the dose used for adult humans on a drug-to-bodyweight basis, tear production remained unaffected but the lacrimal peroxidase secretion decreased by 60% of the baseline level. After withdrawal of acetazolamide the peroxidase secretion returned to the baseline level.

Acetazolamide↗
PubMed1985

M-7 lowers rabbit intraocular pressure.

Changes in intraocular pressure (IOP) and pupil diameter were studied in albino rabbits following topical administration of TL-99, M-7 (N,N-dimethyl analogues of 2-aminotetralin), DiPr-5,6-ADTN, DiPr-6,7-ADTN (dipropyl analogues of aminotetralin) and DPDA (N,N-di-n-propyl-dopamine), known as mixed alpha-adrenoceptor/dopamine receptor agonists with variable alpha 1/alpha 2-adrenoceptor/selectivity. The potencies of those compounds to decrease IOP were compared with each other. We found that M-7 has the most potent IOP-lowering properties, caused minimal ocular discomfort and is of interest as a potential antiglaucoma agent. The ocular hypotension was completely inhibited by rauwolscine and slightly antagonized by various other blocking agents. The results strongly suggest that the IOP-lowering effect of M-7 is mediated by the stimulation of alpha 2-adrenoceptors.

Animals↗
PubMed1985

Comparison of tears and lacrimal gland fluid in the rabbit and guinea pig.

The excretory duct of the lacrimal gland of rabbits and guinea pigs was cannulated in situ for collection of pure lacrimal gland fluid, not contaminated by secretions from the Harderian gland or contributions of desquamating cells of the conjunctival and corneal epithelium. Tears as well as lacrimal gland fluid of both species showed a species-specific and molecular weight-dependent pattern after sodium dodecylsulphate-polyacrylamide (SDS-PAA) gradient slab gel electrophoresis. The most striking difference in both species was a protein corresponding to serum albumin present in tears and almost lacking in lacrimal gland fluid. Likewise, a variety of enzymes, total protein and PGE2 were measured in tears and lacrimal gland fluid. For rabbit tears the lacrimal gland is the primary tissue source of lysozyme (LZM), beta-hexosaminidase (beta-hex), angiotensin-converting enzyme (ACE), plasminogen activator (PA) and total protein, while lactate dehydrogenase (LDH) and the greater part of prostaglandin E2 (PGE2) are present in rabbit tears mainly as products from other ocular tissue sources. In guinea pig tears peroxidase (POD), ACE, PA and less PGE2 are exceted by the lacrimal gland, amylase (AMY), LDH and a substantial amount of PGE2 are added to the guinea pig tears by other ocular tissue sources. Beta-hex and total protein are released from the lacrimal gland and from other ocular tissue sources as well.

Animals↗
PubMed1984

Cotton-thread tear test: an experimental study for testing drugs suspected of side effects on lacrimation.

We tested tear fluid production and lacrimal peroxidase secretion in rats without and with drug consumption with the cotton-thread tear test. Twelve frequently prescribed drugs in patients were given in recommended therapeutic and excessive doses to rats. Daily oral doses during five days of Sudafed Plus (chlorpheniramine/pseudoephedrine combination), promethazine, atropine, timolol, aspirin, diazepam and furosemide equivalent to the doses used for adult humans on a drug-to-body-weight basis or excessive doses, resulted in about 20-60% reduction of tearing. Changes in lacrimal peroxidase secretion were found after administration of atropine, aspirin, furosemide, indomethacine and pilocarpine. Generally, tear production and lacrimal peroxidase secretion returned to baseline levels after withdrawal of the drugs.

Animals↗
PubMed1984

Comparison of enzymes of tears, lacrimal gland fluid and lacrimal gland tissue in the rat.

A variety of enzymes were identified in rat tears and lacrimal gland fluid. The use of a tapered glass cannula in the opening of the excretory duct was found to be an useful method to collect samples of rat lacrimal gland fluid, i.e., the fluid directly originated from the main excretory duct of the lacrimal gland, uncontaminated by secretions from the Harderian gland and from desquamating conjunctival and corneal epithelial cells. Based upon comparison of the enzyme pattern in tears, lacrimal gland fluid and the lacrimal gland tissue, we concluded that the lacrimal gland is the primary tissue source for peroxidase (POD), amylase (AMY) and total protein in rat tears, while plasminogen activator and lactatedehydrogenase (LDH) may be present in tears primarily as secretion products from other ocular tissue sources. beta-hexosaminidase (beta-hex) is released from the lacrimal gland and from other ocular tissue sources as well.

Amylases↗
PubMed1983

The fine-thread method: lacrimation test for measuring ocular side-effects of drugs in the rat.

Tear production was measured by means of the fine-cotton-thread method in rats. Sedation with hypnorm had no pharmacological effect on normal tear production. Daily oral administration of atropine which was comparable with the dose used for human adults on a drug-to-weight basis, resulted in a 60-percent reduction of tearing. Tearing returned to base-line levels after withdrawal of atropine.

Animals↗
PubMed1983

Peroxidase secretion from rat lacrimal gland cells in vitro. I. Alpha-adrenergic stimulation in the absence of alpha-adrenoceptors.

The identification of alpha-adrenergic receptors and subdivision into alpha 1- or alpha 2-subtypes were studied by measuring the specific binding of the radioligands [3H]-prazosin as well as [3H]-clonidine to membranes prepared from homogenized rat lacrimal glands. The absence of high-affinity binding for [3H]-prazosin as well as for [3H]-clonidine indicates that rat lacrimal glands do not possess a substantial amount of alpha 1- and alpha 2-adrenoceptors. The binding data correspond with the characterization by pharmacological means. Monolayers of lacrimocytes were incubated with various selective alpha 1-, alpha 2-, beta-adrenergic agonists and antagonists or other substances, and peroxidase discharge was measured over a period of 1 hr. Among various substances only L-norepinephrine, L-phenylephrine, tyramine and ionophore A 23187 were stimulants of peroxidase secretion, whereas the adrenergic-stimulated secretory response was only suppressed by phentolamine.

Animals↗
PubMed1983

Peroxidase secretion from rat lacrimal gland cells in vitro: II. The role of calcium in stimulus-secretion coupling.

The role of calcium in stimulus-secretion coupling in rat lacrimocytes was investigated. Monolayers of lacrimocytes released peroxidase into the incubation medium upon stimulation with calcium ionophore A 23187, L-norepinephrine, L-phenylephrine and tyramine. Our lacrimocyte preparation can be considered free of endogenous catecholamines, because lacrimocytes derived both from normal and from reserpinized rats responded to tyramine with respect to peroxidase secretion. Phenoxybenzamine, cocaine, verapamil and sodiumorthovanadate failed to inhibit the L-phenylephrine-evoked peroxidase secretion. The stimulatory effects of A 23187, L-norepinephrine and L-phenylephrine required extracellular Ca2+ and could be blocked by phentolamine. The action of tyramine was insensitive to all these measures. It is suggested that the stimulus-secretion of peroxidase from lacrimocytes may consist of a Ca2+-dependent phase for stimulants as A 23187, L-norepinephrine and L-phenylephrine and a Ca2+-independent phase for the non-specific tyramine action.

Animals↗
PubMed1983

Immunological characterization and possible origin of plasminogen activator in human tear fluid.

Human tear fluid has plasminogen activator activity. The type of plasminogen activator activity in unstimulated and stimulated tears was determined, using antibodies that specifically neutralize tissue plasminogen activator or urokinase. All plasminogen activator activity was tissue plasminogen activator-related in both types of tears. Correlations between activities of beta-hexosaminidase, lysozyme and lactate dehydrogenase with tissue plasminogen activator activity indicate that the contribution to plasminogen activator activity of conjunctival and corneal epithelium is more important in unstimulated tears than stimulated tears. In stimulated tears the tissue plasminogen activator activity originates mainly from the lacrimal gland. It is suggested that a constant concentration of plasminogen activator is released from the lacrimal gland and that this concentration is independent of the secretion rate of tear fluid and that the release from the conjunctiva is due to desquamation of cells.

Adult↗
PubMed1982

The role of bacterial adherence in the pathogenesis of infective endocarditis.

Bacterial adherence as a result of specific surface properties may be a contributory factor in the pathogenesis of bacterial endocarditis giving certain types of bacteria a selective advantage to cause this disease. Adherence could interact with other pathogenetic mechanisms, and this interaction could promote or hamper the development of endocarditis. Dextran production by streptococci, the activation of the clotting system by monocyte tissue thromboplastin, and phagocytic removal of bacteria from the vegetational surface by granulocytes and monocytes are examples of interacting mechanisms that could contribute to the pathogenesis of bacterial endocarditis.

Adhesiveness↗
PubMed1980

Effects of immunization and anticoagulation on the development of experimental Escherichia coli endocarditis.

The effects of immunization and anticoagulation in experimental Escherichia coli endocarditis were studied. Immunization of rabbits with E. coli resulted in the development of specific agglutinating and opsonic activity of the serum, but not in bactericidal activity. These antibody activities also developed in nonimmunized rabbits during the course of bactericidal endocarditis. Immune serum promoted phagocytosis in vitro but did not enhance intracellular killing of E. coli by elicited rabbit peritoneal macrophages. The presence of specific antibodies in rabbits after immunization had no effect on the induction or course of E. coli infection of endocardial vegetations. Anticoagulation was found to affect the induction of the infection. In anticoagulated rabbits, larger bacterial inocula were needed to induce an infection, but in animals with bacterial endocarditis the number of bacteria in the vegetations did not differ significantly from that of the control animals.

Agglutination↗
PubMed1980

Effects of monocytopenia and anticoagulation in experimental Streptococcus sanguis endocarditis.

The role of blood monocytes in the attachment of streptococci to endocardial vegetations was investigated in an experimental Streptococcus sanguis endocarditis by depletion of blood monocytes with the cytostatic drug VP 16-213 alone and combined with anticoagulant treatment with warfarin sodium. The numbers of streptococci in the vegetations of control, monocytopenic, and monocytopenic/anticoagulated rabbits were comparable. In the vegetations streptococci were found mainly in areas free of phagocytic cells. It is concluded that streptococci do not have to be phagocytosed by monocytes in the circulation before being deposited on the surface of endocardial vegetations. Even the vegetations of intensively anticoagulated/monocytopenic rabbits showed colonies of streptococci embedded in polymerized fibrin and cellular material, this matrix possibly being held together by streptococcal dextran.

Animals↗
PubMed1980

Experimental Streptococcus sanguis endocarditis: immune complexes and renal involvement.

An increase of agglutinins and circulating immune complexes (CIC) was observed in the sera of rabbits after the induction of bacterial endocarditis (BE) by intravenous injection of live streptococci into animals with a non-bacterial thrombotic endocarditis. Rabbits immunized for 12 days with heat-killed streptococci developed higher levels of agglutinins and CIC than did those unimmunized during BE. The levels remained elevated in the immunized rabbits after the induction of streptococcal endocarditis. In rabbits with very high levels of CIC complement activation occurred in vivo, possibly via the classical pathway. Kidneys from both unimmunized and immunized rabbits with streptococcal endocarditis contained bacteria and also showed inflammatory reactions but only the renal tissue of immunized rabbits with endocarditis showed a little mesangial deposition of immunoglobulin. The findings in this study indicate that in rabbits, renal inflammation due to BE is initiated more often by septic emboli than by immune complex deposition, at least during the first 12 days after infection.

Agglutinins↗