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Biomedical subjects

M Wiederholt

Publications and source records attributed to M Wiederholt.

At least 127 records · Page 7Linked to original sources
PubMed1984

Effect of bicarbonate, pH, methazolamide and stilbenes on the intracellular potentials of cultured bovine corneal endothelial cells.

Micropuncture of cultured bovine corneal endothelial cells led to registrations stable for hours. Intracellular potentials were mainly in the range of -40 to -55 mV, average 46.3 +/- 0.6 mV (SEM). Changes of extracellular [HCO-3] led to voltage transients, their amplitude depending logarithmically on [HCO-3] with a mean slope of 37.3 +/- 8.8 (SD) mV. After removal of bicarbonate/CO2, a steady-state depolarization was seen. This steady-state depolarization, but not the voltage transients, could be reduced by 1 mM Ba++. After removal of bicarbonate, the voltage response to changes of extracellular potassium was reduced. Alteration of pHi induced by permeable buffers (butyrate, glycodiazine and ammonium) also resulted in voltage transients, internal acidification being correlated with a hyperpolarization, and internal alkalinization with a depolarization. Also changes of external pH caused voltage responses, alkalinization causing a hyperpolarization, acidification a depolarization. Methazolamide, an inhibitor of carbonic anhydrase, as well as stilbenes (SITS or DIDS) caused a reduction of the voltage response to HCO-3 and pH. Their effects were additive. It is suggested that corneal endothelial cells possess one or two electrogenic transporters for HCO-3 or related species, one of which is inhibitable by stilbenes.

Animals↗
PubMed1984

Relationship between peritubular membrane potential and net fluid reabsorption in the distal renal tubule of Amphiuma.

Amphiuma kidneys were isolated and perfused with modified Ringer solution and peritubular and transepithelial membrane potentials (p.d.s) in distal tubules measured with micro-electrodes during rapid changes of luminal electrolyte concentrations. Peritubular membrane potential and net fluid reabsorption (split-oil-droplet method) were also measured with and without application of various drugs known to alter transport. Raising the luminal sodium concentration from 10 to 100 mM reversibly increased the peritubular p.d. The magnitude of the peritubular p.d. was a saturable function of luminal sodium concentration. In the presence of chloride in the lumen the peritubular hyperpolarization following increased luminal sodium could be inhibited by luminal amiloride (10(-4)M). Sodium-induced hyperpolarization of the peritubular p.d. could be completely inhibited by 10(-5)M-ouabain. Adding amiloride (10(-4)M) to the luminal fluid rapidly and reversibly depolarized the peritubular p.d. and inhibited fluid reabsorption. Addition of amphotericin B (20 micrograms/ml) to the luminal perfusion solution had no effect on peritubular p.d. at 100 mM-luminal NaCl but at 10 mM-NaCl, peritubular p.d. hyperpolarized. Fluid reabsorption was stimulated (with 100 mM-NaCl in the lumen). Addition of amphotericin when the tubule was perfused on both sides with solutions containing a constant potassium concentration of 78 mM and a variable sodium concentration ranging from 7.8 to 34.5 mM revealed strong dependence of the peritubular hyperpolarization on the sodium concentration. Luminal furosemide (10(-4)M) and chlorothiazide (10(-4)M) and peritubular ethacrynic acid (10(-4)M) all reduced fluid reabsorption but hyperpolarized the peritubular p.d. The data suggest the presence of an electrogenic sodium transport process in the peritubular membrane that directly contributes to the generation of the peritubular potential. In addition, chloride transport has an important role in determining this potential.

Absorption↗
PubMed1984

Decrease of intracellular chloride activity by furosemide in frog retinal pigment epithelium.

We found that intracellular chloride activity in frog retinal pigment epithelium (RPE) was significantly higher than predicted from the equilibrium distribution across the cell membranes. When transepithelial chloride transport was inhibited by furosemide intracellular chloride activity decreased and approached electrochemical equilibrium. These data indicate that RPE possesses an active, furosemide-sensitive chloride transport across the apical membrane.

Animals↗
PubMed1984

Corticosteroids and the active ion transport of the isolated human lens.

Glucocorticoids may induce posterior subcapsular cataract in man following topical or systemic administration. Translenticular potential difference (PD) and short circuit current (SCC) measurements were performed on the isolated human lens. 6-methylprednisolone 10(-4)mol 1(-1) did not change PD and SCC. However, 10(-3) and 10(-2)mol 1(-1) prednisolone reduced PD and SCC already 45 min after administration. An inhibition of SCC from 5.4 microA cm-2 to 3.8 microA cm-2 was obtained after prednisolone. PD was reduced from 6.2 mV (anterior side positive) to 4.6 mV, while resistance was unchanged. The effect on PD and SCC could only be demonstrated when prednisolone was given to the epithelial (anterior) side of the lens. After the 2-3 hr incubation of human lenses in 10(-2)mol 1(-1) prednisolone macroscopically visible opacities under the posterior lens capsule could be seen regularly. Aldosterone had no effect on PD, SCC and transparency. The data are consistent with the hypothesis that in the human lens glucocorticoids may induce cataract formation by inhibition of epithelial electrolyte transport.

Adrenal Cortex Hormones↗
PubMed1983

Adrenergic regulation of sodium and chloride transport in the isolated cornea of rabbit and man.

Isolated corneas were mounted in Ussing-Zerahn-type chambers and short circuit current (SCC) was measured before and after application of drugs (5 X 10(-5) mol X 1(-1)) interfering with adrenergic receptors. Epinephrine increased SCC in the rabbit cornea and decreased SCC in the human cornea. alpha-Adrenergic stimulation or inhibition did not affect SCC. The increase in SCC observed after terbutaline (beta 2-agonist) was similar to the increase after isoproterenol (beta 1- and beta 2-agonist). SCC was not influenced by the beta 1-antagonist atenolol but was modified, although differently in rabbit and man, by the beta 1- and beta 2-antagonist propranolol. Thus, the catecholamine response of the rabbit and human cornea is mainly mediated by beta 2-adrenergic receptors. However, species differences were observed when testing the effect of propranolol on the transcorneal flux of 22Na and 36Cl. In the rabbit cornea the net Cl flux (directed from the aqueous to the tear side) was inhibited by propranolol, whereas net Na flux (from the tear to the aqueous side) was not influenced by the drug. In the human cornea propranolol reduced unidirectional Na flux from the aqueous to the tear side. Thus, the regulatory effect of propranolol on corneal transparency is different in man and the rabbit.

Adrenergic beta-Agonists↗
PubMed1982

Human precorneal tear film pH measured by microelectrodes.

The pH value in human precorneal tear film was measured with micro- and semimicro-pH-electrodes; the mean was pH 7.6. Stimulation of tear secretion and blinking led to a decrease in the pH value. When the eyelid was open, the precorneal tear film was alkalized by equilibration with the partial pressure of the CO2 in the surrounding air. When the eyelid remained open for 60 s or longer, an equilibrium value of greater than pH 9 was attained.

Blinking↗
PubMed1982

Rabbit corneal allograft survival following topical administration of cyclosporin A.

Cyclosporin A (CS-A), selectively inhibited cellular immunity, delayed the skin graft-induced rejection of corneal allografts in rabbits when administered subconjunctivally in the dose of 3 mg/kg/day or in the form of 5% water-soluble drops five times daily for 28 days. The subconjunctival application of CS-A was irritating, whereas the topical instillation of the water-soluble preparation was well tolerated. The corneal grafts were rejected after discontinuation of the therapy. Rejection was confirmed by scanning and transmission electron microscopy. The mechanism by which CS-A delayed corneal graft rejection seems to depend mainly on the specific and/or the nonspecific effect of topical CS-A on lymphocytes.

Administration, Topical↗
PubMed1981

Effect of calcium, furosemide and chlorothiazide on net volume reabsorption and basolateral membrane potential of the distal tubule.

In the distal tubule of the isolated kidney of Amphiuma net volume reabsorption (split-oil droplet method) and basolateral membrane potential (psi b) were measured. Luminal perfusion solution could be changed rapidly from 108 mmol . 1-1 NaCl plus 0.1 mmol . 1-1 calcium to solutions containing 103 or 97 mmol . 1-1 NaCl plus 3.6 or plus 7.2 mmol . 1-1 calcium. Furthermore, 10(-4) mol . 1-1 furosemide or chlorothiazide were applied luminally. (1) Addition of 7.2 mmol . 1-1 calcium hyperpolarized psi b from -73.4 mV to -108.3 mV and inhibited net volume reabsorption. (2) Similarly, when furosemide was injected, psi b was hyperpolarized and net volume reabsorption reduced. Application of both high calcium and furosemide further inhibited volume reabsorption. (3) The effects of chlorothiazide were similar to those of furosemide. However, when both high calcium and chlorothiazide were administered psi b and volume reabsorption were almost normalized. (4) The data are consistent with the hypothesis that calcium and the diuretics interfere primarily with chloride uptake across the luminal membrane and thus reduce sodium chloride transport. When chlorothiazide in the presence of high luminal calcium almost normalized chloride transport, it is likely that its effects were by stimulating calcium transport and thus increasing intracellular calcium activity.

Animals↗
PubMed1980

The effects of extracellular potassium, ouabain, and prostaglandins on intracellular potassium activity in sheep cardica Purkinje fibers.

(1) Intracellular K activity (aKi) of sheep heart Purkinje fibers was measured using K-selective microelectrodes (liquid ion exchanger). aKi in the resting state with an extracellular K of 4 mmol . l-1 EK was 112.9 +/- 6.1 mmol . l-1 (n = 47) for a membrane potential (VM) of -73.3 +/- 0.9 mV. VM deviated from the calculated potassium equilibrium potential (EK = -93mV). (2) When extracellular K was decreased to 2 mmol . l-1 or increased to 6 and 10 mmol . l-1 EK changed from -114 to -84 and -73 mV, with little change in aKi. (3) aKi and VM significantly decreased after administration of 10(-6) mol . l-1 ouabain. (4) Prostaglandins (PGI2 10-100 micrograms . l-1 and PGE2 0.01-1 microgram . l-1) decreased aKi without greatly changing VM. The differences between VM and EK became smaller. These effects indicate an increase in K permeability and may explain the antiarrhythmic action of prostaglandins.

Animals↗
PubMed1980

[Treatment of central retinal venous and arterial occlusion by isovolemic hemodilution (author's transl)].

(1) Ten patients (mean age 71) with fully developed central retinal venous occlusion were treated by isovolemic hemodilution over a period of four to six weeks. Hematocrit was lowered in steps to about 30% to improve retinal microcirculation. For two to four days, 500 ml whole blood were exchanged daily for about 250 ml hydroxyethyl starch and 250 ml plasma. The procedure was repeated every five to ten days whenever the hematocrit exceeded 35%. Visual acuity was considered to be improved when the patient could read at least two more lines on the test card. Four to six weeks after starting hemodilution therapy visual acuity had improved in seven patients, deteriorated in one, and was unchanged in two. In the follow-up study six months after treatment visual acuity, as compared to data before treatment, had improved in four patients, deteriorated in two and was unchanged in four. Three patients developed a neovascular glaucoma and had to undergo photocagulation treatment. (2) As expected, hemodilution failed to improve visual acuity in five patients who had had a complete central retinal arterial occlusion for more than four hours. (3) This is the first time that a beneficial effect of isovolemic hemodilution on visual acuity, probably mediated by an improvement in retinal blood flow, has been demonstrated in man. However, only in retinal tissue with at least minimal blood flow (venous but not arterial occlusion) can this method be effective. Except for severe anemia or thrombocytosis there are no absolute contraindications. No adverse side-effects were observed. To prevent neovascularization it is planned to use a combination of hemodilution and photocoagulation.

Aged↗