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Biomedical subjects

A Röckel

Publications and source records attributed to A Röckel.

At least 37 records · Page 2Linked to original sources
PubMed1985

Parotid kallikrein secretion in the rat after alterations of electrolyte transport and cAMP activity.

The effects of pharmacologically induced alterations of electrolyte transport and cAMP activity on kallikrein secretion - measured as amidolytic activity - in rat parotid gland were tested in vivo. Changes in transepithelial sodium/potassium transport caused a significant alteration of parotid kallikrein handling. Amidolytic activity was inhibited by sodium channel blockade (via amiloride) and stimulated by an increased sodium influx (via the sodium ionophore monensin). Enhanced intracellular cAMP activity (via dibutyryl cAMP and theophylline) caused a significant increase of ductal kallikrein and potassium secretion. Alterations of intracellular calcium-ion concentration (via A 23187 and verapamil) did not influence parotid kallikrein secretion. Parotid kallikrein secretion seems to be dependent on intracellular sodium and cAMP concentration.

Amiloride↗
PubMed1985

Effects of haemodialysis on the pharmacokinetics of muzolimine.

UNLABELLED: High ceiling diuretics allow a better control of fluid balance in dialysis patients with a minimum urine flow of 500 ml/day. The pharmacokinetics of the high ceiling, long acting diuretic muzolimine (M) was investigated in 6 patients on regular dialysis therapy. METHODS: Concentrations of unchanged M in plasma were determined by high performance thin-layer chromatography (HPTLC) after a single oral dose of 240 mg up to 26 h: A) during and after the performance of dialysis lasting for 3 h, B) 20 h after finishing haemodialysis therapy (non-blind randomized cross-over study). RESULTS: The M plasma levels and the M half-lives did not differ between the two treatment groups (half-life A: 5.1 +/- 0.24 h; B: 4.8 +/- 0.51 h). The M peak concentrations were between 2 and 5 micrograms/ml and were reached 2 h post administration or even earlier. The mean M plasma levels 24 h after administration were in the same range (A: 0.33 +/- 0.16 microgram/ml; B: 0.33 +/- 0.11 microgram/ml).

Adult↗
PubMed1985

Three cases of hemodialysis-associated hypersensitivity reactions.

According to the United States Food and Drug Administration, untoward reactions to capillary hemodialyzers occur at a rate of 3.5 of every 100,000 dialyzers sold. Allergic symptoms immediately after initiation of dialysis consist of burning retrosternal pain, sensation of diffuse heat, cold perspiration, periorbital and facial edema, flushing, laryngeal stridor, bronchial hypersecretion, hypotension, bradycardia, and loss of consciousness. In 1982 Popli et al. reported four patients suffering from such allergic manifestations; three were successfully managed after being taken off dialysis. These investigators thought that inadequate rinsing of cuprammonium cellulose capillary dialyzers was responsible for the reactions, and recommended rinsing the blood compartment with 2 liters of normal saline, and the dialysate compartment with 10 liters of dialysate, both in a single-pass fashion over 20 minutes. Nichols and Platts (1982) (3) reported 15 patients with urticaria, severe bronchospasm, and shock occurring immediately after the blood had been returned from the dialyzer. These authors suggested that the sterilizing agent, ethylene oxide (ETO), was responsible. Poothullil et al. (1975) (4) described a patient with pruritus, severe dyspnea, and hypotension during dialysis. On the basis of a positive skin prick test (dermal reaction to ETO-exposed human albumin) and of antigen-induced histamine release from peripheral leucocytes, these workers suggested that ETO was responsible for the allergic reactions. Marshall et al. (1984) (5) reported that 8.9% of hemodialysis patients had positive skin tests to ETO and that 12.1% were ETO-radioallergosorbent test (RAST) positive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Elimination of low molecular weight proteins during hemofiltration.

In patients on regular dialysis treatment, uremic symptoms (anemia, osteopathy, myopathy, neuropathy, and disorders of carbohydrate, fat, and protein metabolism) may be partly due to an accumulation of low molecular weight (MW) proteins (10,000 to 60,000 daltons). We tested this hypothesis using membranes with a higher permeability than conventional Cuprophan membranes. The primary aim of the study was to test the cutoff of various hemofilters (Cuprophan [Highflux], polyamide [FH 20], cellulose acetate [Duoflux], and polyacrylonitrile [Hospal RP 7 + 8 and Asahi PAN]) under in vivo conditions. In addition the effects of hemofiltration on plasma low molecular weight protein concentrations, polyneuropathy, and autonomic insufficiency were also tested in a long-term (six-month) study using the membrane with the highest cutoff and most constant sieving coefficient, i.e., Highflux. Low MW proteins with a defined MW were used as marker substances. Sieving coefficients of beta 2-microglobulin, lysozyme, retinol-binding protein, alpha 1-glycoprotein, alpha 1-antitrypsin, prealbumin, albumin, and transferrin were determined during a four-hour hemofiltration (20 L ultrafiltrate). Proteins were analyzed using an immunodiffusion technique. In the long-term study, motor nerve conduction velocity, the Schellong test, and Valsalva maneuver were tested prior to and three and six months after hemofiltration therapy. Highflux, Duoflux, and FH 202 membranes were permeable to proteins with molecular weights up to 15,000 daltons, and the Highflux module had the most constant sieving coefficient during hemofiltration. In the six-month hemofiltration study with the Highflux filter, plasma beta 2-microglobulin and lysozyme decreased significantly as expected. Parameters of polyneuropathy and autonomic insufficiency were slightly improved.

Adult↗
PubMed1980

Effects of acute haemodialysis-induced changes in sodium balance upon experimentally hypertensive rats.

In two-kidney Goldblatt hypertensive, spontaneously hypertensive, and normotensive control rats, the activity of the renin-angiotensin system was tested during variation of sodium balance. Acute, exactly calculable and selective changes in total body sodium were achieved by haemodialysing conscious rats, using dialysates with high and low sodium contents. The activity of the renin-angiotensin system was evaluated by blood pressure response to angiogtensin II blockade (saralasin bolus injection; 25 micrograms/kg b.w., i.v.) and plasma renin activity. During sodium-depletion, blood pressure maintenance became renin-dependent; sodium-loading caused a decrease of renin-angiotensin activity in renovascular hypertension. A weak direct correlation between depressor response to saralasin and the plasma renin activity could be established in the different sodium-depleted and sodium-loaded states.

Animals↗
PubMed1979

Salivary kallikrein excretion in hypertension.

According to immunohistochemical investigations kallikrein in the majors salivary glands is located predominantly at the apical border of the striated duct cells and as a luminal rim in the main excretory ducts. Comparatively the highest concentrations are observed in the submandibular gland of rats and cats in the cytoplasmic granules of the granular tubules. In normal humans and rats the kallikrein activity of parotid saliva is inversely related to flow rate and sodium concentration. An increased salivary kallikrein concentration is found in human essential hypertension and renoparenchymal hypertension associated with impaired kidney function. Furthermore in rats with various forms of hypertension (genetic hypertension, DOCTMA salt and renovascular hypertension) the salivary kallikrein secretion - as determined by the BAEE-esterase activity - is enhanced. In contrast to the kallikrein secretion the flow dependent sodium concentration of parotid saliva is reduced in human essential and renoparenchymal hypertension as well as in rats with various forms of experimental and genetic hypertension, which indicates an enhanced sodium reabsorption in the glandular duct system. Furthermore in most forms of hypertension, there is a tendency of higher potassium levels in the saliva. The pathogenesis of the enhanced glandular kallikrein secretion in hypertension is discussed with regard to a counterregulatory mechanism in hypertension as well as to a sympathicoadrenergic activation. The enhanced sodium reabsorption in the duct system in the various forms of hypertension could be the cause as well as a consequence of the enhanced kallikrein secretion.

Absorption↗
PubMed1979

[Saralasin in resistant hypertensive crisis (author's transl)].

4 patients with hypertensive crisis (glomerulonephritis [n = 2], phaeochromocytoma [n = 1], reno-vascular hypertension [n = 1] combined with encephalopathy, showed a normalisation of blood-pressure up to 18 days during angiotensin-II-blockade with saralasin. Prior, blood pressure was treated insufficiently by intravenous diazoxide and Na-nitroprusside. Increased plasma-renin-activity and plasma levels of catecholamines pointed to an activation of the renin-angiotensin- and sympathico-adrenergic system. A trial of therapy with saralasin--especially, if blood-pressure response to diazoxide and sodium-nitroprusside is insufficient--could be indicated. Side-effects like pressor-reactions are excluded by very low priming doses (0,1 microgram/kg/min); rebound-hypertension at the end of the therapy is avoided by an overlapping therapy with renin suppressing drugs (beta-receptor blockers, clonidine, guanfacinum).

Adrenergic beta-Antagonists↗
PubMed1979

Effects of acute hemodialysis-induced changes in sodium balance on the renin-angiotensin system in renovascular and spontaneously hypertensive rats.

In two-kidney Goldblatt hypertensive, spontaneously hypertensive, and normotensive control rats the activity of the renin-angiotensin system was tested during variation of sodium balance. Acute, exactly calculable and selective changes of total body sodium were achieved by hemodialyzing the conscious rats using dialysate with either high or low sodium content. The activity of the RAS was evaluated by blood pressure response to AT II blockade (saralasin bolus injection; 25 micrograms/kg b.w., i.v.) and the plasma-renin activity. During sodium depletion blood pressure maintenance became renin-dependent; sodium loading caused a decrease of renin-angiotensin activity in renovascular hypertension. A weak direct correlation between deprssor response to saralasin and the PRA could be established in the different sodium-depleted and -loaded states.

Angiotensin II↗
PubMed1979

Uraemic sympathetic neuropathy after haemodialysis and transplantation.

Autonomic function in patients with uraemia treated conservatively, by haemodialysis, and by transplantation was evaluated by the pupillary reaction to tyramine, the Valsalva manoeuvre and a postural tolerance test. The pupillary reaction to tyramine is diminished in haemodialysis patients compared with control subjects. Renal transplantation improves, but does not correct the pupillary reaction to tyramine. The frequency of the diminished response roughly correlates with the degree of renal insufficiency, with results of a Valsalva manoeuvre, and with postural tolerance tests. Our data show that uraemic autonomic dysfunction is improved by successful renal transplantation, but not by adequate haemodialysis.

Adult↗