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Biomedical subjects

R Larsson

Publications and source records attributed to R Larsson.

At least 253 records · Page 14Linked to original sources
PubMed1981

Polarographic pO2 sensors with heparinized membranes for in vitro and continuous in vivo registration.

The membranes of the pO2 sensor in a conventional blood gas analyser and a commercially available catheter pO2 electrode were coated with a glutardialdehyde stabilized heparin layer. It was analysed whether or not the "non-thrombogenic" heparin surface could improve the accuracy of in vitro pO2 registration and continuous in vivo paO2 monitoring. The in vivo experiments were performed on anaesthetized and non-anticoagulated dogs. Two identical blood gas analysers were used, one furnished with a heparin coated pO2 membrane and the other with a standard pO2 membrane. In vitro pO2 determinations exhibited--when simultaneously analysing the same blood sample--identical mean values. For repeated pO2 determinations, however, the standard deviation was significantly lower on the analyser furnished with a heparinized membrane. The non-heparinized catheter pO2 electrode showed a marked deterioration in accuracy with time as compared with blood-gas analysis on reference blood samples. Falsely low paO2 values were presented. The heparinized catheter electrode monitored values in full agreement with those of the conventional blood gas analyser using standard membranes. It is concluded that the heparin surface on the oxygen diffusible membranes diminishes the variability of the diffusion characteristics both at contact with anticoagulated blood in vitro and during in vivo paO2 monitoring. The "non-thrombogenic" heparin surface prevents diffusion impeding clot formations when an arterial catheter pO2 sensor is used.

Animals↗
PubMed1980

The effects of cimetidine (Tagamet) on renal function in patients with renal failure.

Cimetidine has been administered during 7 days to 28 patients with different degrees of renal failure. Thirteen of these patients had a further week's treatment at least one month later. The daily dose of cimetidine was reduced in relation to pretrial values of creatinine clearance. There was a clear rise in serum creatinine all through the trial (22.3 +/- 2.6% at day 7) (p < 0.001). Maximal decreases in creatinine clearance occurred on day 2 (21.8 +/- 2.2%) and day 3 (23 +/- 2.0%) (p < 0.001), but were still present on days 6 (16.4 +/- 2.9%) and 7 (17.3 +/- 2.8%) (p < 0.001). There was a small rise in serum uric acid all through the trial (p < 0.05). Three days after finished treatment there were no significant differences in serum creatinine, creatinine clearance and serum uric acid when compared to pretrial values. The pattern of changes in serum creatinine and creatinine clearance was the same in both mild and severe renal failure. Glomerular filtration rate determined by |52Cr¿ EDTA clearance before, on day 3 of treatment and 3 days after treatment did not show any differences. No change was seen in serum beta 2-microglobulin during the trial. The decrease in creatinine clearance during treatment with cimetidine is probably not caused by a reduction of glomerular filtration rate, but could be explained by competition by cimetidine for tubular secretion of creatinine. Treatment with cimetidine of patients with renal failure may invalidate measurements of serum creatinine and creatinine clearance as standard routine tests for glomerular filtration rate.

Adult↗
PubMed1979

Oral absorption of cimetidine and its clearance in patients with renal failure.

The plasma concentration curve after a single oral dose of cimetidine 200 mg was followed in 27 patients with varying degrees of chronic renal failure (creatinine clearance 1--52 ml/min) and in 46 patients with normal serum creatinine. Compared to the latter patients, the plasma concentration was higher and the elimination rate was slower in all uraemic subjects, including a group with moderate renal impairment. The preliminary recommendations of dosage for patients with a creatinine clearance below 5 ml/min, and for patients on regular haemodialysis, is cimetidine 200 mg every 12 h, 5-15 ml/min 200 mg every 12 to 8 h, 15-30 ml/min 200 mg every 8 h and 30-52 ml/min 200 mg every 6 h.

Adult↗
PubMed1979

The effect of cimetidine, a new histamine H2-receptor antagonist, on renal function.

Serum creatinine, endogenous creatinine clearance, (51Cr)EDTA plasma clearance and the concentration of beta2-microglobulin in serum and urine were determined in 19 patients before and during treatment with cimetidine for peptic ulcer disease. The mean concentrations of creatinine and beta2-microglobulin in serum increased significantly within normal limits after 2 and 6 weeks' treatment. However, creatinine clearance and (51Cr)EDTA plasma clearance were unchanged during the treatment. Thus, the observed increases in serum creatinine and beta2-microglobulin could not be explained by a diminished glomerular filtration rate. Inhibited tubular secretion of creatinine may explain the observed increase in serum creatinine during cimetidine treatment. Another hypothetical possibility is that a small increase in tubular reabsorption of both creatinine and beta2-microglobulin would account for the observed increases in creatinine and beta2-microglobulin in serum. It is concluded that, although statistically significant, the increases in serum creatinine and beta2-microglobulin are small and therefore of little relevance for the patient's treatment with cimetidine.

Adult↗
PubMed1979

Serotonin uptake and release by platelets adhering to polyethylene.

Heparinized human blood containing platelets labelled with 14C-serotonin and 51Cr was exposed to a polyethylene surface by rotation in Chandler loops. Both uptake of platelets on the surface and platelet aggregation in the blood occurred. More 14C- than 51Cr activity accumulated on the surface. It was demonstrated that this was due to an active uptake of 14C-serotonin by the surface-adherent platelets, which also retained their capacity to exert a release reaction.

Blood Platelets↗
PubMed1978

Reciprocal inhibition during the tonic stretch reflex in the decerebrate cat.

1. The aim of this study was to investigate post-synaptic reciprocal Ia inhibition during the stretch reflex; particularly the extent to which an increased Ia excitation of the Ia inhibitory interneurones will be counteracted by recurrent inhibition from motor axon collaterals. For this purpose we investigated depression of monosynaptic test reflexes antagonist flexors (reciprocal inhibition) during static stretch of quadriceps or triceps surae in unanaesthetized decerebrate cats. 3. With increasing stretch of the extensor muscle there was first a linear augmentation of reciprocal inhibition, but along with the stretch reflex in the extensor a plateau appeared in the inhibition of the flexors, although the extensor stretch reflex (judged by the e.m.g.) increased with further stretching. Within the range of stretching of triceps surae which gave increased stretch reflexes the plateau in the reciprocal inhibition was usually maintained, while during stretching of quadriceps a second phase of augmenting reciprocal inhibition often appeared. Stretch beyond the level which increased the stretch reflex activity gave augmenting reciprocal inhibition both in case of quadriceps and triceps surae. 3. Excitability measurements from central terminals of Ia afferents revealed that the increasing reciprocal inhibition during increasing stretch reflex activity in quadriceps was associated with a primary afferent depolarization in knee flexor Ia afferents; there was no corresponding effect in ankle flexor Ia afferents during stretch reflexes in triceps surae. 4. The primary afferent depolarization evoked in knee flexor Ia afferents by electrical nerve stimulation was then compared with the presynaptic inhibition of knee flexor monosynaptic test reflexes produced by the same stimuli. The results suggest that the second phase of increasing reciprocal inhibition in knee flexors is due to presynaptic inhibition and accordingly that the depth of post-synaptic reciprocal inhibition remains constant at different degrees of stretch reflex activity in both knee and ankle extensors. 5. It is postulated that during increasing stretch reflex activity the increment in Ia excitation and recurrent inhibitio; on to the Ia inhibitory interneurones almost exactly balance each other. It is suggested that recurrent inhibition of Ia inhibitory interneurones may serve as a segmental autoregulatory mechanism to keep 'alpha-gamma-linked reciprocal inhibition' at a constant depth during different levels of agonist activity.

Animals↗
PubMed1977

Prevention of platelet adhesion and aggregation by a glutardialdehyde-stabilized heparin surface.

A stable heparinized surface was prepared by sequential treatment of polyethylene with water solutions of hexadecylamine hydrochloride, heparin and glutardialdehyde. In order to explain the "non-thrombogenic" properties of this surface, it was evaluated with regard to prevention of platelet adhesion and aggregation. Human heparinized blood (2 and 10 IU/ml) with 51Cr-labelled autologous platelets was rotated for 60 minutes in untreated and heparin-treated circular tubings. The surface area/blood volume ratio was varied and an air-blood interface was present. In untreated tubings, platelet adhesion and aggregation increased in proportion to the size of the surface area/blood volume ratio, irrespective of the heparin concentrations of the blood. In the heparin-treated tubings, there was no measurable platelet adhesion to the surface and no platelet aggregation in the blood. The difference between the heparinized and the untreated surfaces with regard to platelet adhesion was discernible even after 10 minutes storage of stagnant blood. It is concluded that platelet adhesion and aggregation induced by exposure of blood to a foreign surface in an in vitro experimental model can be prevented by a stable heparin coating of the surface.

Aldehydes↗
PubMed1977

Activity pattern and convulsions in the abstinence period after barbital treatment in the rat.

Barbital solution was given as the only drinking fluid to male rats for 50 weeks (daily dose around 200 mg/kg). During the treatment and in the abstinence period activity and convulsive episodes were recorded with jiggle cages. Sensitivity to hexobarbital was tested with a threshold method. A 12:12 HR L:D schedule was used. During the barbital treatment the activity of the treated rats started earlier (prior to light off) and ended earlier (prior to light on) compared with controls. A clear 24-hr pattern remained and the total activity was same as in the controls. In the first part of the abstinence period there was a large increase in activity with loss of the 24-hr pattern. Later in the abstinence period the activity was still increased both during light and darkness but a 24-hr pattern influenced by the L:D cycle was re-established. The changes in activity seemed to occur in a least two phases with the second phase lasting between abstinent Days 20-60. A similar two phase pattern was seen also in the changes of the hexobarbital thresholds. The convulsive episodes had several maxima during the abstinence period. The first one occurred around abstinent Days 3--4 and the second one was seen around Day 12. After Day 37 no convulsions were seen. All recorded changes can tentatively be explained by a common increased excitation in the central nervous system.

Animals↗
PubMed1977

Evaluation of the sulphapyridine acetylator phenotyping test in healthy subjects and in patients with cardiac and renal diseases.

The acetylator phenotype of 35 healthy, drug-free volunteers and 21 patients with cardiac and/or renal disease has been assessed using oral sulphapyridine. Comparative evaluation of a simplified and a more selective method of sulphapyridine analysis was performed. Thirteen of the patients were also phenotyped by determination of plasma isoniazid half-life. 81% of the patients were slow acetylators, compared with only 51% of the volunteers. When phenotyping healthy, drug-free subjects the analytical procedure, involving a direct estimation of sulphapyridine in urine with the Bratton-Marshall procedure, was satisfactory. On the other hand, in patients receiving concomitant drug therapy the more selective analytical procedure was necessary in order to diminish the risk of methodological interference.

Acetylation↗
PubMed1977

Spontaneous systemic lupus erythematosus and acelylator phenotype.

Fifteen patients with spontaneous systemic lupus erythematosus (SLE) have been phenotyped by determination of plasma isoniazid (INH) half-life. Seven patients had signs of renal insufficiency. Of the 15 patients, 13 were slow and only 2 rapid acetylators. No correlation was found between the plasma INH half-lives and the renal function. Thus, there is the same marked predominance of slow acetylators in patients with spontaneous SLE as in patients with the drug-induced SLE-like syndrome.

Acetylation↗
PubMed1977

Quinton-Scribner arteriovenous shunts for hemodialysis. A review of 6.5 years' experience.

Quinton-Scribner shunts have been used as a reliable access to the blood-stream in 56 patients treated with intermittent hemodialysis in the years 1965-71. The mean age of 29 men and 27 women was 39 years. Two hundred and thirty-two cannulae showed a mean survival time of 11.2 months for 103 arterial cannulae and 9.0 months for 129 venous cannulae. 700 shunt clotting episodes occurred during 1157 patient months, i.e. 0.6 clotting episode/month. In 350 episodes where saline flushing could not remove the clot, the effect of treatment with streptokinase was considered evident in 79.7%. Shunt cannula infection was a common complication while aseptic cutaneous necrosis and bleeding from the cannulated vessel were seen less frequently. Both severe and less harmful bleeding episodes were seen as a complication of dicumarol therapy. The number of complications to streptokinase treatments was low. The advantages and disadvantages of the Quinton-Scribner shunt for hemodialysis are discussed.

Adolescent↗