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Biomedical subjects

R Laven

Publications and source records attributed to R Laven.

16 recordsLinked to original sources
PubMed1978

Adrenergic and nonadrenergic activation of isolated human renal veins of normotensive and hypertensive patients.

In human renal venous strips from normotensive and hypertensive patients, adrenergic- and nonadrenergic-induced contractions were elicited. The maximal amplitude of contractions remained unchanged whatever the mode of activation. However, in the hypertensive group the forces generated reached only about 20% of those in the normotensive group. Furthermore, preparations from hypertensive patients showed a reduced sensitivity for noradrenaline: the ED50 was shifted from 0.13 +/- 0.03 to 0.66 +/- 0.19 microgram/ml (p less than 0.01). This reduced sensitivity is discussed in connection with the pathogenesis of hypertension.

Adolescent↗
PubMed1978

Modulation of the prostaglandin-induced intestinal motility in humans through the transmitters of the vegetative nervous system.

Research was done on the reciprocity between adrenergic and cholinergic stimulating or inhibiting pharmaceuticals and the prostaglandin-induced intestinal motility. By cholinergic activation, the amplitudes of the prostaglandin-dependent rhythmical contractions of human taenia coli were intensified. There was very little influence on the frequency of contractions, however. Simultaneous stimulation of adrenergic beta-receptors by increasing doses of adrenaline or noradrenaline caused the contraction amplitude and frequency to decrease continually until the contractions were completely eliminated. The cholinergic effect could be suppressed with atropine, the adrenergic-stimulated reaction was reversed by the blockage of beta-receptors. It was completely abolished by simultaneous addition of alpha- and beta-receptor-blocking drugs.

Acetylcholine↗
PubMed1978

[Colon dynamics in ileus].

All forms of ileus have one thing in common, namely a disorder of the intestinal motility, which, with increasing distension of the intestinal wall, finally leads to paralysis of the intestine. With the increase in distension mechanical and functional colon changes take place which are discussed in this study. During peristalsis the strain on the wall is directed against the intra-luminal course of pressure. In spite of the increase of the internal pressure from 5 cm H2O to 100 cm H2O, the tension of the wall remains low or even decreases (roughly 500 dyn/mm2). In ileus patients, however, the strain on the intestinal wall increases enormously (about 100000 dyn/mm2). The maximum contraction capacity of the large intestine's muscle system (50,000 dyn/mm2) is high and similar to that of the skeletal muscles.

Colon↗
PubMed1978

[Impairment of adrenergic innervation in achalasia (author's transl)].

Length tension diagrams and diagrams of isometrically developed active tension were set up for normal and aganglionic cardia-circular muscles. The effects of acetylcholin, adrenergic stimulating and inhibiting drugs were examined. The physiological parameters in healthy cardia and the cardia muscle system in achalasia did not vary significantly from one another. The acetylcholin threshold was higher in aganglionic cardia, while the maximum effective dose in healthy and aganglionic cardia remained the same. In achalasia no sensitisation to acetylcholine was detectable. There was a marked impairment in the balance between adrenergic alpha- and beta-receptors, with the contraction-inducing alpha-receptors obviously predominating.

Acetylcholine↗
PubMed1978

The role of prostaglandines in peristalsis of the human colon.

Prostaglandines (PG) of the E and F series cause peristaltic activity in isolated longitudinal muscle strips of the human colon. As this phasic motor reaction can be varied by acetyl choline and adrenaline it was supposed, that prostaglandines contribute to peristalsis. The role of PG E and F in the human colon was studied by inhibiting the prostaglandine synthesis and by antagonizing the prostaglandine-effects. Indomethacin proved to be a suitable inhibitor. HR 546 was found a powerful antagonist. The effect of Pentagastrin and Cholecystokinin (CCK) on peristaltic activity were suppressed by Indomethacin and HR 546. The inhibition of peristalsis by Indomethacin and HR 546 was removed by high doses of PG E and F. On the basis of these results the role of PG for the motility of the gut is discussed.

Cholecystokinin↗
PubMed1977

[Adrenergic receptors in the pathogenesis of congenital megacolon (author's transl)].

Contractions of fresh specimens of taenial musculature from human colon were investigated under the influence of depolarization (bathing in solutions high in potassium), of acetylcholine, and of adrenaline; definite changes of contractile tension could be induced by these agents. The investigations were carried out using normal musculature as well as specimens from patients with congenital megacolon taken from the narrow segment. Contractions after depolarization and after cholinergic stimulation were equal in all specimens investigated, pre-extension of these specimens not differing significantly. Relaxation of colon musculature mediated by adrenergic receptors was very pronounced in normal musculature, but was lacking in specimens taken from the narrow segments of congenital megacolon. Sympathetic stimulation of normal taenial musculature does abolish completely cholinergically induced contractions. On the other hand, a preparation relaxed by adrenaline contracts very little after additional application of acetylcholine. These findings do suggest a severe disturbance of adrenergic receptors in the colon, or of adrenergic neuromuscular transmission in congenital megacolon.

Humans↗
PubMed1977

[Computer assisted heart and circulation analysis in experimental septic shock (author's transl)].

Developping a model of shock applying to the clinical manifestation is necessary to investigate the pathogenesis of septic shock and to identify the letality causing organ. Perhaps the hyperkinetic syndrome may play an important role. The extensive experimental data is processed by a digital computer. Explanations are given for the experimental apparatus and the structure of the Fortran-program.

Animals↗
PubMed1977

[Functional studies of the cardia muscles in achalasia].

1. The mechanical properties - extension behaviour and ability to contract per muscle cross-section - were the same for healthy and aganglionic cardiac sphincter. 2. The acetyl choline threshold is higher in aganglionic muscle strips. The maximum effective acetyl choline dose (2 microgram/ml) remained the same. 3. Achalasia is characterized by a considerable reduction of adrenergic beta-receptor activity and alpha-receptor predominance.

Acetylcholine↗
PubMed1976

Force velocity relations in vascular smooth muscle: the influence of pH, pCa, and noradrenaline.

The kinetics of vascular smooth musclw activity was studied by means of afterloaded isotonic contractions of the tetanized rat portal vein at varied pH (8.0-5.9), pCa (3.4-2.1), and during noradrenaline incubation (0.4 mug/ml). Under control conditions (pH 7.3, pCa 2.6) the following parameters of the force velocity relation were calculated: a of Hill's equation (relating to the isometric peak tension) = 0.36; b (relating to the actual muscle length) = 0.19 ML/s; VM Trelating to the actual muscle length) = 0.56 ML/s. Within the range of pCa between 2.0 and 3.2 the amount of force generation (= delta P) depended on the extracellular calcium level whereas the extrapolated velocity of shortening of the unloaded preparation (= VM) did not. Also pH changes between 8.0 and 6.8 as well as noradrenaline incubation at a pH of 5.9 affected delta P quite considerably, but VM only scarcely. At a pH of 6.3, however, VM was distinctly diminished, and a reduced calcium sensitivity of the ATPase was inferred from the shift of ED50 of extracellular calcium from 0.66 mM Ca at a pH of 7.3 to 1.56 mM Ca at a pH of 6.3 (P less than 0.0005). It is concluded from these results that the experimental conditions-pCa between 2.0 and 3.2, pH between 8.0 and 6.8, and noradrenaline added at a pH of 5.9-obviously change the intracellular calcium concentration which influences the number of activated interaction sites rather than the velocity of crossbridge movement.

Animals↗
PubMedDate not supplied

The influence of temperature and calcium on the degree of stretch-activation in isolated K-depolarized vascular smooth muscle strips.

Stretching of K-depolarized contracted helically cut strips of pig coronary arteries produced a delayed increase in tension. The influence of temperature and extracellular calcium on this active response to stretch was investigated. Reference for all tension values was the amplitude of contraction (induced by K-depolarization) starting from the high resting tension. 1. The mean amplitude of the delayed tension increase after stretch amounted to 27.5 plus or minus 4.8% (x plus or minus SEM, n equals 9); lowering the bath temperature from 37 degrees C to 27 degrees C caused a drop to 10.8 plus or minus 1.5% (n equals 9; P smaller than 0.0025); increasing the calcium concentration of the bath solution from 2.7 to 6.9 mM produced negligible effects on both the amplitude of the delayed tension increase (24.6 plus or minus 1.0%; n equals 9), and the amplitude of contraction after depolarization. 2. The peak tension time of the active response to stretch was not changed by the 6.9 mM calcium, but prolonged from 27.9 plus or minus 4.0 to 40.7 plus or minus 4.4 minutes (P smaller than 0.025) by lowering the bath temperature to 27 degrees C. At the high calcium level the preparation contracted faster after depolarization than at the normal calcium level. 3. The experimental results correspond with the conception of the sliding filament mechanism as the basic process of contraction also in vascular smooth muscle preparations. The delayed tension increase after stretch may be caused by a recruitment of interaction sites between contractile proteins.

Animals↗