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Biomedical subjects

B Diamant

Publications and source records attributed to B Diamant.

At least 37 records · Page 2Linked to original sources
PubMed1988

Ergogenic effect of inhaled beta 2-agonists in asthmatics.

To investigate the effect of beta 2-agonists on exercise performance, eight asthmatics performed an incremental exercise test on a treadmill. Five minutes before the start of the exercise, they were treated with inhaled salbutamol or placebo in a double-blind manner. The exercise started at a low intensity (2 mph, 10% inclination), and every 3 min the speed was increased by 0.5 mph at the same inclination until the subjects were exhausted. Every minute peak expiratory flow, heart rate, blood lactate concentration, and rating of perceived exertion were measured. The same parameters were also measured following the completion of the exercise. No significant difference was seen in total working time, maximal lactate concentration, heart rate, or rating of perceived exertion, whereas the decrease in peak expiratory flow was reduced following pretreatment with salbutamol. It is concluded that the release of inhaled beta 2-agonists for use in competitive events is justified as no ergogenic effect was seen.

Adrenergic beta-Agonists↗
PubMed1988

Beta 2-mediated changes in central haemodynamics, coronary circulation and myocardial metabolism in canine.

The combined effect of terbutaline on systemic and coronary circulation was investigated in dogs to clarify its influence on myocardial oxygen supply and lactate balance. The dogs were anaesthetized and the chest opened. Coronary sinus blood flow and cardiac output were monitored by thermodilution, aortic pressure was measured by tip-transducer and heart rate by RR-interval on ECG, coronary sinus blood were analyzed for lactate, oxygen and carbon dioxide. Terbutaline caused a substantial systemic vasodilation and an increased heart rate, the total external cardiac work increased to a minor degree. Terbutaline increased arterial lactate concentration. Coronary vascular resistance was reduced after terbutaline. Even if myocardial perfusion pressure was reduced and an increased external cardiac work was present, no signs of myocardial distress was observed in lactate metabolism or coronary sinus oxygen content. In fact a tendency to increased myocardial aerobic metabolism was observed, as myocardial lactate consumption increased after terbutaline. Terbutaline seems to be a coronary vasodilator in dogs. However, the demand for oxygen secondary to both an increase in cardiac work and aerobic metabolism can be hazardous to the potentially ischaemic myocardium.

Animals↗
PubMed1984

Inhibitory effect of aprotinin on gastric acid secretion.

Aprotinin was found to inhibit the amplitude of electrically stimulated contractions of the isolated guinea pig ileum with an ID50 of 6.75 X 10(-6) M. Aprotinin inhibited pentagastrin-stimulated gastric acid secretion in the rat, cat, and pig after oral or intraventricular administration. No inhibition of gastric acid secretion was seen after intravenous infusion of aprotinin. When segments of antrum, duodenum, and ileum were incubated in vitro with increasing concentrations of aprotinin, increasing amounts of somatostatin were released from the organs. It is suggested that aprotinin's effects, which are similar to those of somatostatin, may be due to a local release of somatostatin from the D-cells in the gastrointestinal tract.

Animals↗
PubMed1983

Dissociation of the spasmolytic and metabolic effects of glucagon.

Glucagon and glucagon-(1-21)-peptide were equipotent with regard to inhibitory effect on the amplitude of electrically evoked contractions of the isolated guinea-pig ileum. The effect was not potentiated by isobutylmethylxanthine (IBMX) nor inhibited by phentolamine or propranolol. Both peptides inhibited intestinal motility in rabbits in vivo. Glucagon and equimolar doses of glucagon-(1-21)-peptide exerted a relaxing effect on the rabbit gall bladder in vitro and in vivo and increased bile flow in rats. Both peptides inhibited pentagastrin stimulated gastric acid secretion in cats. However, contrary to glucagon, glucagon-(1-21)-peptide did not increase blood glucose and plasma IRI levels after intravenous administration to rats in vivo. Whereas the entire glucagon molecule was required for the metabolic effects, the amino acid sequence (1-21) of glucagon exerted a full spasmolytic action on the enteric muscles and the biliary tree. The spasmolytic effects on these organs are therefore likely to be mediated via a mechanism that does not involve the activation of adenyl cyclase.

Animals↗
PubMed1982

Pancreatic spasmolytic polypeptide (PSP): III. Pharmacology of a new porcine pancreatic polypeptide with spasmolytic and gastric acid secretion inhibitory effects.

Pancreatic spasmolytic Polypeptide (PSP) is a new porcine pancreatic polypeptide, which inhibits gastrointestinal motility and gastric acid secretion in laboratory animals after parenteral as well as oral administration. (1) PSP inhibits the amplitude of electrically stimulated contractions of the isolated guinea pig ileum. PSP's inhibitory effect is antagonized by phentolamine, but not by yohimbine. (2) PSP inhibits the motility of isolated guinea pig intestinal segments after intraluminal dosing. (3) PSP reduces intestinal motility in rabbits in vivo after intravenous and intraluminal administration, and in mice in vivo after subcutaneous injection. (4) PSP delays absorption of protein hydrolysate when it is administered orally in capsules to pigs and to pancreatectomized dogs. (5) PSP inhibits pentagastrin induced gastric acid secretion in rats after oral administration and in cats after subcutaneous and oral administration. The mechanism of action of PSP has so far not been finally elucidated. It seems likely that PSP interferes with endogenous acetylcholine release. Furthermore it might act by release of somatostatin from somatostatin cells in the gastrointestinal tract. It may have a direct or an indirect stimulant effect on alpha 2-receptors.

Administration, Oral↗
PubMed1980

The influence of hypertonicity on histamine release from isolated rat mast cells.

Increasing the tonicity of the incubation medium gradually inhibited histamine release from isolated rat mast cells when induced A-23187, ATP, Thapsigargin, sodium fluoride and compound 48/80 in the presence of extracellular calcium, as well as by the latter in the presence of calcium. In contrast, hypertonicity had but negligible effect on the release caused by the monovalent cation inophore X-537A. The swelling action induced by both ATP and X-537A on rat mast cells was markedly depressed by hypertonicity. Thus, the swelling action seemed to be inherent to the mechanism by which ATP stimulates mast cells to a calcium-dependent histamine secretion, whereas this was not the case with X-537A. For Thapsigargin and sodium fluoride it was demonstrated that only the secretory step, induced by calcium, was inhibited by hypertonicity, and this could be reversed by adjusting the incubation medium to isotonicity. Therefore, the results suggest that the uptake of calcium in the rat mast cells after stimulation is a passive process.

Adenosine Triphosphate↗
PubMed1979

On the mechanism of histamine release induced by thapsigargin from Thapsia garganica L.

Thapsigargin (Tg) is a pure chemical compound isolated from Thapsia garganica with a molecular weight of 650. It releases histamine from isolated rat mast cells but not from isolated histamine-retaining mast cell granules. The rate of release is markedly influenced by pretreatment of mast cells with Tg prior to the addition of calcium. In agreement with the effect of the ionophore A23187 but in contrast to many other calcium-dependent histamine-releasing agents, cells preincubated with Tg respond to the secretory action of calcium whenever the ion is introduced. However, after dilution of Tg-pretreated cells histamine release induced by the addition of calcium became dependent on the time of its addition. The secretory reaction induced by Tg and calcium can be divided into a two-step reaction at 37 degrees C. Pretreatment of mass cells with Tg renders the cells insensitive to the secretory action of compound 48/80 in the absence of calcium, and this effect could be partly counteracted if 1 mM of strontium was added together with compound 48/80. It is concluded that among various calcium- and energy-dependent histamine-releasing agents Tg most closely resembles the action of fluoride on isolated rat mast cells.

Animals↗
PubMed1978

The mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells. II. The relationship between increase of cell volume and histamine release.

The ionophore X537A induced swelling of isolated rat mast cells parallel to histamine release. Both actions were depressed by extracellular calcium and BSA, temperatures below 37 degrees C, NEM, PMSF, and TTX, and were enhanced by high potassium and pretreatment of the cells with ATP. DSCG, theophylline, and DFP enhanced the histamine release noted after 10 min of incubation without influencing the swelling action of X537A. The swelling action could not be separated from histamine release and it is suggested that it might be inherent in the mechanism of secretion induced by X537A. The present results further distinguish histamine release induced by the two ionophores X537A and A23187.

Animals↗
PubMed1978

The mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells. I. Significance of monovalent cations, calcium, metabolic energy and temperature.

Histamine release induced by X537A from isolated rat mast cells was dependent on the presence of sodium or potassium but not on calcium in the incubation medium. The rate of release was faster in potassium than in sodium, but the final release was the same after prolonged incubation. Extracellular calcium as well as metabolic inhibitors depressed the rate or release induced by X537A. Pretreatment of mast cells with either EDTA or the ionophore A23187 in the absence of extracellular calcium did not influence subsequent release induced by X537A. The findings of release at 45 degrees C and lack of release at 0 degrees C distinguish the mechanism of action of X537A from calcium- energy-dependent releasing agents like compound 48/80 and A23187 on the one hand and the simple lytic action of decylamine on the other.

Animals↗
PubMed1978

Mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells.

X537A released histamine from isolated histamine-retaining mast cell granules incubated at 37 degrees C in Tris-sodium (150 mM) or Tris-potassium (150 mM), but not in Tris-glucose (300 mM). The release was depressed at 0 degrees C. In contrast, decylamine released all histamine bound to the granules irrespective of the presence of monovalent cations in the incubation medium of temperature. X537A did not release histamine from an artificial heparin-protamine complex when incubated in deionized water. The mechanism of histamine release by X537A can be explained by the ability of the ionophore to carry monovalent cations across cellular membranes, hereby making the ions available for exchange with histamine bound to the granular matrix. This mechanism can be distinguished from that of agents triggering an exchange between cations and bound histamine through a calcium- and energy-dependent exocytotic process on the one hand and through membrane lysis on the other. Based on the observation that the ionophore was able to carry histamine into the bulk of an organic phase, various possibilities exist to explain how histamine escapes from the cells following release from intracellular granular stores.

Animals↗