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Biomedical subjects

W Feldberg

Publications and source records attributed to W Feldberg.

At least 19 recordsLinked to original sources
PubMed1991

Concordance of indirect methods for the detection of lactose malabsorption in diabetic and nondiabetic subjects.

In order to collect data on (1) the prevalence of lactose malabsorption and (2) the value of indirect diagnostic methods for hypolactasia in diabetics, we compared lactose tolerance tests using serum glucose, serum galactose (after oral ethanol intake) and breath hydrogen excretion as diagnostic cutoff in 144 nondiabetic and 46 diabetic subjects. A good rate of concordance was found for the hydrogen breath test and galactose-dependent lactose tolerance test. The glucose-dependent lactose tolerance test was found to be of satisfactory diagnostic value in nondiabetic subjects and was useless for diagnostic purposes in diabetics. Lactose malabsorption was no more frequent in diabetics than in controls and lactose intolerance was found to be less frequent in the diabetic group. A distinction between hypolactasia and other gastrointestinal disorders in diabetics is possible by ambulatory indirect tests.

Adult↗
PubMed1986

Analysis of cardiovascular effects of morphine in the cat.

In cats anaesthetized with chloralose, the effect of morphine on arterial blood pressure and heart rate was examined by injecting the drug through different routes. When injected into the cerebral ventricles, it acted on structures in the walls of the third ventricle and produced a naloxone resistant tachycardia through a sympathetic discharge to the heart. When injected into the cisterna magna or subcutaneously, it produced a naloxone sensitive long-lasting fall in blood pressure and bradycardia resulting from inhibition of sympathetic tone to blood vessels and heart; increased vagal tone played a minor role in the development of bradycardia. When injected intracisternally or subcutaneously, morphine acted near the obex at the dorsal surface of the medulla, because it produced the same circulatory effects but in much smaller doses when applied to this region on a piece of filter paper. Conversely, small doses of naloxone similarly applied abolished or prevented the circulatory effects of subcutaneous morphine. The action of morphine may be on the commissural nucleus of the tractus solitarius. Intravenous naloxone restored the circulatory effects of intracisternal and subcutaneous morphine and sometimes produced a pronounced overshoot, but without a preceding injection of morphine, naloxone had no effect on circulation. It is suggested that inhibition of sympathetic tone to the cardiovascular system by an action on structures near the obex is the mechanism by which morphine produces in man orthostatic hypotension and its beneficial effect in left ventricular failure.

Animals↗
PubMed1986

Blood pressure effects of leptazol applied to the ventral surface of the brain stem of cats.

In anaesthetized cats leptazol (200 mg/ml) and sodium pentobarbitone (30 mg/ml) were applied topically to an area of the exposed ventral surface of the medulla oblongata, which lies between the rootlets of the twelfth cranial and first cervical nerve. The drugs were applied either bilaterally by means of paired Perspex rings or unilaterally by means of a single Perspex ring. Their effects on arterial blood pressure, heart rate and respiration were examined during two stages of anaesthesia, during 'surgical anaesthesia' produced by an intravenous injection of chloralose at 60 mg/kg, and during deeper anaesthesia attained by two additional intravenous injections of chloralose at 30 mg/kg. Both the bilateral and unilateral application of leptazol produced a fall in arterial blood pressure during surgical anaesthesia, but a rise during deepened anaesthesia. After a preceding topical application of sodium pentobarbitone the fall became attenuated or abolished, whereas the rise became potentiated. Sodium pentobarbitone itself affected blood pressure as well as respiration when applied bilaterally. It then produced pronounced tachypnoea independent of the depth of anaesthesia and a fall in arterial blood pressure during deepened anaesthesia. Its unilateral application did not affect respiration, nor did it affect usually arterial blood pressure, although during deepened anaesthesia it occasionally produced a fall in blood pressure. The area from which the pressor response to leptazol was obtained lay 7-11 mm caudal to the lower border of the trapezoid bodies, i.e. about 2 mm more caudally than the 'nicotine-sensitive area' from which a depressor response to leptazol is evoked. Thus the two areas, though not identical, overlap. The result obtained with sodium pentobarbitone suggest that the area for the pressor response to leptazol plays a role in maintaining vasomotor tone during deepened anaesthesia and exerts a strong inhibitory effect on the respiratory rate during both surgical and deepened anaesthesia.

Anesthesia, General↗
PubMed1985

Hyperglycaemia: imitating Claude Bernard's piqûre with drugs.

Hyperglycaemia lasting for hours, has been produced in unanesthetized cats, rabbits and rats by injection into the cerebral ventricles or the cisterna magna of a variety of drugs (morphine, etorphine, pethidine, beta-endorphin, enkephalin, bombesin, TRH, cholecystokinin, naloxone, propranolol, phentolamine, chloralose, magnesium chloride and GABA). These drugs probably act at the ventral surface of the brainstem and initiate a sympathetic discharge to the adrenals which results in a prolonged release of relatively small amounts of adrenaline. When adrenaline is released in this way hyperglycaemia may be the only effect. The mechanism of the piqûre hyperglycaemia of Claude Bernard may be the same, although Bernard assumed that it resulted from an effect on the floor of the fourth ventricle, i.e. on the dorsal surface of the brainstem. However, it is clear from his description that his trochar not only pricked the floor of the fourth ventricle but penetrated to the ventral surface of the brainstem. Release of adrenaline from the adrenals is usually regarded as a stress response, as in fight, flight, fear or rage when it is suddenly released in large amounts and produces its typical cardiovascular and ocular reactions. The results now obtained with drugs injected intraventricularly or intracisternally suggest an additional physiological role for adrenaline when it is released over prolonged periods and in relatively small amounts producing only hyperglycaemia. Such a release may play a role in the day-to-day control of blood glucose, and its disturbance might underlie non-insulin-dependent diabetes.

Adrenergic beta-Antagonists↗
PubMed1981

Inhibition of vasopressin release to carotid occlusion by gamma-aminobutyric acid and glycine.

1 In cats anaesthetized with pentobarbitone sodium or chloralose, the amino acids, gamma-aminobutyric acid (GABA) and glycine, were applied to the ventral surface of the brain through paired Perspex rings placed across the medulla. 2 Applied to a region situated at the transition between medulla and cord, both amino acids greatly attenuated and even abolished the vasopressin release in response to carotid occlusion. Glycine was about 100 times more potent than GABA and effective in a concentration of 0.1 mg/ml. The pressor response to carotid occlusion was not affected. 3 Applied to a region situated 5 to 6 mm more rostrally, the amino acids did not affect vasopressin release but in strong concentrations, greatly attenuated the pressor response to carotid occlusion. 4 The two responses to carotid occlusion, vasopressin release and the pressor response, can thus be influenced independently. 5 It is concluded that the pathways carrying afferent impulses from the baroreceptors in the carotid sinus reach the ventral surface of the brain stem at two regions. At both, synaptic transmission can be blocked by the application of an inhibitory amino acid and thus prevent either the release of vasopressin at the caudal site, or the increase of vasomotor tone at the rostral site.

Animals↗
PubMed1979

Cardiovascular effects of hypertonic sodium chloride solutions when injected into the liquor space of anaesthetized cats.

1 In cats anaesthetized with chloralose, hyper- and hypotonic solutions were injected into the cisterna magna (in 0.5 ml) or into a lateral cerebral ventricle (in 0.2 to 0.3 ml), with aqueduct cannulated to prevent the injected solution from entering the subarachnoid space, and the effects on blood pressure and heart rate were examined. 2 Cisternal injections of hyper- and hypotonic solutions of NaCl (0.51 M and 0.05 M), glucose (1.03 M and 0.10 M), or sucrose (1.02 M and 0.10 M), as well as distilled water produced a rise in arterial blood pressure with tachycardias. Isotonic solutions of NaCl, glucose or sucrose were ineffective. 3 Ventricular injections of the hypertonic NaCl solution, also produced a pressor response with tachycardia effects when injected in this way. 4 The pressor responses and the tachycardias occurred after bilateral vagotomy and resulted from a sympathetic discharge which, on cisternal injection, originated from structures reached from the subarachnoid space, and on ventricular injection, from structures in the ventricular walls, probably in the hypothalamus. 5 The stimuli responsible for the discharge, were, on cisternal injection, the changes in osmolarity and on ventricular injection, the sodium ions.

Anesthesia↗
PubMed1978

Vasopressin release produced in anaesthetized cats by antagonists of gamma-aminobutyric acid and glycine.

1 In cats anaesthetized with chloralose, the central excitatory substances, tubocurarine, picrotoxin, bicuculline, leptazol and strychnine, were applied to the exposed ventral surface of the brain stem through paired Perspex rings placed across the medulla and their effects on vasopressin release and arterial blood pressure were examined.2 The excitatory substances released large amounts of vasopressin when applied to an area 6-9 mm caudal to the trapezoid bodies. From this area vasopressin release was previously obtained with nicotine.3 With nicotine, the vasopressin release occurred almost instantaneously and tachyphylaxis developed rapidly. With the excitatory substances the release increased gradually and there was no tachyphylaxis. When these substances were applied for several minutes, the release reached its maximum a considerable time after their removal, except with leptazol when release diminished at once after removal.4 The excitatory substances had little or no effect on arterial blood pressure when applied to the vasopressin releasing area, but produced strong pressor responses when applied to a more rostrally situated area.5 It is concluded that the excitatory substances release vasopressin and raise arterial blood pressure because they are antagonists of gamma-aminobutyric acid and/or glycine and that numerous inhibitory neurones which release these amino-acids synapse at the ventral surface of the medulla. The physiological function of those which synapse at the vasopressin releasing area may be to act as a brake on vasopressin release, and of those which synapse at the more rostrally situated area to act as a brake on arterial blood pressure.

Aminobutyrates↗
PubMed1978

Effects of propylbenzilylcholine mustard on injection into the liquor space of cats.

In unanaesthetized cats the effects were examined of propylbenzilylcholine mustard (PrBCM) on injection into the cannulated cerebral ventricles and cisterna magna. Extreme motor excitation, vocalization, shivering leading to fever, tachypnoea, panting, piloerection and salivation were produced on ventricular, vigorous scratching bouts on cisternal, injections. The sites of these actions are discussed. None of the effects was produced by atropine similarly injected. All effects were suppressed by anaesthetizing doses of pentobarbitone sodium injected intraperitoneally.

Animals↗
PubMed1978

Release of vasopressin by enkephalin.

Leu-enkephalin, its stable analogue [D-Ala2-D-Leu5]-enkephalin and the C-fragment of lipotropin (beta endorphin) injected intravenously in the rat produced antidiuretic responses which were inhibited reversibly by naloxone. It was shown for Leu-enkephalin that injection into the cerebral ventricles was at least ten times more effective than intravenous injection and for [D-Ala2-D-Leu5]-enkephalin that the antidiuretic response was associated with increased excretion of vaspressin in the urine.

Animals↗
PubMed1977

C-fragment of lipotropin--an endogenous potent analgesic peptide.

1 A series of peptides derived from porcine lipotropin was examined for analgesic and other morphine-like properties on infusion into the cannulated third ventricle of cats.2 Lipotropin (LPH 1-91) itself produced no analgesia or other morphine-like effects when infused in a dose of 150 mug.3 C-fragment (LPH 61-91) produced strong long-lasting analgesia when infused in a dose of 10 or 20 mug; on a molar basis the potency was between 90 and 180 times that of morphine. The following morphine-like effects were also produced: shivering leading to fever, vasodilatation of the pinnae, mydriasis, opening of the palpebral fissures, tachypnoea with bouts of panting, vocalization, hyperexcitability, restlessness and catalepsy. All the effects, including analgesia, were abolished by an intraperitoneal injection of naloxone (1 mg/kg).4 Hyperglycaemia, another central effect produced by morphine, was obtained with C-fragment infused in a dose of 60 mug.5 On intravenous injection, C-fragment produced analgesia with a dose of about 200 mug/kg. Administered by this route, C-fragment was again more potent than morphine.6 C'-fragment (LPH 61-87), LPH 61-78 and LPH 61-69, either had no analgesic effect or produced weak short-lasting analgesia when infused in doses up to 100 mug.7 Methionine enkephalin (LPH 61-65) either produced very weak short-lasting analgesia or had no analgesic effect when infused in doses of between 30 and 400 mug.8N-methyl methionine enkephalin amide in which both termini of methionine enkephalin were protected against degradation by exopeptidases produced long-lasting analgesia when infused in doses of 150 to 180 mug; its analgesic potency was approximately 100 times less than that of C-fragment. Blocking only one terminus of methionine enkephalin did not appear to endow the peptide with analgesic properties. The N-methyl pentapeptide amide produced other morphine-like effects of which the most striking was catalepsy. All the effects were abolished by intraperitoneal naloxone (1 mg/kg).

Analgesics↗