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Biomedical subjects

G Nilsson

Publications and source records attributed to G Nilsson.

At least 271 records · Page 15Linked to original sources
PubMed1978

A quantitative study of the insulin release induced by vagal stimulation in anesthetized cats.

Insulin was released by vagal stimulation in anesthetized and eviscerated cats. The plasma insulin concentration and blood flow in the portal vein were determined concomitantly and the insulin output was calculated. Stimulation of either the right or the left cervical vagus released the same amount of insulin, whereas bilateral stimulation released twice as much. Following a stimulation that depleted the "vagally-releasable pool", a recovery period of 15--20 min was needed before the same maximal output could be obtained again. With shorter interstimulatory periods the amounts of insulin released were reduced. When less than 2--3 00 impulses were applied during a stimulation period, the amount of insulin released per impulse was constant. Atropine (0.2--2 mg/kg) did not reduce the vagally-induced insulin release.

Animals↗
PubMed1978

A gastrin releasing peptide from the porcine nonantral gastric tissue.

This paper presents evidence for the existence in extracts from porcine non-antral gastric tissue of a peptide capable of causing substantial rises of plasma immunoreactive gastrin levels in a dose dependent manner and of stimulation of gastric acid and pepsin secretion. Obtained data show that the peptide is basic and that its gastrin releasing properties are at least partially resistant to atropinisation and beta-receptor blockade. Antrectomy almost eliminates the rise in plasma IRGa when the peptide is administered. The possible relationship of this peptide to amphibian bombesin is discussed.

Animals↗
PubMed1977

On the occurrence of substance P-containing fibers in sympathetic ganglia: immunohistochemical evidence.

Several sympathetic ganglia of the guinea pig, cat and rat were studied with indirect immunofluorescence technique using antibodies to substance P (SP) and dopamine-beta-hydroxylase (DBH), the latter of which represents a marker for noradrenaline containing neurons. In all ganglia studied SP-like immunoreactivity could be observed in certain nerve fibers (SP-positive fibers). Their number, localization fluorescence intensity and 'fluorescence morphology' varied considerably between the different ganglia as well as between species. In the inferior mesenteric ganglion and the coeliac-superior mesenteric ganglion complex of all species, and in particular of the guinea pig, a dense plexus of varicose SP-positive fibers was observed around the mostly DBH-positive, principal ganglion cells. In contrast no such fibers were seen in relation to the DBH-positive SIF cells of the ganglia. No SP-positive ganglion cells were observed in any of the ganglia studied. Previous biochemical and immunohistochemical studies have indicated that peripheral SP-positive fibers may represent the branches of primary sensory neurons. The rich supply of varicose, SP-positive nerve terminals, often surrounding the noradrenergic ganglion cells in a basket-like manner, may indicate that these fibers may play a functional role within the ganglia. Instead of merely passing through the ganglion they may be involved in special types of reflex arches.

Animals↗
PubMed1977

Insulin release in response to vagal stimulation in anaesthetized cats.

Peripheral and portal plasma insulin concentrations were determined in eviscerated cats before, during and after vagal stimulation. Basal peripheral insulin levels averaged 2.4 ng/ml and portal levels 18 ng/ml. The portal blood flow was recorded continuously, thus enabling the insulin output/min to be calculated. In addition, the total insulin content of the pancreas was determined, which permitted quantitative comparisons of insulin release and pancreatic insulin content to be made. About 2% of the insulin store was released during one hour under basal conditions. Unilateral vagal stimulation with frequencies ranging between 1 and 20 Hz induced an almost immediate release of insulin into the portal vein. Following stimulation with frequencies of 3-4 Hz, the release mechanism was fatigued by a total of 2000-3000 impulses. The insulin output produced by such a supramaximal stimulation averaged 1.5 microgram and constituted about 2% of the total pancreatic insulin content. 15-20 min was needed for the release mechanism to recover.

Animals↗
PubMed1977

Immunohistochemical analysis of peptide pathways possibly related to pain and analgesia: enkephalin and substance P.

The distribution of Met-enkephalin- and substance P-immunoreactive neurons was studied by indirect immunofluorescence in some areas related to pain and analgesia. Met-enkephalin- and substance P-positive cell bodies and nerve terminals were observed in the periaqueductal central gray, the nucleus raphe magnus, the marginal layers and substantia gelatinosa of the spinal trigeminal nucleus, and the dorsal horn of the spinal cord. Lesion experiments suggest that Met-enkephalin neurons in the dorsal horn and possibly in the spinal trigeminal nucleus are interneurons or propriospinal neurons with nerve terminals in the laminae I and II of the cord and in the superficial layers of the spinal trigeminal nucleus, respectively. These areas are also very rich in substance P-positive nerve terminals, mainly representing central branches of primary afferent neurons. The present immunohistochemical-anatomical findings support the hypothesis that stimulation-produced analgesia is related to activation of spinal and spinal trigeminal enkephalin interneurons forming axo-axonic synapses with (substance P?) pain afferents in the superficial laminae of the dorsal horn and the spinal trigeminal nucleus. These interneurons may be activated by sensory fibers and by descending fibers from medullary stimulation sites. Transmitter substances in these descending fibers may be 5-hydroxytryptamine and substance P.

Analgesia↗
PubMed1977

Divergent changes of serum 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine in patients with acute myocardial infarction.

The serum levels of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3, rT3), thyroxine-binding globulin and thyroid-stimulating hormone have been monitored in 13 patients with acute myocardial infarction. The major changes recorded were a transient decrease in T3 and a transient increase in rT3. They reached a nadir and a peak, respectively, within three days. A conceivable explanation for these alterations is that the monodeiodination of T4 is diverted from the activating pathway (T4 to T3) to the inactivating pathway (T4 to rT3).

Acute Disease↗
PubMed1977

Studies on replacement and suppressive dosages of 1-thyroxine.

Serum thyrotropin (TSH) levels were studied in 55 hypothyroid patients in order to determine adequate replacement and suppression dosages of 1-thyroxine (T4). In accordance with previous reports it was found that most patients had normal TSH levels and were clinically euthyroid at daily doses of 0.10-0.15 mg T4. None of the patients required a dose exceeding 0.20 mg. When the TSH levels normalized, serum thyroxine and serum triiodothyronine also fell to levels within their normal ranges. The effectiveness of various doses of T4 in suppressing the temporary rise in serum TSH concentration normally induced by thyrotropin-releasing hormone was examined in 57 patients treated with T4 for atoxic goitre or after subtotal surgical removal of such a goitre. The rise in TSH was not usually inhibited by a T4 dose of less than 0.20 mg, a finding which at least theoretically has implications for the adequate suppressive dose of T4.

Female↗
PubMed1977

Effect of teasing and sham feeding on plasma glucagon concentration in dogs.

Plasma glucagon concentration was determined by radioimmunoassay during fasting and following teasing and sham feeding. Teasing and sham feeding for 1--10 min raised the plasma glucagon concentration which then within a short period of time returned to the basal level. Atropinization (0.2 mg/kg) almost abolished the glucagon response to 10 min of sham feeding. Glucose concentration was slightly elevated in response to 10 min of sham feeding. The results show that physiological stimulation that is induced by the smell, sight and taste of food releases glucagon in the dog. The release is mediated by a cholinergic mechanism.

Animals↗