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Biomedical subjects

J Holmberg

Publications and source records attributed to J Holmberg.

At least 55 records · Page 3Linked to original sources

Controlled blocking of hepatic artery flow with enzymatically degradable microspheres combined with oncolytic drugs.

A new method for intermittent hepatic arterial flow arrest has been used in combination with intraarterial 5-fluorouracil (5-Fu) for the treatment of secondary liver neoplasms in 12 patients. Polysaccharide microspheres with a half-life of 1 h were infused together with 5-Fu via a percutaneously introduced catheter into the hepatic artery. There were no significant side effects to the treatment. Clinical effects and overall survival were comparable to those of hepatic artery ligation.

Clinical Trials as Topic↗

Reflex plasma hyperglycemia and hyperosmolality evoked by unloading of the carotid baroreceptors.

Hemorrhage is usually accompanied by a considerable increase in the plasma osmolality and glucose concentration due to an augmented release of glucose from the liver. In the present cat experiments an attempt was made to investigate the possible role of different vascular receptors in mediating this hyperglycemic (hyperosmolar) response. Bilateral vagotomy or stimulation of the carotid chemoreceptors by perfusion of the carotid sinus with venous blood at normal pressure only slightly increased the arterial plasma glucose concentration. On the other hand, when the sinus nerves were cut in the vagotomized animal, thereby simulating complete unloading of the carotid baroreceptors, the arterial plasma glucose concentration rose by about 8 mM/L and the arterial plasma osmolality by about 10 mOsm/kg H2O. Perfusion of the carotid baroreceptors with arterial blood at different levels of hypotension showed that the baroreceptor-induced hyperglycemia was graded in relation to the pressure level. Regional hypotension of the liver, pancreas, intestine, kidneys or brain did not significantly affect plasma glucose concentration or osmolality. We conclude that the reflex release of glucose from the liver during hemorrhage mainly is initiated from the unloading of arterial baroreceptors.

Animals↗

Hyperglycemic and hyperosmolar responses to graded hemorrhage.

Changes of the arterial plasma osmolality and of the glucose concentration were followed during a 30 min period of graded hemorrhagic hypotension (80, 50, and 30 mmHg) in the cat. Bleeding evoked a significant plasma hyperosmolality at all three hypotension levles and the responses were quantitatively related to the degree of hypotension. An approximate steady state increase in the arterial plasma osmolality was reached about 20 min after the start of the bleeding and it then averaged 8. 20, and 25 mOsm/kg H2O at 80, 50, and 30 mmHg, respectively. Bleeding also evoked an increase in the plasma glucose concentration, which almost entirely accounted for the observed hyperosmolality, especially at 80 and 50 mmHg. In late stages of hypotension at 30 mmHg, elevated plasma lactate and potassium concentrations contributed to the overall hyperosmolality. --Previous hemorrhagic hypotension experiments at 50 mmHg (Järhult 1975 b) have shown that hyperosmolality serves as an important regulator of the plasma and extracellular fluid volumes during bleeding. The present results indicate that such an osmolar compensatory mechanism is operating over wide ranges of hemorrhagic hypotension.

Animals↗

Tissue hyperosmolality as a causal factor in vasodilatation following sympathetic stimulation of the submandibular gland.

In a previous investigation, parasympathetic activation of the submandibular gland in the cat was found to cause a considerable increase of regional tissue osmolality, the degree of which was related to the evoked functional hyperemia; intra-arterial hypertonic infusion to the resting gland producing tissue hyperosmolality of similar magnitudes caused graded and marked dilatations (Lundvall and Holmberg 1974). It was concluded that hyperosmolality contributes significantly to the functional hyperemia response. In the present study evidence is presented to indicate that tissue hyperosmolality is a mediator of the dilatation associated with sympathetic activation as well. An increase of tissue hyperosmolality, as traced in the venous effluent, was found at all frequencies of sympathetic stimulation (2-16 Hz). At high stimulation rates it sometimes exceeded the resting control level by more than 20 mOsm/kg H2O. There was a direct relation between the degree of venous hyperosmolality and the hyperemia response observed immediately after cessation of stimulation. Comparison of the dilator effects evoked by sympathetic stimulation and by hypertonic infusion to the resting gland indicated that tissue hyperosmolality is an important causal factor for the nerve induced dilatation, especially at low and moderate stimulation rates.

Animals↗

The secretory nerves of the parotid gland of the dog.

1. Secretory nerve fibres to the parotid gland of the dog have been found in the adventitia of the internal maxillary artery. In dogs under chloralose anaesthesia the course of these fibres from the mandibular nerve to the gland was determined by electrical stimulation at different sites. Secretion induced by these nerves was abolished by atropine but not by hexamethonium.2. In dogs in light barbiturate anaesthesia parotid secretion was evoked reflexly by pouring citric acid on the tongues. After division of the auriculo-temporal nerve and the nerves on the artery this secretion disappeared in about half the experiments and was greatly reduced in the others.3. The maximal secretory rate which could be obtained reflexly from the normally innervated parotid gland was first estimated in light barbiturate anaesthesia. Chloralose was then given and the auriculo-temporal nerve and the nerves on the artery were electrically stimulated together; in about half the experiments this could produce secretion at a rate as high as that obtained reflexly.4. By separate and simultaneous stimulation of different sets of nerve fibres convergence of the secretory fibres to the glandular cells could be demonstrated.5. It is concluded that a large number of post-ganglionic, cholinergic secretory fibres to the canine parotid gland run on the internal maxillary artery. In some dogs a small number of fibres seem to have escaped detection. Possibly they may reach the gland by way of the facial nerve.

Anesthesia↗