Search PubMed⌕ Search

Biomedical subjects

I Guldvog

Publications and source records attributed to I Guldvog.

34 records · Page 2Linked to original sources
PubMed1983

The effect of alpha- and beta-adrenergic agonists and blockers on postprandial pancreatic polypeptide release in dogs.

The influence of adrenergic agonists--phenylephrine (alpha), isoproterenol (beta), and salbutamol (beta 2)--and of adrenergic blockers--phentolamine (alpha), pranolol (beta), and practolol (beta 1)--on the postprandial pancreatic polypeptide (PP) release has been assessed in five Labrador retrievers. Infusions of phenylephrine, 0.12 mg kg-1h-1; isoproterenol, 3 micrograms kg-1h-1; salbutamol, 12 micrograms kg-1h-1, did not significantly affect PP release. Propranolol, 0.5 mg kg-1, and propranolol, 0.5 mg kg-1, + phentolamine, 1 mg kg-1, combined, given as intravenous boluses before the meal significantly reduce PP release (44% and 58% of controls, p less than 0.05), whereas phentolamine, 1 mg kg-1, and practolol, 1 mg kg-1, had no effect. Phenylephrine combined with phentolamine and isoproterenol combined with propranolol and practolol did not influence PP secretion. It is concluded that the postprandial PP release is stimulated by beta 2-adrenergic mechanisms.

Adrenergic alpha-Agonists↗
PubMed1983

The effect of histamine, H1 and H2 agonists, and H1 and H2 antagonists on postprandial pancreatic polypeptide release in dogs.

The influence of histamine, H1 and H2 agonists (2-AETD and dimaprit), and H1 and H2 antagonists (mepyramine and cimetidine) on the postprandial release of pancreatic polypeptide (PP) was assessed in five Labrador retrievers. Infusions of histamine, 0.25 mumol kg-1 h-1; 2AETD, 4 mumol kg-1 h-1; and dimaprit, 1 mumol kg-1 h-1, enhanced postprandial release (131-189% of control values). The response to 2-AETD and dimaprit was significantly different from control values (p less than 0.05). An increase was observed even when 50 mg mepyramine and 400 mg cimetidine were injected as intravenous boluses (131-139% of control values (p less than 0.05]. The action of the antagonists may be explained by partial agonism or histamine release induced by these agents. It is concluded that postprandial PP release is stimulated by H1 and H2 receptors.

Animals↗
PubMed1982

Experimental post-traumatic lung insufficiency in dogs: ultrastructure of lung lesions.

The ultrastructure of developing lung lesions in two groups of dogs exposed to a combination of haemorrhagic hypotension and liver trauma was studied with particular attention to changes at the alveolar level and lung micro-vessels. Lung samples were obtained every four hours and at collapse in one group and 12 hrs after initiation of the trauma in the other. An interstitial oedema was recognized in biopsies obtained 4 hrs after initiation of the trauma, and before marked lesions were observed at the ultrastructural level in endothelial cells. Endothelial damage was, however, evident in biopsies obtained at 8 hrs and at collapse. Aggregates of degranulated and degenerated leucocytes and platelets were occasionally found to obstruct respiratory capillaries together with erythrocytes, some of which seemed to be haemolysing. A considerable amount of protein-rich oedema, cellular debris and fibrinoid material was found in alveolar lumina at collapse. The present experiments indicate that increased vascular permeability in lung micro-vessels is of importance for the development of the characteristic lesions seen in shock lung. Possible pathogenetic mechanisms, initiating the lung lesions, are discussed with special emphasis on the significance of kinin activation and the presence of polymorphonuclear leucocytes and microthrombi.

Animals↗
PubMed1982

Changes of components of the plasma kallikrein-kinin system during experimental lung insufficiency in dogs.

Lung insufficiency was induced in 11 dogs by combined hemorrhagic hypotension (55 mm Hg for two hours) and clamping the portal triad (20 minutes). Four dogs were ventilated spontaneously (group 1). In seven dogs thoracotomy was done giving access to lung biopsies and central hemodynamic measurements (group 2). Five dogs were used as controls without hypotension or clamping. All the dogs in group 1 and 2 developed morphological changes in the lungs characteristic of post-traumatic lung insufficiency. A significant decrease of prekallikrein levels (42% and 34% of initial levels in the two groups, respectively) was found. A significant elevation of the kallikrein activity compared to initial values and the control group was found as well. The antikallikrein levels were reduced to 76% and 67% of initial levels in group 1 and 2, respectively. This reduction was statistically significant. A significant lowering of high molecular weight kininogen was also found, 50% and 28% of initial levels in the two groups. These results demonstrate activation of the kallikrein-kinin system in this experimental model. This can give information on the pathogenesis of post-traumatic lung insufficiency and can explain, for instance, the hypotension and oedema found in this condition. This study also demonstrates that homeostatic functions are altered, this probably being of greater interest than the specific lung alterations described by several authors. Determination of the components of the kallikrein-kinin system can be of diagnostic and prognostic value in post-traumatic lung insufficiency in clinical medicine.

Animals↗
PubMed1982

Angiotensin II and renal excretion of sodium and potassium in unanaesthetized dogs.

Aldosterone is a kaliuretic hormone. It is also widely believed to be instrumental for physiological renal sodium sparing. How, then, can mammals respond to incipient dehydration or low sodium intake without inappropriate potassium loss? To study this problem angiotensin II (A II) was infused intravenously in six dogs. The dose rate was 10 ng per kg per min, probably maintaining plasma A II in the upper physiological range. The A II infusions lasted 3 h, i.e. long enough for the effects of increased aldosterone release to be observable. Mean arterial blood pressure increased by 8% while effective renal plasma flow and glomerular filtration rate fell by 28% and 7%, respectively. Renal sodium excretion fell to near 8% of the preinfusion control values. Plasma aldosterone increased three-fold. Yet no kaliuresis occurred. Potassium and chloride excretion declined by 50% and 80%, respectively. In five of the six dogs urine flow decreased 50% or more with concomitant increase of urine osmolality. Our data indicate that physiological increments of A II can bring about sustained renal sodium sparing without inducing potassium wasting.

Aldosterone↗
PubMed1981

The influence of hormones and drugs on gastric pepsin secretion. The role of vagal innervation.

Seven double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated and denervated mucosa at the same time in the same animal. Stimulation was done by food, a mixture of liver, heart and bonemeal, 10 g/kg. Cimetidine, 25, 50, 100, 200, and 400 mg; atropine, 0.031, 0.125, 0.5 and 1.0 mg; somatostatin, 0.5, 1.0, and 2.0 micrograms/kg/h; and secretin 2 U/kg/h, were given 60 min after the meal, one single dose on each day. Atropine and somatostatin lowered pepsin secretion in both pouches, significantly more in denervated mucosa for all doses of somatostatin and for the lower doses of atropine. Higher doses of atropine nearly abolished the secretion in both pouches. Cimetidine lowered pepsin output only in denervated mucosa. In innervated mucosa the output was unchanged or significantly increased (50 mg) by cimetidine. Secretin increased pepsin output significantly in both pouches, more in innervated mucosa. When the infusion of somatostatin was topped, a marked rebound effect was seen in the innervated pouch.

Animals↗
PubMed1981

Food-stimulated gastric acid secretion inhibited by hormones and drugs. The role of vagal innervation.

Seven double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP) made possible comparison of gastric secretion from innervated and denervated mucosa at the same time in the same animal. Stimulation was done by food--a mixture of liver, heart, and bonemeal, 10g/kg. Cimetidine, 25, 50, 100, 200, and 400 mg; atropine, 0.031, 0.125, 0.5 and 1.0 mg; somatostatin, 0.5, 1.0, and 2.0 micrograms/kg/h; and secretin, 2 U/kg/h, were given 60 min after the meal, one single dose on each day. All compounds and all doses showed inhibition of gastric acid secretion in both pouches, significantly more pronounced in denervated mucosa for smaller doses of all compounds. In addition, the effect lasted longer in denervated mucosa. After somatostatin a pronounced rebound effect was seen. Cimetidine and atropine also showed significantly higher output than controls after the inhibition, but only in innervated mucosa.

Animals↗
PubMed1981

Physiological stimulation of pepsin secretion. The role of vagal innervation.

The studies were performed on eight double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. Food stimulation was done with a mixture of liver, heart, and bonemeal in doses of 1.25, 2.5, 5, 10, and 20 g/kg body weight, plus maximal stimulation by repeated meals of 5 g/kg every 15 min up to 10 times. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl dissolved in 0.15 M NaCl. The pepsin secretion in the HP equalled the 'non-active' output for all doses of food. In the innervated pouch there was an immediate, very high pepsin output similar to the response that can be elicited by 2-deoxy-D-glucose and bethanechol chloride. The secretion of pepsin was gradually reduced, but it was, as long as the volume and electrolyte secretion lasted. well above the 'non-active' level. The results show that stimulation of pepsin secretion by food is completely dependent on intact vagal innervation. The volume and acid output were increased as the dose of food was increased, but the concentration of pepsin was stepwise reduced when the volume increased, resulting in approximately the same output of pepsin for all doses of food. The pepsin to acid ratio was statistically higher in juice secreted from innervated than from denervated mucosa for all doses of food, for lower doses of histamine and pentagastrin, and for higher doses of bethanechol chloride.

Animals↗
PubMed1980

Blood flow in arteries determined transcutaneously by an ultrasonic doppler velocitymeter as compared to electromagnetic measurements on the exposed vesels.

We have compared the instantaneous mean blood velocity measured transcutaneously from total cross-sections of arteries in dogs by the use of a new pulsed heterodyne ultrasound doppler equipment, with instantaneous blood flow as measured simultaneously by an electromagnetic flowmeter applied on the exposed vessels. The experiments were performed on the common carotid and the femoral arteries in a variety of flow situations, always with a close fit between the two curves. The results show that the output from the ultrasound equipment is proportional to flow.

Animals↗
PubMed1980

Vagally innervated and denervated gastric pouch in one and the same dog--a new model.

A new model for studies of gastric secretion is introduced. Two pouches separated from the stomach are constructed in one and the same dog. A vagally denervated pouch is taken from the corporo-fundic part of the stomach, and a vagally innervated pouch is constructed from a pear-shaped piece of the anterior wall with basis in the corporeal part of the lesser curvature. Intact vagal innervation is tested with 2-deoxy-D-glucose. The maximal histamine response is used as reference value for each pouch. A dose-response study for histamine stimulation is presented. The model has proved to be surgically well reproducible: of the first 16 dogs operated upon, 12 have shown appropriate magnitude of secretion. The dogs can live for months and years; a tendency to hypopotassaemia is easily normalized by oral KCl.

Animals↗
PubMed1980

Comparison of physiological and pharmacological stimulation of acid secretion in vagally innervated and denervated gastric pouches in the same dog.

The double-pouch dog with one vagally innervated Amdrup pouch (AP) taken from the lesser curvature side of the stomach and one denervated Heidenhain pouch (HP) from the corporo-fundic part permitted comparison of gastric secretion from innervated and denervated mucosa at the same time in the same animal. Food stimulation with a mixture of liver, heart, and bonemeal showed significantly higher response from AP than from HP for all doses, and the difference between the pouches in total acid output was constant for all doses, indicating that the relative contribution of vagal innervation is diminished when the size of the protein meal is increased. The difference between innervated and denervated mucosa is achieved by an immediate high response from the AP. After 150 min the responses to the larger meals were identical in the two pouches. Acid output during stimulation with pentagastrin reached 64.4% of maximal response to histamine in the AP and 36.2% in the HP, the innervated mucosa giving a statistically significant higher response for all doses. Absence of innervation gave an HP response similar to non-competitive inhibition with significantly lower calculated maximal response and a CD50 not different from the CD50 for the AP. Twenty-four hour secretion studies during optimal physiological conditions with the dog fed two daily meals of standard composition showed sparse secretion from denervated mucosa, whereas a great part of the capacity of innervated mucosa is utilized during daily conditions.

Animals↗
PubMed1980

'Non-active' pepsin secretion compared with stimulated secretion by bethanechol, histamine, pentagastrin, and 2-deoxy-D-glucose. The role of vagal innervation.

The present studies were performed on a double-pouch dog with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl, 0.15 M NaCl, and 0.03 M phosphate buffer, and well-known stimulators of gastric secretion such as histamine, pentagastrin, bethanechol, and 2-deoxy-D-glucose (2-DG) were tested as pepsigogues. Cholinergic stimulation by 2-DG and bethanechol (Urecholine) was clearly the most potent stimulus of pepsin secretion. 2-DG elicited secretion only from innervated mucosa, whereas the responses to bethanechol were similar in the two pouches. Histamine and pentagastrin were weak stimulators, but both provoked active and sustained secretion of pepsin when given in small doses. Higher doses of histamine strongly inhibited pepsin output. The effects of histamine were independent of vagal innervation. By contrast, the active stimulation by pentagastrin only took place in innervated mucosa. The highest outputs were seen in the lowest doses, but also very high doses of pentagastrin elicited active pepsin secretion in the AP. Medium doses of pentagastrin brought the secretion down the the 'non-active' level. The chief cells in the denervated mucosa were quite insensible to pentagastrin, and the pepsin output in the HP equalled the non-active' response at all dose levels.

Animals↗
PubMed1980

Plasma antiplasmin activities in experimental lung insufficiency.

Components of the fibrinolytic system including functional activities of plasma antiplasmins were studied in experimental lung-insufficiency in a canine model. The procedure included hemorrhagic hypotension for 2 hours and occlusion of the hepatic artery, portal vein and common bile duct for 20 minutes of the hypotensive period. Plasma levels of plasminogen decreased gradually during the experiments. Using chromogenic peptide substrate assays, significant reductions of both "immediate" and "time dependent" antiplasmin activities were observed during the first few hours of the experiments. After 4 hours, both antiplasmin activities gradually increased. In 2 of the animals studied "time dependent" antiplasmin activities were 113 and 118 per cent of initial values at 12 hours. These findings emphasize that increased antiplasmin activities may be of great importance for fibrin deposition, leading to a state of microembolism in the lung in this condition.

Animals↗
PubMed1980

Blood cells and coagulation during experimental lung insufficiency in dogs.

Thromboembolism of minor vessels in the lungs is almost constantly seen in posttraumtic lung insufficiency. Many investigators consider it as the primary factor in the pathogenesis of this condition. The present paper deals with screening of the coagulation system as part of a more extended project also investigating changes in the fibrinolytic system and the kallikrein-kinin system. The data are also to be compared with morphological findings during the development of experimental posttraumatic lung insufficiency. The experimental syndrome was evoked in Labrador retriever dogs by haemorrhagic hypotension combined with clamping of the portal triad. The surgical procedure was extended to additional thoracotomy in one group of dogs. Group I, without thoracotomy, were followed for 12 hours. Group II, with thoracotomy, were followed until they succumbed (3-14 hours). Thrombotest (TT) showed a steady prolongation of clotting time in both groups, whereas Cephotest did not reveal any alterations, except for a significant prolongation in group II just before collapse. Fibrinogen was markedly reduced in both groups. Platelets and leucocytes were significantly reduced, but only in group II. It is concluded that the present data are indicative of disseminated intravascular coagulation. The involvement of the intrinsic coagulation system is questioned.

Animals↗