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Biomedical subjects

W F Immink

Publications and source records attributed to W F Immink.

9 recordsLinked to original sources
PubMed1992

Hyperadrenocorticism in four cats.

This paper describes four cats with hyperadrenocorticism. Cat 1 showed polydipsia and polyphagia. Diabetes mellitus was initially diagnosed. As the animal appeared to be insulin resistant, pituitary and adrenocortical function tests were performed and the diagnosis of hyperadrenocorticism was made. Resistance to the high-dose dexamethasone suppression test was noticed in this cat. Pathological examination revealed a pituitary chromophobe adenoma. Cat 2 presented with diabetes mellitus, which was treated with insulin. The animal had a pendulous abdomen and its coat was in a poor condition. The low-dose dexamethasone suppression test demonstrated hyperadrenocorticism. Necropsy findings of pituitary tumour and hyperplasia of the adrenal cortex confirmed the diagnosis. Cat 3 showed clinical abnormalities indicative of hyperadrenocorticism, for instance, muscle weakness, alopecia, multiple abscesses. The diagnosis of hyperadrenocorticism was confirmed by the results of the lowe-dose dexamethasone suppression test. Pathological examination revealed an adrenocortical carcinoma. Cat 4 presented with polydipsia. The cause of this symptom was not found initially. One and a half years later additional symptoms, such as nephritis and polyphagia developed. Hyperadrenocorticism was diagnosed because of a palpable mass cranial to the left kidney. The diagnosis was confirmed by the results of the lowe-dose dexamethasone suppression test and the necropsy findings.

Animals↗
PubMed1985

[Experiences with a paste used as an anthelmintic in cats].

When the anthelmintic Banminth 'Katze' was administered twice to ninety-two cats, the owners were questioned on the method by which the animals took this paste. Minor, if any, problems were observed in 94.5 per cent of the cats. Major problems occurred in 5.5 per cent of the animals. Significantly more adult than young cats had difficulties in taking the paste.

Animals↗
PubMed1984

Vasoactivity of adrenaline in regions covering the canine gastrointestinal tract.

Little is known about the action adrenaline has on vascular areas of functionally different parts of the stomach and intestine. Therefore the vasoactivity of adrenaline (1-1024 ng/kg i.v.) was studied by electromagnetic flow measurements in 8 vascular beds covering the gastrointestinal tract. Adrenaline induced 1) a vasodilation in the lesser curvature and antrum of the stomach; 2) a vasoconstriction in the greater curvature of the stomach; 3) a vasoconstriction followed by a vasodilation in the duodenum and jejunum; 4) a vasoconstriction in the ileum, caecum/colon and colon/rectum. Phenoxybenzamine (750 micrograms/kg i.v.) blocked systematically the vasoconstriction in the duodenum and jejunum but not in the ileum and colon. Vasodilation could be blocked by propranolol (100 micrograms/kg i.v.). It is concluded that 1) adrenaline-effects are mediated predominantly by beta-receptors in the antrum and lesser curvature of the stomach; predominantly by alpha-receptors in the greater curvature of the stomach; by alpha- and beta-receptors in the duodenum and jejunum; 2) receptors in the large intestine are of another alpha-adrenergic type than those in the small intestines. Evidence was provided for a gradient of diminishing vasodilating effects of adrenaline from cranial to caudal of the gut.

Animals↗
PubMed1978

alpha- and beta-receptor blockade of isoproterenol- and norepinephrine-induced effects on regional blood flow and blood flow acceleration.

The effects of the beta-receptor blocking agent propranolol (100 microgram/kg i.v.) and of the alpha-receptor blocking agent dihydroergotamine (50 microgram/kg i.v.) on hemodynamic responses to isoproterenol and norepinephrine (both 1--1024 ng/kg) were investigated in anesthetized dogs. The effects studied were: (1) flow in the ascending aorta and the coronary, common hepatic, gastroduodenal, splenic, cranial mesenteric, renal and femoral arteries: (2) maximal flow acceleration in the splenic, cranial mesenteric and femoral arteries; (3) maximal rate of change of left ventricular pressure (LV dP/dt max). Propranolol shifted the dose-response curves for the isoproterenol-induced flow increases in the common hepatic, gastro-duodenal, and cranial mesenteric arteries to the right. It did not influence the flow responses to isoproterenol in the ascending aorta or the coronary, splenic, renal and femoral arteries. Propranolol prevented the decrease of arterial pressure evoked by isoproterenol. Propranolol shifted the isoproterenol-induced increase of LV dP/dt max and maximal blood flow to the same extent. Propranolol blocked the flow to the liver and gastrointestinal tract to a greater extent than the LV dP/dt max and maximal flow acceleration. Propranolol had no effect on the norepinephrine-induced increases in flow in the splenic, femoral and coronary arteries, but blocked the norepinephrine-evoked increases of flow accelerations and LV dP/dt max to the same extent. Dihydroergotamine inhibited the norepinephrine-induced increase in flow in the femoral artery and the decreases in flow in the hepatic, splenic, cranial mesenteric and renal arteries, and reversed the reduction of flow in the gastroduodenal artery. It is argued that dihydroergotamine may inhibit the increase in femoral flow through two mechanisms: (1) blocking the flow reduction to norepinephrine in the abdomen, and thereby passively shunting blood from the abdomen in preference to the femoral bed; (2) attenuating the norepinephrine-evoked reflexogenic femoral vasodilatation. It is concluded that: (1) propranolol is a beta-receptor blocking agent with a preference for blockade of isoproterenol-induced vascular effects; (2) norepinephrine-induced flow increases are not direct actions on vascular beta-receptors; (3) the increase of maximal blood flow accelerations after isoproterenol and norepinephrine is mediated by stimulation of cardiac beta-receptors; (4) dihydroergotamine is an alpha-receptor blocking agent particularly in the splanchnic vascular region.

Adrenergic alpha-Antagonists↗
PubMed1976

Hemodynamic effects of norepinephrine and isoprenaline in various regions of the canine splanchnic area.

Responses to norepinephrine (NE) and isoprenaline (ISO) (1-1024 ng/kg i.v.) were assessed by electromagnetic flowmetry on 18 arteries of the splanchnic region in anesthetized dogs. Measurements were judged according to the 2 criteria: 1. direction of effect; 2.sensitivity of vascular areas to catecholamines, expressed as D50 (i.e. the calculated dose inducing 50% of the maximum effect). NE decreased flow in all arteries (40-80%), but caused additionally an increase in the celiac, splenic and splenic artery proper. Thus changes in the spleen are responsible for the increase with NE. Flow reduction in the pancreatic branch of the cranial mesenteric artery was small. All flow reductions induced by NE had a similar D50 (about 30 ng/kg), except that in the hepatic artery (100 ng/kg).

Animals↗
PubMed1976

Norepinephrine and isoprenaline induced changes of peripheral blood flow acceleration caused by changes of cardiac inotropy.

In anesthetized dogs the norepinephrine (NE) and isoprenaline (ISO) (1--1024 ng/kg i.v.)--induced increase of maximum peripheral flow acceleration (celiac artery, cranial mesenteric artery, renal artery; and femoral artery) and the changes of the maximum first derivative of arterial pressure were compared with the increases of maximum ascending aortic flow acceleration and maximum first derivative of left ventricle pressure (LV dP/dt max). The maximum effect of each dose on maximum acceleration of flows (dF/dt max) and maximum first derivative of pressures (dP/dt max) occurred simultaneously for all v56--512 ng/kg) and for ISO (D50:128--256) ng/kg). We demonstrated that other varure) played only a minor role in the increases of LV dP/dt max in our studies. In contrast with the uniform response of dF/dt max and dP/dt max, the reaction of peripheral vascular resistance varied. In particular in the gastrointestinal tract the resistance could either be increased (NE, D50:115 ng/kg) or decreases (ISO, D50:15 ng/kg). Gastrointestinal resistance was a more sensitive variable for catecholamine stimulation than dF/dt max and dP/dt max. The data show that under the present experimental conditions induced by NE and ISO is due to increase of cardiac inotropy.

Animals↗
PubMedDate not supplied

Distinction between alpha-adrenergic receptors in eight vascular areas of the dog.

The study concerns the heterogeneity of the vascular alpha-adrenergic receptor population studied in anesthetized dogs. Two groups of animals were used: a control group that received only the agonists noradrenaline (1-1024 ng/kg i.v.) and phenylephrine (64-16384 ng/kg i.v.) and a group that additionally received the antagonist phenoxybenzamine (67-2250 micrograms/kg i.v.). Arterial pressure was measured and the vascular responses were simultaneously monitored in liver, stomach, duodenum, jejunum, ileum, colon, kidney and hindleg, simultaneously with electromagnetic blood flow sensors. Phenoxybenzamine with regard to noradrenaline only blocked the renal vasoconstriction. Effects of some dosages of noradrenaline were inhibited only by the highest dose of phenoxybenzamine. In contrast, phenoxybenzamine inhibited phenylephrine-induced vasoconstriction in all the investigated vascular beds, but not completely in the hindleg. The response in the stomach was even reversed to a vasodilation. It is concluded that (1) all vascular beds studied contain alpha 1-adrenergic receptors; (2) noradrenaline exerts its vasoconstrictive activity by interaction with alpha 1-adrenergic receptors but also with phenoxybenzamine-insensitive alpha-adrenergic receptors. This conclusion indicates a heterogeneity of alpha-adrenergic receptors in the vascular beds studied.

Animals↗