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Biomedical subjects

J Gagne

Publications and source records attributed to J Gagne.

8 recordsLinked to original sources
PubMed1997

Inflammatory liver disease.

The histopathologic and clinical features of feline inflammatory liver disease are incompletely under-stood. Results of recent studies indicate that feline inflammatory liver diseases can be classified as acute (suppurative) and chronic (nonsuppurative) cholangiohepatitis and lymphocytic portal hepatitis. Histopathologic features of cholangiohepatitis include infiltration of neutrophils into walls and lumens of bile ducts and portal areas, periportal necrosis, and variable degrees of fibrosis and bile duct hyperplasia. Lymphocytic portal hepatitis is characterized by increased numbers of lymphocytes and plasma cells in portal areas, bile duct hyperplasia, and fibrosis. Liver biopsy is needed to establish a definitive diagnosis but trends in clinical laboratory test results may be helpful in establishing a tentative diagnosis. Specific treatment for cholangiohepatitis include antibiotic therapy. Corticosteroids have been recommended for treatment of lymphocytic portal hepatitis.

Animals↗
PubMed1996

Mechanism of altered synaptic strength due to experience: relation to long-term potentiation.

An increase in medial perforant synaptic strength can be observed for hippocampal slices from rats exposed to environmental enrichment. The expression of enhanced synaptic strength exhibits properties similar to long-term potentiation (LTP), a physiological model of memory storage. Similarities include an increase in strength of the synaptic response in the absence of an altered paired-pulse ratio and an increase in the binding of the glutamate agonist alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. Furthermore, environmental enrichment interacts with the mechanisms responsible for the induction of LTP by inhibiting further increases in synaptic strength following LTP-inducing stimulation. The results provide evidence for experience-mediated influences on postsynaptic mechanisms regulating medial perforant path synaptic strength.

Analysis of Variance↗
PubMed1990

Alpha 2-adrenoceptor modulation of catecholamine and neuropeptide Y responses during haemorrhagic hypotension in anaesthetized dogs.

The acute effects of oxymetazoline, an alpha 2-adrenoceptor agonist, and idazoxan, an alpha 2-adrenoceptor antagonist, on the release of neuropeptide Y were evaluated during haemorrhage in pentobarbital-anaesthetized dogs. Plasma concentrations of neuropeptide Y and catecholamines (adrenaline, noradrenaline, and dopamine) were determined in samples simultaneously collected from aorta, portal vein, and adrenal veins. In control dogs, adrenal catecholamine output, aortic concentrations neuropeptide Y and catecholamines markedly increased during the hypotension period. However, adrenal neuropeptide Y output decreased significantly during this period. Portal venous noradrenaline and neuropeptide Y concentrations increased significantly. In dogs treated with idazoxan, catecholamine output from the adrenals increased to an extent similar to that observed in control dogs. However, the increase in noradrenaline and neuropeptide Y in aortic or portal venous blood during haemorrhage was significantly potentiated in the presence of idazoxan. Administration of oxymetazoline abolished this increase, but did not alter adrenal catecholamine or neuropeptide Y output. The present study demonstrates that neuropeptide Y is co-released with noradrenaline from sympathetic nerve fibers during haemorrhage. Since the release of neuropeptide Y appeared to follow a similar time course to that of noradrenaline release, the present observations suggest that haemorrhagic hypotension enhances both neuropeptide Y and noradrenaline release presumably through a common releasing mechanism. These results also indicate that, in peripheral sympathetic nerves but not in the adrenal gland, neuropeptide Y release is also modulated presynaptically by the inhibitory alpha 2-adrenoceptors in conjunction with the noradrenaline release.

Adrenergic alpha-Antagonists↗
PubMed1990

Corelease of neuropeptide Y like immunoreactivity with catecholamines from the adrenal gland during splanchnic nerve stimulation in anesthetized dogs.

The release of neuropeptide Y like immunoreactivity (NPY-li) from the adrenal gland was studied in relation to the secretion of catecholamines (CA: NE, norepinephrine; E, epinephrine) during the left splanchnic nerve stimulation in thiopental-chloralose anesthetized dogs (n = 16). Plasma concentrations of NE, E, and NPY-li were determined in the left adrenal venous and aortic blood. Adrenal outputs of NPY-li, NE, and E were 2.4 +/- 0.4, 1.4 +/- 0.2, and 7.3 +/- 1.7 ng/min, under basal conditions, respectively. These values increased significantly (p less than 0.05; n = 8) in response to a continuous stepwise stimulation at frequencies of 1, 3, and 10 Hz given at 3-min intervals during 9 min, reaching a maximum output of 4.6 +/- 0.9 (NPY-li), 240.2 +/- 50.2 (NE), and 1412.5 +/- 309.7 ng/min (E) at a frequency of 10 Hz. Burst electrical stimulation at 40 Hz for 1 s at 10-s intervals for a period of 10 min produced similar increases (p less than 0.05) in the release of NPY-li (4.8 +/- 1.0 ng/min, n = 8), NE (283.5 +/- 144.3 ng/min, n = 8), and E (1133.5 +/- 430.6 ng/min, n = 8). Adrenal NPY-li output was significantly correlated with adrenal NE output (r = 0.606; n = 24; p less than 0.05) and adrenal E output (r = 0.640; n = 24; p less than 0.05) in dogs receiving the burst stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1989

Plasma catecholamine and glucose concentrations during hemorrhagic hypotension in anesthetized dogs.

Hemorrhage-induced hepatic glycogenolytic responses were compared in pentobarbital-anesthetized dogs with a temporary functional adrenalectomy (ADRX) and in dogs with an acute hepatic denervation (HNX). Plasma concentrations of catecholamines [CAs; epinephrine (E), norepinephrine (NE), and dopamine (DA)] were determined in aortic (AO), hepatic venous (HV), portal venous (PV), and adrenal venous (ADV) blood collected simultaneously before, during, and after hemorrhage (H). Plasma glucose (GL) concentrations were measured in AO and HV blood. AO blood was bled (5.3 +/- 0.5 ml.kg-1.min-1, n = 42) until AO systolic pressure dropped to half (72.9 +/- 4.7 mmHg) of its control value (148.0 +/- 4.4 mmHg), and the hypotension was maintained for 5 min. In control dogs (CTL; n = 12), H markedly increased ADV CAs with a predominant increase in E over NE and DA. AO CAs increased similarly. By contrast, however, changes in HV CAs were characterized by a significant increase in NE that was more pronounced than the increases in E and DA. The increases in NE were associated with significant increases in both HV GL and AO GL. In dogs with ADRX (n = 10), AO CAs remained unchanged during H, but both HV NE and HV GL rose concomitantly to an extent similar to that observed in CTL dogs. In dogs with HNX (n = 10), HV NE remained unchanged during H, but HV GL increased to an extent similar to that observed in dogs with ADRX, along with significant increases in AO CAs. In dogs with HNX combined with ADRX (n = 10), HV NE and AO CAs did not change at all during H, resulting in a marked attenuation (50%, P less than 0.05) of the increasing response of HV GL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗