Gabaergic inhibition of the pituitary release of adrenocorticotropin and α-melanotropin is impaired in dogs with hepatic encephalopathy

Rothuizen, J.; Kok, Yung-Yean; Slob, Adri; Mol, Jan A.

doi:10.1016/0739-7240(95)00044-5

Cited by 7 publications

(3 citation statements)

References 43 publications

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“…Discordant with previous studies of CPSS dogs, we found no significant differences between preoperative baseline cortisol concentrations of healthy and CPSS dogs. Previous reports describe significantly increased baseline cortisol concentrations in CPSS dogs; hypercortisolemia subsequently resolved within 4 weeks after shunt attenuation 28–30 . Potential etiologies for hypercortisolemia in dogs with CPSS include decreased hepatic synthesis of cortisol binding proteins, abnormal counter‐regulatory response to hypoglycemia, reduced hepatic clearance of cortisol, peripheral resistance to cortisol, or stress associated with chronic nonadrenal illness 21,28–33 .…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports describe significantly increased baseline cortisol concentrations in CPSS dogs; hypercortisolemia subsequently resolved within 4 weeks after shunt attenuation. [28][29][30] Potential etiologies for hypercortisolemia in dogs with CPSS include decreased hepatic synthesis of cortisol binding proteins, abnormal counter-regulatory response to hypoglycemia, reduced hepatic clearance of cortisol, peripheral resistance to cortisol, or stress associated with chronic nonadrenal illness. 21,[28][29][30][31][32][33] In our study, no dog with preoperative hypoglycemia had increased cortisol concentrations; thus, postoperative hypoglycemia was unlikely to be the cause of baseline postoperative hypercortisolemia.…”

Section: Discussionmentioning

confidence: 99%

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Adrenal Response to Adrenocorticotropic Hormone in Dogs before and after Surgical Attenuation of a Single Congenital Portosystemic Shunt

Holford

Tobias

Bartges

et al. 2008

Veterinary Internal Medicne

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Background: Dogs with single congenital portosystemic shunts (CPSS) often develop postoperative hypoglycemia and prolonged anesthetic recovery. These abnormalities could be attributable to inadequate adrenal response. However, adequacy of adrenal response after CPSS surgery is unexplored.Hypothesis: Dogs with CPSS have inadequate postoperative adrenal response. Animals: Eight nonoperated, 8 ovariohysterectomy (OHE), and 16 CPSS dogs. Methods: Consecutive day ACTH stimulation tests were performed on nonoperated healthy dogs, healthy dogs before and after OHE, and CPSS dogs before and after surgery. Adequate response was defined as 450% or 430 ng/mL increase in cortisol after ACTH administration. Blood glucose (BG) was monitored before and after surgery. Prolonged anesthetic recovery and refractory hypoglycemia episodes were recorded.Results: Results of consecutive day ACTH stimulation tests did not vary in normal dogs. Results of preoperative ACTH stimulation tests of CPSS and OHE dogs were not significantly different. Dogs with CPSS had higher postoperative baseline cortisol concentrations (median, 329 ng/mL) than OHE dogs (median, 153 ng/mL). Postoperative cortisol increase after ACTH in CPSS was 50% in 10/16 and 30 ng/mL in 6/16. After surgery, BG was 60 mg/dL in 7/16 CPSS dogs. Cortisol concentrations were not correlated with BG. Two CPSS dogs had refractory hypoglycemia and 4 had delayed recovery; all improved with dexamethasone administration (0.1-0.2 mg/kg/IV).Conclusions and Clinical Importance: Contrary to previous reports, baseline cortisol concentrations in CPSS and healthy dogs are similar. Many CPSS dogs have postoperative hypercortisolemia. Response to ACTH does not correlate with postoperative hypoglycemia or prolonged anesthetic recovery.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Adrenal Response to Adrenocorticotropic Hormone in Dogs before and after Surgical Attenuation of a Single Congenital Portosystemic Shunt

Holford

Tobias

Bartges

et al. 2008

Veterinary Internal Medicne

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“…Deranged GABAergic neurotransmission, suggesting an increased GABAergic tone, has been documented in dogs with HE. 87 Further support for the role of an increased GABAergic tone in the pathogenesis of canine HE is provided by the apparent improvement in clinical signs noted following administration of benzodiazepinereceptor partial inverse agonists. In a study using dogs with HE due to Eck fistulae, there was a positive response to treatment with the benzodiazepine-receptor partial inverse agonist sarmazenil.…”

Section: Neurosteroidsmentioning

confidence: 99%

Hepatic encephalopathy in dogs and cats

Lidbury

Cook

Steiner

2016

J Vet Emergen Crit Care

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HE is a potentially life-threatening condition that is probably underdiagnosed in companion animals. Although various treatment recommendations have been proposed, there is a lack of evidence in the veterinary literature regarding optimal strategies for the management of this condition. As our understanding of the pathogenesis of HE in dogs and cats evolves, novel diagnostic tests and therapeutic agents may become available.

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The Brain in Sepsis

Philips¹,

Bennett²

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Gabaergic inhibition of the pituitary release of adrenocorticotropin and α-melanotropin is impaired in dogs with hepatic encephalopathy

Cited by 7 publications

References 43 publications

Adrenal Response to Adrenocorticotropic Hormone in Dogs before and after Surgical Attenuation of a Single Congenital Portosystemic Shunt

Adrenal Response to Adrenocorticotropic Hormone in Dogs before and after Surgical Attenuation of a Single Congenital Portosystemic Shunt

Hepatic encephalopathy in dogs and cats

The Brain in Sepsis

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