Blood glycated hemoglobin concentration reflects long-term serum glucose levels in dogs. In this study, the effects of several diseases on blood glycated hemoglobin levels have been evaluated. For this study, blood samples were drawn from 93 unhealthy dogs. The animals were distributed into 10 groups according to pathological process (group 1, digestive problems; group 2, leishmaniasis; group 3, anemia; group 4, dermatological disorders; group 5, urinary problems; group 6, cardiorespiratory problems; group 7, diabetes mellitus; group 8, insulinoma; group 9, general diseases; group 10, control group). Blood glucose and glycated hemoglobin concentrations and hemoglobin and hematocrit values were analyzed in all the animals. In diabetic dogs, a strong increase in blood glycated hemoglobin was observed when compared with the other groups (P < 0.01). In contrast, dogs with insulinoma showed a decrease in blood glycated hemoglobin, though significant differences were not reported in all cases. No change in blood glycated hemoglobin concentrations were reported in dogs affected by other diseases. So, we can suppose that only the chronic alterations in glucose metabolism (chronic hyper- or hypoglycemia) can induce significant changes on the blood glycated hemoglobin concentrations in dogs.

The commercial snake venom extract, Protac, is a specific activator of the anticoagulant zymogen, protein C (PC) in human plasma. This specific action has led to its use in developing coagulation-based and amidolytic-based assays for the diagnosis of quantitative and/or qualitative PC deficiency states in human beings. The purpose of the present study was to compare the effects of Protac on the activated partial thromboplastin times (APTT) of human, bovine, equine, and canine plasmas in order to determine the potential value of this venom extract as an activator in functional PC assays in these domestic animal species. As expected, Protac significantly prolonged the APTT of normal human plasma, but had no effect on plasma known to be devoid of PC. Clotting times were prolonged by 34%-214% with concentrations of venom activator ranging from 0.1-1.0 U/mL. Under identical conditions, Protac prolonged the APTT of equine plasma by 11%-98% over control times. Even more dramatic was the inhibitory effect of Protac on the clotting of bovine plasma, extending the APTT more than 3-fold at a venom concentration of 0.1 U/mL. At higher venom concentrations, most bovine plasmas remained unclotted after 300 s (control time 34.1 s). Under similar conditions, the canine APTT was unaffected by Protac, even when the venom concentration was increased to 3 U/mL. In order to determine the reason for the lack in response of canine plasma, the concentration of the APTT reagent was altered (decreased), exposure time of the plasma to the Protac was increased from 2 min to 9 min, and the plasma was diluted to assess for the potential existence of plasma PC inhibitors. Protac caused an unexpected shortening of the APTT when the contact activator reagent was diluted. Increasing the exposure time had no effect. Although a slight prolongation of the canine APTT was detected when the plasma was diluted, the presence of strong plasma PC inhibition was considered an unlikely cause of the lack of significant anticoagulant action. The failure of Protac to exert a strong inhibitory effect on the canine APTT, as well as to generate amidolytic activity, suggests that this venom extract does not stimulate the production of activated PC activity in canine plasma. This may result from molecular differences in the canine PC molecule that prevent the formation of the stoichiometric complex of venom extract, APTT reagent, and canine protein, a complex thought to be essential for the PC-activating function of Protac. Protac may be suitable as an activator of PC in bovine and equine plasmas; however, it appears ineffective in generating anticoagulant activity in canine plasma.

The tricyclic antidepressant, clomipramine, is an effective treatment for canine compulsive disorder (canine CD). This disorder is a clinical syndrome of abnormal conflict behaviors and its pathophysiology is unknown. However, because clomipramine is an effective treatment, information about the drug's neurochemical effect could enhance the understanding of canine CD. The following experiment used 6 behaviorally normal dogs to assess the effect of clomipramine (3 mg/kg, q24h, PO) on the central turnover of 3 monoamines (serotonin, dopamine, and norepinephrine) as measured by the concentrations of their respective metabolites in cerebrospinal fluid (CSF). In a randomized, placebo-controlled, AB-BA crossover experiment, cisternal CSF was taken after 1, 2, 4, and 6 wk on each treatment. No effect of clomipramine was detected. This contrasts with human studies that have suggested that clomipramine affects the concentrations of monoamine metabolites in lumbar CSF. However, those papers do not address methodological assumptions, such as (i) metabolites in CSF originate only from the brain, and (ii) concentrations of metabolites in cisternal/lumbar CSF reflect the concentrations in local areas of the brain. Notwithstanding the small sample size, our results suggest that more localized sampling techniques (e.g. microdialysis) are needed when examining the effect of drugs on central monoamine metabolites. Clomipramine's efficacy for canine CD indicates the need for neurobiological research and, to our knowledge, our study is the first of its kind in dogs. The resulting data are preliminary but they can inform optimal neurobiological studies of canine CD.