To determine values of F-wave parameters for the tibial nerve in clinically normal Miniature Dachshunds and those with thoracolumbar intervertebral disk herniation (IVDH).
53 Miniature Dachshunds (10 clinically normal and 43 with various clinical grades of thoracolumbar IVDH).
F-waves were elicited in the interosseous muscles of 1 hind limb in each dog by stimulation of the tibial nerve. F-wave parameters were measured for 32 stimuli/dog, and mean values were calculated. Linear regression was performed to assess correlations between F-wave parameters and clinical severity of IVDH.
For clinically normal dogs, mean ± SD values of shortest F-wave latency, mean F-wave conduction velocity, mean F-wave duration, and ratio of the mean F-wave amplitude to M response amplitude were 8.6 ± 0.6 milliseconds, 83.7 ± 6.1 m/s, 6.6 ± 1.5 milliseconds, and 9.8 ± 8.5%, respectively. F-wave persistence was 100%. Mean F-wave duration was positively correlated with clinical grade of IVDH. Linear regression yielded the following regression equation: F-wave duration (milliseconds) = 6.0 + 2.7 × IVDH grade. One dog with grade 2 IVDH had a mean F-wave duration shorter than that of all 5 dogs with grade 1 IVDH; 1 dog with grade 3 IVDH had a longer duration than that of all 10 dogs with grade 4 IVDH.
CONCLUSIONS AND CLINICAL RELEVANCE
Mean F-wave duration was correlated with the severity of inhibitory motor tract dysfunction in the spinal cord of dogs. F-wave examination may be useful for objective functional evaluation of upper motor neurons in the spinal cord.
Objective—To investigate whether the tissue and plasma renin-angiotensin-aldosterone system (RAAS) is activated in dogs with mild regurgitation through the mitral valve and determine the contribution of chymase and angiotensin-converting enzyme (ACE) to the activation of the RAAS and potential production of angiotensin II during the chronic stage of mild mitral valve regurgitation.
Animals—5 Beagles with experimentally induced mild mitral valve regurgitation and 6 clinically normal (control) Beagles.
Procedures—Tissue ACE and chymase-like activities and plasma RAAS were measured and the RAAS evaluated approximately 1,000 days after experimental induction of mitral valve regurgitation in the 5 dogs.
Results—Dogs with experimentally induced mitral valve regurgitation did not have clinical signs of the condition, although echocardiography revealed substantial eccentric hyper- trophy. On the basis of these findings, dogs with mitral valve regurgitation were classified as International Small Animal Cardiac Health Council class Ib. Plasma activity of renin and plasma concentrations of angiotensin I, angiotensin II, and aldosterone were not significantly different between dogs with mitral valve regurgitation and clinically normal dogs. Tissue ACE activity was significantly increased and chymase-like activity significantly decreased in dogs with mitral valve regurgitation, compared with values in clinically normal dogs.
Conclusions and Clinical Relevance—The tissue RAAS was modulated without changes in the plasma RAAS in dogs with mild mitral valve regurgitation during the chronic stage of the condition. An ACE-dependent pathway may be a major route for production of angiotensin II during this stage of the condition.
Objective—To establish a method of F-wave examinations
and to determine values of F-wave conduction
velocity (FWCV) and F-wave latency for the tibial
nerve of clinically normal dogs.
Animals—21 clinically normal dogs.
Procedure—The F-waves were elicited from the
interosseous muscles via stimulation of the tibial
nerve. The FWCV was determined by using the F-wave
shortest value and the surface distance corresponding
to the tibial nerve length. Correlation
between the smallest latency value of the F-wave and
the length of the tibial nerve and between the FWCV
and rectal temperature were closely examined.
Results—F-wave latency was proportional to the
length of the tibial nerve (correlation coefficient,
0.929). Mean ± SD FWCV was 77.98 ± 8.62 m/s.
Regression equation was as follows: F-wave latency =
2.799 + (0.029 X length of the tibial nerve). The FWCV
was increased when the measured rectal temperature
was high. Correlation coefficient between FWCV
and rectal temperature was 0.665.
Conclusion and Clinical Relevance—In the study
reported here, we established a reliable method for
clinical evaluation of the F-wave. When assessing
nerve conduction velocity, it is essential to measure
nerve length along the pathway that the nerve
impulse travels. This method of F-wave examination is
a useful diagnostic tool for the evaluation of suspected
dysfunction of the peripheral nervous system.
(Am J Vet Res 2002;63:1262–1264)
Objective—To establish a method of F-wave evaluation and to determine normative values of F-wave parameters, including F-wave conduction velocity, persistence, and amplitude for the tibial nerve in cats.
Animals—30 clinically normal cats.
Procedures—F-waves elicited in the interosseous muscles by stimulation of the tibial nerve were recorded, and linear regression analyses of the shortest latency versus the length of the tibial nerve and the limb length were performed. F-wave persistence was calculated by dividing the number of recorded F-waves by the number of stimuli.
Results—The correlation coefficient between F-wave latency and nerve length was 0.92, and that between F-wave latency and limb length was 0.58. Mean ± SD F-wave conduction velocity of the tibial nerve was calculated to be 97.1 ± 5.0 m/s. Linear regression analysis yielded the regression equation as follows: F-wave latency (milliseconds) = 2.60 + (0.02 × nerve length [mm]). Mean F-wave persistence and amplitude were 98.7 ± 2.3% and 1.01 ± 0.62 mV, respectively.
Conclusions and Clinical Relevance—Results indicated that nerve length should be used for nerve conduction studies of F-waves in felids. The regression equation for F-wave latency, conduction velocity, persistence, and amplitude may contribute to the diagnosis of nervous system diseases or injury in cats, such as trauma to the spinal cord or diabetic neuropathy.
Objective—To compare the effects of candesartan cilexetil and enalapril maleate on right ventricular myocardial remodeling in dogs with experimentally induced pulmonary stenosis.
Procedures—18 dogs underwent pulmonary arterial banding (PAB) to induce right ventricular pressure overload, and 6 healthy dogs underwent sham operations (thoracotomy only [sham-operated group]). Dogs that underwent PAB were allocated to receive 1 of 3 treatments (6 dogs/group): candesartan (1 mg/kg, PO, q 24 h [PABC group]), enalapril (0.5 mg/kg, PO, q 24 h [PABE group]), or no treatment (PABNT group). Administration of treatments was commenced the day prior to surgery; control dogs received no cardiac medications. Sixty days after surgery, right ventricular wall thickness was assessed echocardiographi-cally and plasma renin activity, angiotensin-converting enzyme activity, and angiotensin I and II concentrations were assessed; all dogs were euthanatized, and collagenous fiber area, cardiomyocyte diameter, and tissue angiotensin-converting enzyme and chymase-like activities in the right ventricle were evaluated.
Results—After 60 days of treatment, right ventricular wall thickness, cardiomyocyte diameter, and collagenous fiber area in the PABNT and PABE groups were significantly increased, compared with values in the PABC and sham-operated groups. Chymase-like activity was markedly greater in the PABE group than in other groups.
Conclusions and Clinical Relevance—Results indicated that treatment with candesartan but not enalapril effectively prevented myocardial remodeling in dogs with experimentally induced subacute right ventricular pressure overload.
Objective—To determine dose dependency of tranexamic acid–induced emesis and the time course of the antifibrinolytic potency of tranexamic acid in dogs.
Procedures—In a dose-escalating experiment, ascending doses of tranexamic acid (10, 20, and 30 mg/kg, IV) were administered at 5-minute intervals until vomiting was observed. In a separate single-dose experiment, ascending doses of tranexamic acid (20, 30, 40, and 50 mg/kg, IV) were administered at 1-week intervals until vomiting was observed. Time to onset of vomiting and number of vomiting episodes were measured in both experiments. In a coagulation experiment, a single 50 mg/kg bolus of tranexamic acid was administered, and blood was obtained 1 hour before and 20 minutes, 3 hours, and 24 hours after administration. Antifibrinolytic potency of tranexamic acid was evaluated by use of a modified rotational thromboelastography method.
Results—Tranexamic acid induced vomiting in a dose-dependent manner. Vomiting frequency was < 2 episodes, and vomiting concluded < 250 seconds after administration. Antifibrinolytic potency of tranexamic acid was significantly higher at 20 minutes following administration, but not different by 24 hours, when compared with the potency measured before administration. No adverse effects were observed in any experiment.
Conclusions and Clinical Relevance—IV administration of tranexamic acid induced emesis in a dose-dependent manner. The antifibrinolytic potency of tranexamic acid decreased in a time-dependent manner and was resolved < 24 hours after administration. Further studies are warranted to investigate the emetic and other adverse effects of tranexamic acid in dogs of various breeds and ages.