Objective—To validate the use of a human enzyme immunoassay (EIA) kit for measurement of plasma antidiuretic hormone (ADH) concentration in dogs and evaluate plasma ADH concentrations in dogs with congestive heart failure (CHF) attributable to acquired cardiac disease, compared with findings in healthy dogs.
Animals—6 healthy dogs and 12 dogs with CHF as a result of chronic degenerative valve disease or dilated cardiomyopathy.
Procedures—Plasma samples from the 6 healthy dogs were pooled and used to validate the EIA kit for measurement of plasma ADH concentration in dogs by assessing intra-assay precision, dilutional linearity, and spiking recovery. Following validation, plasma ADH concentrations were measured in the 6 healthy dogs and in the 12 dogs with CHF for comparison.
Results—The EIA kit measured ADH concentrations in canine plasma samples with acceptable intra-assay precision, dilutional linearity, and spiking recovery. The intra-assay coefficient of variation was 11%. By use of this assay, the median plasma concentration of ADH in dogs with CHF was 6.15 pg/mL (SD, 3.2 pg/mL; range, 4.18 to 15.47 pg/mL), which was significantly higher than the median concentration in healthy dogs (3.67 pg/mL [SD, 0.93 pg/mL; range, 3.49 to 5.45 pg/mL]).
Conclusions and Clinical Relevance—Plasma ADH concentrations in dogs can be measured with the tested EIA kit. Plasma ADH concentrations were higher in dogs with CHF induced by acquired cardiac disease than in healthy dogs. This observation provides a basis for future studies evaluating circulating ADH concentrations in dogs with developing heart failure.
Objective—To evaluate the use of measuring plasma concentrations of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and cardiac troponin-I (cTnI) to detect dogs with occult dilated cardiomyopathy (DCM).
Animals—118 client-owned dogs.
Procedures—Dogs were prospectively examined by use of ECG; echocardiography; and evaluation of concentrations of ANP, BNP, and cTnI. Occult DCM was diagnosed by evaluation of echocardiographic left ventricular dimensions and detection of ventricular arrhythmias on ECG. Sensitivity and specificity of assays for measurement of plasma concentrations of ANP, BNP, and cTnI to detect dogs with occult DCM were determined.
Results—Occult DCM was diagnosed in 21 dogs. A concentration of > 6.21 pg/mL for BNP had a sensitivity of 95.2% and specificity of 61.9% for identifying dogs with occult DCM. In contrast, concentrations of ANP and cTnI had relatively low predictive values.
Conclusions and Clinical Relevance—Blood-based screening for occult DCM in dogs can be accomplished by use of a BNP assay. Additional studies should be performed to optimize this method of screening dogs to detect occult DCM.
OBJECTIVE To compare left ventricle (LV) volume and function variables obtained by use of 1-D, 2-D, and real-time 3-D echocardiography versus ECG-gated multidetector row CT (MDCT) angiography, which was considered the criterion-referenced standard.
ANIMALS 6 healthy, purpose-bred dogs.
PROCEDURES Dogs were anesthetized and administered a constant rate infusion of esmolol, and 1-D, 2-D, and 3-D echocardiography and ECG-gated, contrast-enhanced MDCT were performed. End-diastolic volume (EDV), end-systolic volume (ESV), stroke volume, and ejection fraction (EF) were calculated by use of the Teichholz method for 1-D echocardiography, single-plane and biplane modified Simpson method of disks (MOD) and area-length method for 2-D echocardiography, and real-time biplane echocardiography (RTBPE) and real-time 3-D echocardiography (RT3DE) for 3-D echocardiography. Volumes were indexed to body surface area and body weight. Median values, correlations, and limits of agreement were compared between echocardiographic modalities and MDCT.
RESULTS EDV and ESV measured by use of RTBPE and RT3DE had the strongest correlations with results for MDCT. Values obtained for EDV, ESV, stroke volume, and EF did not differ significantly between echocardiographic methods and MDCT. Use of RT3DE and RTBPE slightly underestimated EDV, ESV, and EF, compared with values for MDCT, as determined with Bland-Altman analysis.
CONCLUSIONS AND CLINICAL RELEVANCE Values for EDV and ESV obtained by use of 3-D echocardiography, including RTBPE and RT3DE, had the highest correlation with slight underestimation, compared with values obtained by use of MDCT. This was similar to results for 3-D echocardiography in human medicine.
Objective—To determine the nucleotide and amino
acid sequence of atrial natriuretic peptide (ANP) in
cats and its typical regions of cardiac expression.
Animals—5 healthy adult mixed-breed cats.
Procedure—Total RNA was extracted from samples
obtained from the left and right atrium, left and right
ventricle, and interventricular septum of each cat. The
RNA was used to produce cDNA for sequencing and
northern blot analysis. Genomic DNA was extracted
from feline blood samples. Polymerase chain reaction
primers designed from consensus sequences of
other species were used to clone and sequence the
feline ANP gene.
Results—The feline ANP gene consists of 1,072
nucleotides. It consists of 3 exons (123, 327, and 12
nucleotides) separated by 2 introns (101 and 509
nucleotides). It has several typical features of eukaryotic
genes and a putative steroid-response element
located within the second intron. Preprohormone
ANP consists of 153 amino acids. The amino acid
sequence of the active form of feline ANP (ANP-30) is
identical to that of equine, bovine, and ovine ANP-30
and differs from that of human, canine, and porcine
ANP-28 only by 2 carboxy-terminal arginine residues.
The ANP mRNA was detected only in the left and
Conclusions and Clinical Relevance—The genetic
and protein structure and principal regions of cardiac
expression of feline ANP are similar to those of other
species. Results of this study should be helpful in
future studies on the natriuretic response in cats to
diseases that affect cardiovascular function.
(Am J Vet Res 2002;63:236–240)
Objective—To evaluate the cardiovascular effects of
the α2-adrenergic receptor agonist medetomidine
hydrochloride in clinically normal cats.
Animals—7 clinically normal cats.
Procedure—Cats were anesthetized with isoflurane,
and thermodilution catheters were placed for measurement
of central venous, pulmonary, and pulmonary
capillary wedge pressures and for determination
of cardiac output. The dorsal pedal artery was
catheterized for measurement of arterial blood pressures
and blood gas tensions. Baseline variables were
recorded, and medetomidine (20 µg/kg of body
weight, IM) was administered. Hemodynamic measurements
were repeated 15 and 30 minutes after
Results—Heart rate, cardiac index, stroke index, ratepressure
product, and right and left ventricular stroke
work index significantly decreased from baseline after
medetomidine administration, whereas systemic vascular
resistance and central venous pressure
increased. However, systolic, mean, and diastolic
arterial pressures as well as arterial pH, and oxygen
and carbon dioxide tensions were not significantly different
from baseline values.
Conclusions and Clinical Relevance—When administered
alone to clinically normal cats, medetomidine (20
µg/kg, IM) induced a significant decrease in cardiac
output, stroke volume, and heart rate. Arterial blood
pressures did not increase, which may reflect a predominant
central α2-adrenergic effect over peripheral
vascular effects. (Am J Vet Res 2001;62:1745–1762)
OBJECTIVE To compare effects of tiletamine-zolazepam, alfaxalone, ketamine-diazepam, and propofol for anesthetic induction on cardiorespiratory and acid-base variables before and during isoflurane-maintained anesthesia in healthy dogs.
ANIMALS 6 dogs.
PROCEDURES Dogs were anesthetized with sevoflurane and instrumented. After dogs recovered from anesthesia, baseline values for cardiorespiratory variables and cardiac output were determined, and arterial and mixed-venous blood samples were obtained. Tiletamine-zolazepam (5 mg/kg), alfaxalone (4 mg/kg), propofol (6 mg/kg), or ketamine-diazepam (7 and 0.3 mg/kg) was administered IV in 25% increments to enable intubation. After induction (M0) and at 10, 20, 40, and 60 minutes of a light anesthetic plane maintained with isoflurane, measurements and sample collections were repeated. Cardiorespiratory and acid-base variables were compared with a repeated-measures ANOVA and post hoc t test and between time points with a pairwise Tukey test.
RESULTS Mean ± SD intubation doses were 3.8 ± 0.8 mg/kg for tiletamine-zolazepam, 2.8 ± 0.3 mg/kg for alfaxalone, 6.1 ± 0.9 mg/kg and 0.26 ± 0.04 mg/kg for ketamine-diazepam, and 5.4 ± 1.1 mg/kg for propofol. Anesthetic depth was similar among regimens. At M0, heart rate increased by 94.9%, 74.7%, and 54.3% for tiletamine-zolazepam, ketamine-diazepam, and alfaxalone, respectively. Tiletamine-zolazepam caused higher oxygen delivery than propofol. Postinduction apnea occurred in 3 dogs when receiving alfaxalone. Acid-base variables remained within reference limits.
CONCLUSIONS AND CLINICAL RELEVANCE In healthy dogs in which a light plane of anesthesia was maintained with isoflurane, cardiovascular and metabolic effects after induction with tiletamine-zolazepam were comparable to those after induction with alfaxalone and ketamine-diazepam.
Objective—To map canine mitochondrial proteins and identify qualitative and quantitative differences in heart mitochondrial protein expression between healthy dogs and dogs with naturally occurring and induced dilated cardiomyopathy (DCM).
Sample Population—Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with induced DCM.
Procedures—Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by ≥ 2-fold between groups were analyzed by matrixassisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry.
Results—Within narrow pH gradients of control canine heart mitochondrial samples, a total of 1,528 protein spots were revealed. Forty subunits of heart mitochondrial proteins that differ significantly from control tissues were altered in tissue specimens from dogs with naturally occurring and induced forms of DCM. The most affected heart mitochondrial proteins in both groups were those of oxidative phosphorylation (55%). Upregulation of manganese superoxide dismutase was suggestive of heart oxidative injury in tissue specimens from dogs with both forms of DCM. Evidence of apoptosis was associated with overexpression of the heart mitochondrial voltage-dependent anion channel-2 protein and endonuclease G in tissue specimens from dogs with induced DCM.
Conclusions and Clinical Relevance—Alterations of heart mitochondrial proteins related to oxidative phosphorylation dysfunction were more prevalent in tissue specimens from dogs with induced or naturally occurring DCM, compared with those of control dogs.
Objective—To identify qualitative and quantitative differences in cardiac mitochondrial protein expression in complexes I to V between healthy dogs and dogs with natural or induced dilated cardiomyopathy (DCM).
Sample Population—Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with DCM induced by rapid right ventricular pacing.
Procedures—Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by 2-fold or greater between groups were analyzed by matrixassisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry.
Results—A total of 22 altered mitochondrial proteins were identified in complexes I to V. Ten and 12 were found in complex I and complexes II to V, respectively. Five were mitochondrial encoded, and 17 were nuclear encoded. Most altered mitochondrial proteins in tissue specimens from dogs with naturally occurring DCM were associated with complexes I and V, whereas in tissue specimens from dogs subjected to rapid ventricular pacing, complexes I and IV were more affected. In the experimentally induced form of DCM, only nuclear-encoded subunits were changed in complex I. In both disease groups, the 22-kd subunit was downregulated.
Conclusions and Clinical Relevance—Natural and induced forms of DCM resulted in altered mitochondrial protein expression in complexes I to V. However, subcellular differences between the experimental and naturally occurring forms of DCM may exist.