Search Results

You are looking at 1 - 10 of 18 items for

  • Author or Editor: Robert L. Hamlin x
  • Refine by Access: All Content x
Clear All Modify Search

Summary

Eighteen rats were anesthetized with xylazine/ketamine and placed in right lateral recumbency, and a small incision was made in the skin of the left hemithorax. A 21-gauge, 1-inch, short-beveled hypodermic needle, attached directly to a pressure transducer filled with degassed saline solution, was advanced through the incision into the left ventricle and then advanced through the septum into the right ventricle. High-fidelity tracings of right and left ventricular pressures and their derivatives were obtained through this approach in 13 rats. In 5 rats, measurements of right ventricular pressures were obtained by additional right ventricular puncture through the incision in the left hemithorax. Right and left ventricular pressures were recorded on single occasions in 18 rats, twice at 2-week intervals in 6 rats, and 3 times at 2-week intervals in 3 rats. Minimal hemopericardium was observed, but most rats had evidence of hemorrhage on the visceral pericardium. Left and right ventricular pressures can be measured rapidly, safely, and repeatedly in anesthetized rats by this method.

Free access
in American Journal of Veterinary Research

Summary

The QT interval is the period from onset of the QRS complex to the end of the T wave. The QT interval is useful for monitoring drug (eg, quinidine) and electrolyte (eg, calcium) effects on the heart. It depends principally on heart rate (hr), and the relationship between QT interval and hr has been expressed for human beings and for dogs. The purpose of the study reported here was to quantify that relationship for dogs and to assess whether body weight also influenced QT interval. The ecg was recorded from 17 dogs, ranging in weight between 7 and 25 kg. Dogs were anesthetized with fentanyl/droperidol/ketamine, and hr was accelerated by administration of graded doses of atropine. A significant relationship was not found between QT interval and body weight. Despite changes in hr during sinus arrhythmia, a significant relationship was not found between QT and RR intervals. The QT interval vs hr accelerated by atropine was analyzed for all dogs and for small (7 to 10 kg, n = 5), medium (10 to 20 kg, n = 7), and large dogs (20 to 25 kg, n = 5). Equations relating QT interval to mean hr were calculated for each group. Our data may serve as a baseline with which to compare QT intervals from dogs with heart disease and/or electrolyte imbalance.

Free access
in American Journal of Veterinary Research

Summary

Although it is known that the QT interval is dependent on the preceding RR interval, QT interval does not vary during respiratory sinus arrhythmia, despite a wide variation in heart rate. To assess the rate of change of the QT interval following an abrupt increase or decrease in heart rate, QT intervals were measured from ecg of healthy, anesthetized, thoracotomized dogs in which a junctional rhythm had been induced by destroying the sinoatrial node. Atria were paced at 800- or 600 -millisecond cycle durations until a steady state was reached, and then the cycle duration was changed suddenly to a new cycle duration (600 or 800 milliseconds, respectively). The time and number of heart beats required until the QT interval achieved a value of 63% (1 time constant) of the new steady state were calculated. Time constants for change in QT interval vs the number of beats following the change were 2.8 (sd = 1.3 s) seconds when heart rate was accelerated and 4.7 (sd = 2.1 s) seconds when heart rate was slowed. Differences were not statistically significant. The time constants for change in QT interval duration vs duration after the sudden change in heart rate were 1.7 (sd = 0.8 s) seconds when heart rate was accelerated and 3.7 (sd = 1.7 s) seconds when heart rate was slowed. These time constants differed significantly (P < 0.01). Response of QT interval, therefore, depended on the number of heart beats following sudden change in heart rate, but not time, except as time determined the number of heart beats. The QT interval did not change until 3 to 5 beats after the heart rate was suddenly changed. This number of beats would be more than that which would occur in 1 respiratory cycle in dogs; therefore, QT interval memory would prohibit changes in QT intervals that occur during respiratory sinus arrhythmia.

Free access
in American Journal of Veterinary Research

SUMMARY

A study was designed to determine whether phenytoin (phe) prevents the myocardial necrosis and subsequent fibrosis produced by isoproterenol (iso). Seven groups of female rats of the Wistar strain were used. Rats in groups 1 and 5 served as controls, Rats in group 3 were injected sc with 85 mg of iso/kg of body weight for 2 consecutive days. Rats in groups 2 and 6 received 100 mg of phe/kg orally. Rats in groups 4 and 7 received both PHE and iso. There were 6 to 9 rats/group. Effects of iso and phe were evaluated gravimetrically, histologically, and electrocardiographically. Heart weight/body weight ratios for each group receiving iso, with or without phe, were greater than for groups not receiving iso (P < 0.05). Light microscopic examination of heart sections of rats given iso alone or iso + phe revealed multiple and diffuse areas of fibrosis. Fibrosis in hearts from rats receiving phe + iso was less severe than that in hearts from rats receiving iso alone, but the difference was not statistically significant. Electrocardiographic changes of statistical significance were not observed in rats receiving any compound (alone or in combination), when compared with the control groups of equal age.

Free access
in American Journal of Veterinary Research

Summary

The purpose of this study was to evaluate changes in the ecg in a strain of rats, SHHF/Mcc-cp that developed cardiomyopathy and congestive heart failure naturally. Lead-I, -aVF, and -V5 ecg were obtained from male rats at approximately 6, 10, and 19 months of age, corresponding to early, mild, and severe heart failure, respectively. Electrocardiograms also were obtained from male Wistar-Furth rats matched for age with SHHF/Mcc-cp rats. Heart rate, amplitude and duration of component deflections, degree of notching of P waves and QRS complexes, and orientation of means QRS vectors in the frontral plane were analyzed from the ecg. Durations of P waves, PQ intervals, QRS complexes, and QT intervals were prolonged and amplitude of R waves in lead aVF was decreased only in SHHF/Mcc-cp rats at the 19-month recording. Increased notching in QRS complexes, but not in P waves, was observed more frequently at all ages, in SHHF/Mcc-cp rats than in Wistar rats, and notching was greatest at 19 months. Arrhythmias were not observed in Wistar rats, but infrequent supraventricular premature depolarizations were observed in 2 of 10 SHHF/Mcc-cp rats at 19 months. In leads aVF and V5, T waves increased in amplitude as Wistar rats aged; however, in SHHF/Mcc-cp rats, T-wave amplitude peaked in all leads at 10 months, but returned to the 6-month value at month 19. We conclude that cardiomyopathy, heart failure, or both, resulted in changes in the ecg, but that these changes could be used to detect heart failure only when rats reached 19 months of age and were severely affected.

Free access
in American Journal of Veterinary Research

Summary

Blood viscosity (bv) was measured in 32 healthy horses at 6 spindle speeds (60, 30, 12, 6, 3, and 1.5 rpm) and for pcv of 40%, using a digital rotational cone and plate microviscometer. Also, in 7 of 32 horses, bv was measured 3 times each, for 3 pcv values (20, 40, and 60%), and at each spindle speed to determine effect of pcv on bv and machine and among-horse variations. Total plasma protein and fibrinogen concentrations were measured in all horses, using a standard refractometer and heat precipitation, respectively. In 7 of 32 horses, quantitative fibrinogen concentration was measured, using a quantitative fibrinogen assay. Plasma protein and fibrinogen concentrations were measured to determine their effect on bv.

Plasma total protein (6.0 to 7.5 g/dl) and fibrinogen (100 to 400 mg/dl) concentrations were within normal reference range for our laboratory. In this study of healthy horses, mean (± sd) bv values obtained for each pcv value and at each spindle speed were: for pcv of 20%, 2.39 ± 0.33 centipoise (cp) at 60 rpm, 2.52 ± 0.35 cp at 30 rpm, 2.80 ± 0.37 cp at 12 rpm, 2.96 ± 0.48 cp at 6 rpm, 3.04 ± 0.62 cp at 3 rpm, and 2.93 ± 0.96 cp at 1.5 rpm; for pcv of 40%, 3.98 ± 0.29 cp at 60 rpm, 4.40 ± 0.38 cp at 30 rpm, 5.26 ± 0.59 cp at 12 rpm, 6.36 ± 0.93 cp at 6 rpm, 7.34 ± 1.46 cp at 3 rpm, and 8.33 ± 2.61 cp at 1.5 rpm; and for pcv of 60%, 7.21 ± 0.91 cp at 60 rpm, 8.27 ± 1.05 cp at 30 rpm, 10.46 ± 1.38 cp at 12 rpm, 13.69 ± 1.82 cp at 6 rpm, 18.12 ± 2.81 cp at 3 rpm, and 23.44 ± 3.45 cp at 1.5 rpm.

Blood viscosity increased with decreasing rpm and shear rate. Blood viscosity also increased with increasing pcv at each spindle speed. The bv for healthy horses at pcv of 40% was fitted to an asymptotic model. The estimated coefficients were:
BV ( PCV=40% ) =4 .346+4 .877e -0 .116 .rpm

Significant (P < 0.05) correlation between total plasma protein concentration and bv was found for pcv of 40% at all spindle speeds. Furthermore, significant (P < 0.05) correlation between quantitative plasma fibrinogen concentration and bv was found for pcv of 60% at the lower spindle speeds (6, 3, and 1.5 rpm).

The sd of measurement error and the among-horse sd for the digital rotational cone and plate microviscometer were greatest at the low spindle speeds for all pcv. The least variation was found for pcv of 20%.

The digital rotational cone and plate microviscometer is an accurate instrument for measuring bv at multiple pcv and spindle speeds in horses. Packed cell volume, plasma protein concentration, and fibrinogen concentration appear to affect bv in horses. Blood viscosity values obtained in this study will give insights into factors affecting bv in horses and will serve as a baseline for comparison with values in diseased horses.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine acute cardiovascular effects and pharmacokinetics of carvedilol in healthy dogs.

Animals—14 mature healthy Beagles.

Procedure—12 dogs were anesthetized with morphine and α-chloralose. Catheters were placed in the aorta, left ventricle, and right atrium to record systemic and pulmonary pressures and determine vascular resistance and cardiac output. Electrocardiograms (leads I, aVF, and V3) were recorded to determine electrocardiographic changes. Variables were measured before and after IV injection of incremental doses of carvedilol (cumulative doses, 10, 30, 70, 150, 310, and 630 μg/kg of body weight; n = 6) or vehicle alone (6). Pharmacokinetic analysis was performed, using 2 conscious dogs given 160 mg of carvedilol/kg as a single IV injection.

Results—Heart rate and velocity of fiber shortening at zero load (Vmax) increased slightly but significantly from baseline values at doses of carvedilol ≥ 310 μg/kg and 10 μg/kg, respectively. Carvedilol did not affect systemic and pulmonary pressures or vascular resistances. Intravenous administration of approximately 150 μg of carvedilol/kg resulted in a plasma carvedilol concentration of approximately 100 ng/ml. Mean elimination halflife was 54 minutes, half-life of distribution was 3.5 minutes, and volume of distribution was 2,038 ml/kg.

Conclusions and Clinical Relevance—The therapeutic plasma concentration of carvedilol in humans is 100 ng/ml. At that plasma concentration in dogs, the reduction in afterload and positive inotropic effect that we observed would be beneficial for treating heart failure and minimizing the cardiotoxic effects of doxorubicin. (Am J Vet Res 2000;61:57–60)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether QT interval is prolonged or sudden death is caused by ventricular fibrillation resulting from torsades de pointes and to identify hemodynamic effects of ontazolast.

Animals—28 Beagles.

Procedure—Physiologic variables were measured for 2 hours in conscious dogs given ontazolast (0, 1, or 3 mg/kg of body weight, IV) and for 1 hour in anesthetized dogs given cumulative doses of ontazolast (0, 1, 3, 6, or 8 mg/kg, IV).

Results—Ontazolast prolonged QT interval and QT interval corrected for heart rate (QTc) at doses of 6 mg/kg in anesthetized dogs. At 8 mg/kg, both variables remained prolonged but tended to decrease. In conscious dogs, ontazolast increased QT interval and QTc 15 minutes after administration, but both variables returned to reference ranges by 60 minutes. In conscious dogs, ontazolast increased maximum rate of increase of left ventricular pressure and maximal velocity of fiber shortening, indicators of inotropy, and increased tau, indicating a decreased rate of relaxation. One conscious dog receiving 3 mg/kg developed nonfatal torsades de pointes, but another conscious dog developed ventricular fibrillation. Two anesthetized dogs receiving 6 mg/kg developed early afterdepolarizations, and all dogs developed secondary components in their T waves.

Conclusion and Clinical Relevance—Ontazolast possesses potent class-III antiarrhythmic properties and induces prolongation of QTc in a dose-dependent fashion. Because there was a clear dosedependent prolongation of QT interval in all instances, ontazolast may serve as a positive-control compound for studying other compounds that are believed to prolong the QT interval. (Am J Vet Res 2000;61:1364–1368)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the use of 24-hour ambulatory electrocardiography (AECG) for the detection of ventricular premature complexes (VPC) in healthy dogs.

Design—Case series.

Animals—50 healthy mature dogs.

Procedure—A 24-hour AECG was performed on each dog and evaluated for the presence of VPC.

Results—Fifty dogs weighing between 18.2 to 40.9 kg (40 and 90 lb) representing 13 breeds were evaluated; there were 4 sexually intact females, 21 spayed females, 4 sexually intact males, and 21 castrated males. Ages ranged from 1 to 12 years. Thirty-four dogs had no VPC; 16 dogs had between 1 and 24 VPC. The grade of arrhythmia ranged from 1 to 4, with 4 dogs having an arrhythmia with a grade > 1. Significant differences were not detected between the group of dogs with VPC and those without VPC with regard to sex, age, and minimum, maximum, or mean heart rate.

Conclusions and Clinical Relevance—We conclude that healthy mature dogs have infrequent VPC, as detected by use of 24-hour AECG. The presence of numerous or sequential VPC may be suggestive of cardiac or systemic disease and may indicate the need for thorough clinical evaluation. (J Am Vet Med Assoc 2001;218:1291–1292)

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate the use of in-hospital electrocardiography (ECG) for detection of ventricular premature complexes (VPC), compared with 24-hour ambulatory ECG.

Design—Original study.

Animals—188 Boxers > 9 months old; 31 had a history of syncope, and 157 were healthy (no history of syncope).

Procedure—In-hospital ECG was performed on all Boxers for at least 2 minutes. Within 7 days after the in-hospital ECG was completed, 24-hour ambulatory ECG was performed.

Results—The specificity of in-hospital ECG was 100% for the detection of at least 50 VPC in a 24-hour period in dogs with syncope and 93% in healthy dogs. In-hospital ECG had poor sensitivity, although sensitivity increased as the number of VPC per 24 hours increased.

Conclusions and Clinical Relevance—Use of in-hospital ECG is highly specific for detection of at least 50 VPC during a 24-hour period. However, in-hospital ECG is insensitive, and a lack of VPC does not suggest that the dog does not have a substantial number of VPC during that same period. The use of in-hospital ECG appears to be inadequate for screening purposes and therapeutic evaluations in mature Boxers with ventricular arrhythmic disease. (J Am Vet Med Assoc 2001;218:222–224)

Full access
in Journal of the American Veterinary Medical Association