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Abstract

Objective

To study long-term effects of enalapril, an angiotensin-converting enzyme inhibitor, and hydralazine, an arteriodilator, on renin-angiotensin-aldosterone system and fluid balance before and after administration of furosemide.

Animals

22 dogs with clinical signs of congestive heart failure (CHF) attributable to mitral regurgitation.

Procedure

After initial examination, 12 dogs received enalapril and 10 received hydralazine. Dogs were re-examined 3 weeks and 6 months after initial examination. Furosemide was added after the 3-week examination, and at 6 months, dogs had received furosemide for at least 4 months.

Results

Angiotensin II and aldosterone plasma concentrations were low before treatment, and only aldosterone became significantly decreased after enalapril monotherapy. Concentrations of both hormones and heart rate increased in dogs receiving hydralazine monotherapy, and fluid retention was evident. After long-term treatment with either of the 2 drugs together with furosemide, angiotensin II and aldosterone values increased in both groups. Natriuresis and kaliuresis developed in all dogs, with greatest effect in those receiving enalapril and furosemide. These dogs had decreased plasma sodium concentration, whereas potassium concentration was equally decreased in both groups. After 6 months, the enalapril group, but not the hydralazine group, had increased cardiac size. All dogs had moderate reduction of weight and were azotemic, although changes were more pronounced in those of the hydralazine group.

Conclusion

The 2 drugs have different effects on the renin-angiotensin-aldosterone system and fluid balance in dogs with CHF. (Am J Vet Res 1996;57:1645–1652)

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

Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia.

All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) > 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 ± 4.5 SD for D and 24.3 ± 4.4 for C) to hypoxia (28.5 ± 4.7 for D and 28.4 ± 3.7 for C), and decreased during hyperoxia (16.9 ± 3.0 for D and 17.4 ± 3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 ± 11.7 mm of Hg for D and 69.4 ± 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease. Supplemental oxygen to dogs with pulmonary hypertension could reduce PPA and right ventricular afterload. This study supports the use of oxygen, but not antihistamine drugs, in the treatment of postadulticide heartworm disease in dogs that are hypoxic, with signs of congestive heart failure or dyspnea.

Free access
in American Journal of Veterinary Research

examination findings indicated progressive increases in heart and respiratory rates and a progressive decrease in blood pressure ( Table 1 ). Clinical signs of congestive heart failure such as weakness, apathy, cachexia, heart murmurs, pulmonary crackles, and

Full access
in American Journal of Veterinary Research

Congestive heart failure is a clinical syndrome caused by chronic heart disease and is characterized by sodium and water retention that results in edema. Loop diuretics (short- and long-acting agents) are commonly used in the management of CHF and

Full access
in American Journal of Veterinary Research

treatment to suppress the RAAS should accompany furosemide treatment, alone or in combination with pimobendan, in dogs. Abbreviations A:C Aldosterone-to-creatinine ratio ACE Angiotensin-converting enzyme CHF Congestive heart failure RAAS

Full access
in American Journal of Veterinary Research

congestive heart failure 21 and in cats following initiation of TPN 22 was predictive of worse outcomes for those animals. The purpose of the study reported here was to investigate the effect of IV administration of dextrose on coagulation in healthy dogs

Full access
in American Journal of Veterinary Research

flow in response to dobutamine infusion. Studies in compromised patients revealed an increase in renal blood flow in humans with congestive heart failure or low-output cardiac insufficiency 51,52 and increased urine output in dogs with experimentally

Full access
in American Journal of Veterinary Research

with HCM include congestive heart failure, supraventricular and ventricular tachyarrhythmias, and systemic hypotension. 10–15 Hypotension develops in healthy cats and cats with HCM anesthetized with inhalation anesthetic agents because of the negative

Full access
in American Journal of Veterinary Research