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Objective: To evaluate the agreement between cardiac output (CO) values obtained using a transpulmonary thermodilution technique (TPTDCO) and conventional thermodilution technique (TDCO) in anaesthetized dogs with fluid overload., Study Design: Prospective experimental study., Animals: Six healthy Beagle dogs aged 7-8 years., Methods: Dogs were anaesthetized with sevoflurane in oxygen, and catheters were inserted for TPTDCO and TDCO measurement. After instrumentation, baseline CO was measured using each technique at a central venous pressure (CVP) of 3-7 mmHg. Dogs were subsequently administered lactated Ringer's solution and 6% hydroxyethyl starch to induce fluid overload. CO measurements were obtained using each technique at CVP values of 8-12 mmHg, 13-17 mmHg, 18-22 mmHg and 23-27 mmHg. Agreements between CO measurements obtained with the respective techniques were analysed using Dunnett's test, Pearson's correlation coefficient and Bland-Altman analysis., Results: Thirty pairs of CO values were obtained, ranging from 1.45 L minute(-1) to 4.69 L minute(-1) for TPTDCO and from 1.30 L minute(-1) to 4.61 L minute(-1) for TDCO. TPTDCO and TDCO values correlated strongly (r(2)  = 0.915, p < 0.001). The bias and mean relative bias between TPTDCO and TDCO were 0.26 ± 0.30 L minute(-1) (limits of agreement - 0.29 to 0.81 L minute(-1) ) and 9.7%, respectively., Conclusions and Clinical Relevance: TPTDCO and TDCO measurements obtained in anaesthetized dogs during fluid overload exhibited good agreement. Accordingly, transpulmonary thermodilution provides an accurate measurement of CO in dogs with fluid overload., (© 2015 Association of Veterinary Anaesthetists and the American College of Veterinary Anesthesia and Analgesia.)

Simple Summary: Since there is a lack of information regarding how epoprostenol, a prostacyclin, affects canine renal blood flow (RBF), we investigated the effects of short-term administration of epoprostenol at human doses of 2, 5, and 10 ng/kg/min intravenously for 20 min on RBF in six healthy dogs under anesthesia. The effects of short-term administration were investigated. As the dose of epoprostenol increased, peak systolic and end diastolic velocities of the renal arteries, maximum and minimum venous flow velocities of the interlobular and renal veins, and heart rate all tended to increase. However, these increases were not significant. These results indicate that the administration of human doses of epoprostenol to dogs does not produce significant changes in renal or systemic circulation. Prostacyclin is an in vivo bioactive substance that regulates renal blood flow (RBF). Information regarding how epoprostenol, a prostacyclin preparation, affects RBF in dogs is lacking. We investigated the effects of short-term epoprostenol administration on RBF in six healthy dogs under anesthesia by administering it intravenously at human doses—2, 5, and 10 ng/kg/min for 20 min. RBF was evaluated before and during epoprostenol administration using pulsed Doppler ultrasonography, and renal perfusion was evaluated using contrast-enhanced ultrasonography. Effects on renal and systemic circulation were evaluated by measuring systolic arterial, mean arterial, diastolic arterial, pulmonary arterial, mean right atrial, and pulmonary capillary wedge pressures; heart rate; and cardiac output. Kruskal–Wallis and Bonferroni multiple comparison tests and Spearman's rank correlation coefficient were used for statistical analyses. As epoprostenol dosage increased, the peak systolic and end diastolic velocity of the renal artery, maximum and minimum venous flow velocities of the interlobular and renal veins, and heart rate all tended to increase, although not significantly. Our results indicate that human-dose epoprostenol administration in dogs does not cause significant changes in renal or systemic circulation. However, the human doses used may have been too low to produce a clinical effect in dogs. [ABSTRACT FROM AUTHOR]

Objective: Acidosis decreases myocardial contractile and myofibrillar responsiveness by reducing the calcium sensitivity of contractile proteins, which could reduce the effectiveness of pimobendan. We aimed to assess the cardiovascular effects of pimobendan in dogs subjected to acute respiratory acidosis. Design: Randomized crossover study with a 2‐week washout period. Setting: University Laboratory. Animals: Six healthy research Beagle dogs. Interventions: Anesthetized dogs were administered 2 doses of IV pimobendan during conditions of eucapnia (Paco2 35–40 mm Hg) and hypercapnia (Paco2 90–110 mm Hg). Eucapnia was maintained by positive pressure ventilation and hypercapnia was induced by adding exogenous CO2 to the anesthesia circuit. Heart rate (HR), systemic arterial blood pressure, cardiac output (CO), systemic and pulmonary vascular resistance (SVR and PVR, respectively), and pulmonary arterial pressure (PAP) were measured at baseline and 60 min after administering 0.125 mg/kg (low) and 0.25 mg/kg (high) pimobendan intravenously. Blood gas and biochemical analyses were performed at baseline and at the end of the experiment. Measurements and Main Results: The median baseline blood pH was 7.41 (range: 7.33–7.45) and 7.03 (range: 6.98–7.09) under conditions of eucapnia and hypercapnia, respectively. The serum concentrations of epinephrine and norepinephrine and the HR, CO, and PAP were higher, and SVR was lower at baseline in hypercapnic dogs. Pimobendan dose‐dependently increased CO in eucapnia (baseline: 3.6 ± 0.2 L/kg/m2 [mean ± SE], low: 5.0 ± 0.4 L/kg/m2, high: 5.8 ± 0.5 L/kg/m2, P < 0.001) and hypercapnia (baseline: 4.9 ± 0.5 L/kg/m2, low: 5.8 ± 0.5 L/kg/m2, high: 6.2 ± 0.5 L/kg/m2, P < 0.001), and increased HR and decreased SVR and PVR under both conditions (P < 0.001). In hypercapnia, the degree of increase or decrease of these cardiovascular measurements (except for PAP) by pimobendan was less than that in the eucapnic dogs. Conclusions: Pimobendan maintains function as an inodilator in anesthetized dogs with induced respiratory acidosis. [ABSTRACT FROM AUTHOR]