Abstract

The purpose of this study was to investigate the cardiopulmonary response, with quantitative M-mode echocardiography, of glycopyrrolate (G, 10 µg kg−1 IM) as a pretreatment (p) or administered concurrently (c) with romifidine (RO) SQ in dogs. Healthy adult dogs (3M, 3F) 18.5–25 kg (mean ± SD, 23 ± 2.4) were utilized in a randomized cross over design. All dogs were conditioned to lie in lateral recumbency with manual restraint. Doppler measurement of systolic blood pressure (SBP), with inflatable cuffs 40% of leg circumference, was performed simultaneously with echocardiographic measurements. Baseline measurements were recorded and one of the treatments was administered: T1, 0.5 mL saline (S)(p) + RO (40 µg kg−1); T2, G(p) + RO (40 µg kg−1); T3, S(p) + RO (120 µg kg−1); T4, G(p) + RO (120 µg kg−1); T5, S(p) + G(c) + RO (120 µg kg−1). Measurements were repeated 15 minutes after G(p) or S(p); RO or G(c) were administered 20 minutes after G(p) or S(p), and further measurements were taken at 10, 20, 30, 60, and 90 minutes after RO. Dimensions of the left ventricle (LVID), interventricular septum (IVS), and left ventricular free wall (LVFW) were obtained in systole (S) and diastole (D). Heart rate (HR) and amplitude of motion (Amp) of the IVS and LVFW were also measured. From these, measures of wall stress (SBPxLVID-S)/([4LVFW-S](1 + [LVFW-S/LVID-S])) and fractional shortening (FS) of the left ventricle (LVID-D – LVID-S)/(LVID-D) were obtained. Data were analyzed by a two-way anova, with an LSD posthoc test and 95% confidence level. Echocardiographic indices of cardiac performance (LVID-D, LVID-S, FS, AMP-LVFW) and HR were decreased in all RO sedated dogs (p < 0.001). The magnitude of change in cardiac indices was minimal with low dose RO. At most, but not all, times high dose RO produced significantly more alteration in cardiac indices, i.e. T1 versus T3 and T2 versus T4 (p < 0.02). G significantly increased HR (p < 0.0001), but, cardiac indices were not improved. Comparisons between T1 versus T2, and T3 versus T4 demonstrated significant differences in Amp-LVFW (p < 0.007), LVID-D (p < 0.007), LVID-S (p < 0.002) and FS (p < 0.0004) between 10 and 90 minutes. Wall stress (WS) showed a significant treatment effect (p < 0.0001) with a dramatic increase in G(c) or G(p) groups. Comparisons between T1 versus T2 and T3 versus T4 were significant from 10 to 90 minutes (p < 0.0001). In conclusion, RO caused a reduction in cardiac performance, which was most dramatic with high dose RO. G(p) or G(c) did not improve indices of cardiac performance despite an increase in HR. G may actually worsen cardiovascular function with an increase in myocardial oxygen demand as suggested by the increase in WS.

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