Effects of avertin versus xylazine-ketamine anesthesia on cardiac function in normal mice

2001 ◽  
Vol 281 (5) ◽  
pp. H1938-H1945 ◽  
Author(s):  
Chari Y. T. Hart ◽  
John C. Burnett ◽  
Margaret M. Redfield
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Lv Function ◽  
Ketamine Anesthesia ◽  
The Difference ◽  
And Function ◽  
Derivatives Of

Anesthetic regimens commonly administered during studies that assess cardiac structure and function in mice are xylazine-ketamine (XK) and avertin (AV). While it is known that XK anesthesia produces more bradycardia in the mouse, the effects of XK and AV on cardiac function have not been compared. We anesthetized normal adult male Swiss Webster mice with XK or AV. Transthoracic echocardiography and closed-chest cardiac catheterization were performed to assess heart rate (HR), left ventricular (LV) dimensions at end diastole and end systole (LVDd and LVDs, respectively), fractional shortening (FS), LV end-diastolic pressure (LVEDP), the time constant of isovolumic relaxation (τ), and the first derivatives of LV pressure rise and fall (dP/d t max and dP/d t min, respectively). During echocardiography, HR was lower in XK than AV mice (250 ± 14 beats/min in XK vs. 453 ± 24 beats/min in AV, P < 0.05). Preload was increased in XK mice (LVDd: 4.1 ± 0.08 mm in XK vs. 3.8 ± 0.09 mm in AV, P < 0.05). FS, a load-dependent index of systolic function, was increased in XK mice (45 ± 1.2% in XK vs. 40 ± 0.8% in AV, P < 0.05). At LV catheterization, the difference in HR with AV (453 ± 24 beats/min) and XK (342 ± 30 beats/min, P < 0.05) anesthesia was more variable, and no significant differences in systolic or diastolic function were seen in the group as a whole. However, in XK mice with HR <300 beats/min, LVEDP was increased (28 ± 5 vs. 6.2 ± 2 mmHg in mice with HR >300 beats/min, P < 0.05), whereas systolic (LV dP/d t max: 4,402 ± 798 vs. 8,250 ± 415 mmHg/s in mice with HR >300 beats/min, P < 0.05) and diastolic (τ: 23 ± 2 vs. 14 ± 1 ms in mice with HR >300 beats/min, P < 0.05) function were impaired. Compared with AV, XK produces profound bradycardia with effects on loading conditions and ventricular function. The disparate findings at echocardiography and LV catheterization underscore the importance of comprehensive assessment of LV function in the mouse.

Adrenomedullin improves cardiac function and prevents renal damage in streptozotocin-induced diabetic rats

2002 ◽  
Vol 283 (6) ◽  
pp. E1291-E1298 ◽  
Author(s):  
Eric Dobrzynski ◽  
David Montanari ◽  
Jun Agata ◽  
Juhong Zhu ◽  
Julie Chao ◽  
...  
Keyword(s):  
Gene Delivery ◽  
Cardiac Function ◽  
Diastolic Pressure ◽  
Pressure Rise ◽  
Protective Role ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Tubular Damage ◽  
Chemical Examination ◽  
Glycogen Accumulation

Adrenomedullin (AM) is a potent vasodilating peptide and is involved in cardiovascular and renal disease. In the present study, we investigated the role of AM in cardiac and renal function in streptozotocin (STZ)-induced diabetic rats. A single tail-vein injection of adenoviral vectors harboring the human AM gene (Ad.CMV-AM) was administered to the rats 1-wk post-STZ treatment (65 mg/kg iv). Immunoreactive human AM was detected in the plasma and urine of STZ-diabetic rats treated with Ad.CMV-AM. Morphological and chemical examination showed that AM gene delivery significantly reduced glycogen accumulation within the hearts of STZ-diabetic rats. AM gene delivery improved cardiac function compared with STZ-diabetic rats injected with control virus, as observed by decreased left ventricular end-diastolic pressure, increased cardiac output, cardiac index, and heart rate. AM gene transfer significantly increased left ventricular long axis (11.69 ± 0.46 vs. 10.31 ± 0.70 mm, n = 10, P < 0.05) and rate of pressure rise and fall (+6,090.1 ± 597.3 vs. +4,648.5 ± 807.1 mmHg/s), (−4,902.6 ± 644.2 vs. −3,915.5 ± 805.8 mmHg/s, n = 11, P < 0.05). AM also significantly attenuated renal glycogen accumulation and tubular damage in STZ-diabetic rats as well as increased urinary cAMP and cGMP levels, along with increased cardiac cAMP and Akt phosphorylation. We also observed that delivery of the AM gene caused an increase in body weight along with phospho-Akt and membrane-bound GLUT4 levels in skeletal muscle. These results suggest that AM plays a protective role in hyperglycemia-induced glycogen accumulation and cardiac and renal dysfunction via Akt signal transduction pathways.

Abstract 17904: Deficiency of Yes-associated Protein Promotes Cardiac Dysfunction in Response to Pressure Overload in the Mouse Heart

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Jaemin Byun ◽  
Dominic P Del Re ◽  
Peiyong Zhai ◽  
Akihiro Shirakabe ◽  
Junichi Sadoshima
Keyword(s):  
Cardiac Hypertrophy ◽  
Mammalian Cells ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Pressure Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Lv Function ◽  
Mouse Heart ◽  
And Control

Yes-Associated Protein (YAP), a downstream effector of the Hippo pathway, plays an important role in regulating cell proliferation and survival in mammalian cells. We have shown that cardiac-specific loss of YAP leads to increased cardiomyocyte (CM) apoptosis and impaired hypertrophy during chronic myocardial infarction in the mouse heart. However, it remains unclear whether YAP mediates hypertrophy of individual CMs under stress conditions in vivo. We hypothesized that endogenous YAP plays an essential role in mediating hypertrophy and survival of CMs in response to pressure overload (PO). Three-month-old YAP+/fl;α-MHC-Cre (YAP-cKO) and YAP+/fl (control) mice were subjected to transverse aortic constriction (TAC). Two weeks later, YAP-cKO and control mice developed similar levels of cardiac hypertrophy (left ventricular (LV) weight/tibia length: 7.27±0.38, 6.93±0.29) compared to sham (5.08±0.14, 4.07±0.33). LV CM cross sectional area was similarly increased by TAC in YAP-cKO and control mice compared to their respective shams. Induction of fetal-type genes, such as Anf and Myh7, was also similar in YAP-cKO and control mice. YAP-cKO and control mice exhibited similar baseline LV systolic function (ejection fraction (EF): 75, 76%). YAP-cKO mice had significantly decreased LV function after TAC compared to Sham-control mice (EF: 51%, 76%, p<0.05) and TAC-control mice (75%, p<0.05). LV end diastolic pressure (LVEDP, mmHg) was significantly increased (19.3 ±3.2, 9.8±1.6, p<0.05), and LV +dP/dt (mmHg/s, 7250±588, 9500±453, p<0.01) and -dP/dt (mmHg/s, 6000±433, 7781± 314, p<0.05) were significantly decreased in YAP-cKO compared to in control mice after TAC. LV end diastolic diameter (mm) was significantly greater in YAP-cKO than in control mice after TAC (3.95±0.11, 3.35±0.15, p<0.05), whereas LV pressure was similar, suggesting that LV wall stress was elevated in YAP-cKO compared to in control mice. Since cardiac hypertrophy in YAP-cKO mice is similar to that in control mice despite elevated wall stress, the lack of YAP appears to limit the extent of cardiac hypertrophy in response to increased wall stress. These data suggest that endogenous YAP plays an important role in mediating adaptive hypertrophy and protecting the heart against PO.

scholarly journals Direct cardiac versus systemic effects of inorganic nitrite on human left ventricular function

2021 ◽  
Author(s):  
Kevin O'Gallagher ◽  
Ana R Cabaco ◽  
Matthew Ryan ◽  
Ali Roomi ◽  
Haotian Gu ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Sodium Nitrite ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Cardiac Contractile Function ◽  
Lv Systolic Function ◽  
Lv Diastolic Function

Background Inorganic nitrite generates nitric oxide (NO) in vivo and is considered a potential therapy in settings where endogenous NO bioactivity is reduced and left ventricular (LV) function impaired. However, the effects of nitrite on human cardiac contractile function, and the extent to which these are direct or indirect, are unclear. Methods and Results We studied 40 patients undergoing diagnostic cardiac catheterisation who had normal LV systolic function and were not found to have obstructive coronary disease. They received either an intracoronary sodium nitrite infusion (8.7-26 mmol/min, n=20) or an intravenous sodium nitrite infusion (50 mg/kg/min, n=20). LV pressure-volume relations were recorded. The primary end point was LV end-diastolic pressure (LVEDP) while secondary end points included indices of LV systolic and diastolic function. Intracoronary nitrite infusion induced a significant reduction in LVEDP, LV end-diastolic pressure-volume relationship (EDPVR) and the time to LV end-systole (LVEST) but had no significant effect on measures of LV systolic function or systemic haemodynamics. Intravenous nitrite infusion induced greater effects, with significant decreases in LVEDP, EDPVR, LVEST, LV dP/dtmin, tau, and mean arterial pressure. Conclusions These results indicate that inorganic nitrite has modest direct effects on human LV diastolic function, independent of LV loading conditions and without affecting LV systolic properties. The systemic administration of nitrite has larger effects on LV diastolic function which are related to reduction in both preload and afterload. These effects of inorganic nitrite indicate a favourable profile for conditions characterized by LV diastolic dysfunction, e.g. heart failure with preserved ejection fraction.

Abstract 2180: Relationship of Left Ventricular Systolic Function to Persistence or Development of Electrocardiographic Left Ventricular Hypertrophy in Hypertensive Patients: Implications for the Development of New Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Peter M Okin ◽  
Kristian Wachtell ◽  
Eva Gerdts ◽  
Kurt Boman ◽  
Markku S Nieminen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Increased Risk ◽  
Cornell Product

Background : We have previously demonstrated that persistence or development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria are associated with an increased risk of developing heart failure (HF) compared with regression or continued absence of LVH. We postulated that this relationship might be in part mediated via worse LV systolic function in patients with new and persistent LVH. Methods : Baseline and year-3 ECG LVH and LV midwall shortening (MWS) were examined in 725 patients in the LIFE echocardiographic substudy. MWS was measured and considered abnormal if <14.2%; stress-corrected MWS (scMWS) was considered abnormal if 2440 mm-msec. Results : Between baseline and 3 years follow-up, there was continued absence (n=260) or regression (n=167) of LVH in 427 patients and persistence (n=259) or development (n=39) of ECG LVH in 298 patients. Although there was no difference in baseline prevalence of abnormal MWS (23.4 vs 26.5%, p=0.389) or abnormal scMWS (24.6 vs 26.4%, p=0.663) between groups, after 3 years follow-up persistence or development of new LVH was associated with significantly lower mean MWS and scMWS and with higher prevalence and odds of abnormal MWS and scMWS than continued absence or regression of LVH (Table ). After controlling for differences in age, gender, race, treatment group, baseline and change from baseline to year-3 of heart rate, Sokolow-Lyon voltage, systolic and diastolic pressure and baseline severity of LVH by Cornell product, persistent or new ECG LVH remained associated with a >2-fold increased risk of abnormal MWS or scMWS at year 3. Conclusions : Persistence or development of new ECG LVH during antihypertensive therapy is associated with an increased risk of LV systolic dysfunction after 3 years of follow-up. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with changing risk of developing HF. < Midwall LV Function in Relation to Persistence or Development of ECG LVH Between Baseline and Year-3

Hyperhomocysteinemia leads to pathological ventricular hypertrophy in normotensive rats

2003 ◽  
Vol 285 (2) ◽  
pp. H679-H686 ◽  
Author(s):  
Jacob Joseph ◽  
Lija Joseph ◽  
Nawal S. Shekhawat ◽  
Sulochana Devi ◽  
Junru Wang ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Ventricular Hypertrophy ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Wall Thickening ◽  
Cardiovascular Morbidity And Mortality ◽  
And Function

A recent report indicated that hyperhomocysteinemia (Hhe), in addition to its atherothrombotic effects, exacerbates the adverse cardiac remodeling seen in response to hypertension, a powerful stimulus for pathological ventricular hypertrophy. The present study was undertaken to determine whether Hhe has a direct effect on ventricular remodeling and function in the absence of other hypertrophic stimuli. Male Wistar-Kyoto rats were fed either an amino acid-defined control diet or an intermediate Hhe-inducing diet. After 10 wk of dietary treatment, rats were subjected to echocardiographic assessment of left ventricular (LV) dimensions and systolic function. Subsequently, blood was collected for plasma homocysteine measurements, and the rats were killed for histomorphometric and biochemical assessment of cardiac remodeling and for in vitro cardiac function studies. Significant LV hypertrophy was detected by echocardiographic measurements, and in vitro results showed hypertrophy with significantly increased myocyte size in the LV and right ventricle (RV). LV and RV remodeling was characterized by a disproportionate increase in perivascular and interstitial collagen, coronary arteriolar wall thickening, and myocardial mast cell infiltration. In vitro study of LV function demonstrated abnormal diastolic function secondary to decreased compliance because the rate of relaxation did not differ between groups. LV systolic function did not vary between groups in vitro. In summary, in the absence of other hypertrophic stimuli short-term intermediate Hhe caused pathological hypertrophy and remodeling of both ventricles with diastolic dysfunction of the LV. These results demonstrate that Hhe has direct adverse effects on cardiac structure and function, which may represent a novel direct link between Hhe and cardiovascular morbidity and mortality, independent of other risk factors.

Effect of repeated episodes of reversible myocardial ischemia on myocardial blood flow and function in humans

2002 ◽  
Vol 282 (5) ◽  
pp. H1603-H1608 ◽  
Author(s):  
Edward Barnes ◽  
David P. Dutka ◽  
Masood Khan ◽  
Paolo G. Camici ◽  
Roger J. Hall
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Blood Flow ◽  
Systolic Function ◽  
Peak Stress ◽  
Left Ventricular ◽  
Lv Function ◽  
Positron Emission ◽  
Artery Disease ◽  
And Function

Nine patients with coronary artery disease and normal left ventricular (LV) function underwent two episodes of dobutamine-induced ischemia to determine whether repeated episodes of ischemia lead to cumulative stunning. Positron emission tomography (PET) and oxygen 15-labeled H2O was used to assess myocardial blood flow (MBF) at baseline, peak stress, and after stress for each ischemic episode. Quantitative echocardiographic assessment of global ejection fraction (EF) and regional systolic function (SF) was performed at rest and regular intervals after dobutamine. SF was assessed for regions subtended by a coronary artery with a >70% diameter stenosis. Both EF and SF were more severely impaired 45 min after the second episode of stress compared with 45 min after the first (both P < 0.01), despite no difference in duration of the two dobutamine infusions or MBF at peak stress (1.72 vs. 1.69). After both episodes of ischemia, when LV function was impaired but subsequently recovered, MBF (1.15 ± 0.39 and 1.20 ± 0.43, respectively) was no different to baseline MBF (1.02 ± 0.35), confirming that repeated episodes of dobutamine-induced ischemia lead to cumulative myocardial stunning.

scholarly journals A new model of congestive heart failure in rats

2011 ◽  
Vol 301 (3) ◽  
pp. H994-H1003 ◽  
Author(s):  
Jiqiu Chen ◽  
Elie R. Chemaly ◽  
Li Fan Liang ◽  
Thomas J. LaRocca ◽  
Elisa Yaniz-Galende ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Function ◽  
Systolic Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Remote Myocardium ◽  
Male Rats ◽  
Lv Function ◽  
New Model

Current rodent models of ischemia/infarct or pressure-volume overload are not fully representative of human heart failure. We developed a new model of congestive heart failure (CHF) with both ischemic and stress injuries combined with fibrosis in the remote myocardium. Sprague-Dawley male rats were used. Ascending aortic banding (Ab) was performed to induce hypertrophy. Two months post-Ab, ischemia-reperfusion (I/R) injury was induced by ligating the left anterior descending (LAD) artery for 30 min. Permanent LAD ligation served as positive controls. A debanding (DeAb) procedure was performed after Ab or Ab + I/R to restore left ventricular (LV) loading properties. Cardiac function was assessed by echocardiography and in vivo hemodynamic analysis. Myocardial infarction (MI) size and myocardial fibrosis were assessed. LV hypertrophy was observed 4 mo post-Ab; however, systolic function was preserved. LV hypertrophy regressed within 1 mo after DeAb. I/R for 2 mo induced a small to moderate MI with mild impairment of LV function. Permanent LAD ligation for 2 mo induced large MI and significant cardiac dysfunction. Ab for 2 mo followed by I/R for 2 mo (Ab + I/R) resulted in moderate MI with significantly reduced ejection fraction (EF). DeAb post Ab + I/R to reduce afterload could not restore cardiac function. Perivascular fibrosis in remote myocardium after Ab + I/R + DeAb was associated with decreased cardiac function. We conclude that Ab plus I/R injury with aortic DeAb represents a novel model of CHF with increased fibrosis in remote myocardium. This model will allow the investigation of vascular and fibrotic mechanisms in CHF characterized by low EF, dilated LV, moderate infarction, near-normal aortic diameter, and reperfused coronary arteries.

Temporal evaluation of left ventricular remodeling and function in rats with chronic volume overload

1996 ◽  
Vol 271 (5) ◽  
pp. H2071-H2078 ◽  
Author(s):  
G. L. Brower ◽  
J. R. Henegar ◽  
J. S. Janicki
Keyword(s):  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular Remodeling ◽  
Isolated Heart ◽  
Volume Overload ◽  
Left Ventricular ◽  
Control Value ◽  
Chronic Volume Overload ◽  
And Function

The left ventricle (LV) significantly dilates and hypertrophies in response to chronic volume overload. However, the temporal responses in LV mass, volume, and systolic/diastolic function secondary to chronic volume overload induced by an infrarenal arteriovenous (A-V) fistula in rats have not been well characterized. To this end, LV end-diastolic pressure, size, and function (i.e., isovolumetric pressure-volume relationships in the blood-perfused isolated heart) were assessed at 1, 2, 3, 5, and 8 wk post-A-V fistula and compared with age-matched control animals. Progressive hypertrophy (192% at 8 wk), ventricular dilatation (172% at 8 wk), and a decrease in ventricular stiffness (257% at 8 wk) occurred in the fistula groups. LV end-diastolic pressure increased from a control value of 4.2 +/- 3.1 mmHg to a peak value of 15.7 +/- 3.6 mmHg after 3 wk of volume overload. A subsequent decline in LVEDP to 11.0 +/- 6.0 mmHg together with further LV dilation (169%) corresponded to a significant decrease in LV stiffness (222%) at 5 wk post-A-V fistula. Myocardial contractility, as assessed by the isovolumetric pressure-volume relationship, was significantly reduced in all A-V fistula groups; however, the compensatory remodeling induced by 8 wk of chronic biventricular volume overload tended to preserve systolic function.

Abstract 17500: A Crisis of the Heart

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Joyce Njoroge ◽  
Michael H Crawford
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Arterial Oxygen Saturation ◽  
Left Ventricular ◽  
Coronary Vasospasm ◽  
Arterial Oxygen ◽  
Heart Catheterization ◽  
Carcinoid Crisis ◽  
Tace Procedure

A 59 year old female with past medical history of metastatic neuroendocrine tumor without cardiac involvement was admitted for transarterial catheter embolization (TACE) procedure of liver lesions. During the TACE procedure, she developed hypertensive urgency treated with intravenous beta blocker therapy and continuous octreotide for carcinoid reaction. The following day she developed acute pulmonary edema and labile blood pressures requiring low dose norepinephrine. Octreotide infusion was up-titrated to 500 mcg/hour with concern for carcinoid crisis. On physical exam, she was tachycardic and regular without notable murmurs or extra cardiac sounds, no elevated jugular venous distension, and no lower extremity edema. She had bilateral crackles on pulmonary exam and was diaphoretic and delirious. There were sub-millimeter lateral ST- segment elevations on her electrocardiogram but her troponin levels were elevated to 14 ng/dL. Point of care cardiac ultrasound demonstrated severely impaired left ventricular systolic function without regional wall motion abnormalities. Coronary angiogram revealed diffuse coronary vasospasm and elevated left ventricular end-diastolic pressure. On right heart catheterization, she had elevated filling pressures, pulmonary arterial oxygen saturation of 25%, and cardiac index of 1.42 L/min/m2. Our patient was diagnosed with cardiogenic shock secondary to octreotide mediated coronary vasospasm causing diffuse myocardial injury. Continued multidisciplinary discussions were needed to determine appropriate vasopressor and inotropic agent use to support cardiac function without triggering further hormonal dysregulation during carcinoid crisis. Her cardiac function eventually improved with left ventricular Impella support and gradual down-titration of octreotide dose. Norepinephrine, epinephrine, and phenylephrine were avoided in favor of vasopressin, and dobutamine was switched to milrinone to prevent further sympathetic activation. She was able to wean off Impella and pressor support and had improvement of her left ventricular function on repeat echocardiography one month later. She has not had recurrence of heart failure symptoms and continues to follow up with oncology via tele-visits.

scholarly journals Pregnancy Effect on Echocardiographic Parameters in Great Dane Bitches

Animals ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1992
Author(s):  
Monica Melandri ◽  
Ilaria Spalla ◽  
Luca Fanciullo ◽  
Salvatore Alonge
Keyword(s):  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Myocardial Diseases ◽  
Uncomplicated Pregnancy ◽  
Statistical Effect ◽  
Maternal Adaptation ◽  
Echocardiographic Parameters ◽  
And Function ◽  
Great Dane

Pregnancy is associated with adaptation of the left ventricular (LV) function. Due to differences between breeds in baseline echocardiographic values and specific predispositions for myocardial diseases, breed-specific echocardiographic parameters may be helpful to evaluate whether the systolic function varies during pregnancy. This study enrolled nine healthy Great Dane bitches with uncomplicated pregnancy. Echocardiographic M-mode and B-mode data were collected before ovulation and within 7 days of the predicted parturition term. Evaluated parameters were: LV dimension in diastole (LVd) and systole (LVs), end-diastolic (EDVI) and end-systolic (ESVI) volumes indexed to body surface area (BSA), end-diastolic (EDV) and end-systolic (ESV), end-point-septal-separation (EPSS), left atrium to aortic root ratio (LA/Ao), sphericity index (SI), ejection fraction (EF), fractional shortening (FS), stroke volume (SV), heart rate (HR), and cardiac output (CO). The ANOVA showed a statistical effect of the age of gestation (p < 0.01) on the increase of diastolic dimensions and functional parameters and on the decrease of systolic dimensions. The CO increase parallels the rise in SV and HR (p < 0.01). No statistical differences were observed for EPSS, LA/Ao, and SI. The changes in cardiac chambers and function are likely to reflect maternal adaptation to allow the fetal development in uncomplicated pregnancy. The present study provides specific echocardiographic values in uncomplicated pregnancy of Great Danes, showing that the systolic function is enhanced and that the increase in preload, observed during gestation, is the likely mechanism.

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