Search Results (664)

Background and Objectives: Cardiac injury caused by cancer therapy can be detected early using high-sensitivity cardiac troponins (hs-cTns), and this is crucial for preventing irreversible consequences. Clinically relevant issues regarding hs-cTns in oncologic settings—such as reliable cut-off values, the optimal assessment timeframe, factors influencing their levels, and their prognostic ability in relation to functional echocardiographic parameters—require further investigation. In this study, we aimed to examine the determinants of hs-cTnT variations during cancer therapy and the relationship between the biomarker and functional conventional echocardiographic parameters. Materials and Methods: We prospectively evaluated adult patients scheduled for chemotherapy for either breast or gastrointestinal cancers, excluding those with pulmonary and cardiac disorders. We enrolled 40 patients who underwent a minimum of one cycle of potentially cardiotoxic regimens containing at least one of the following agents: anthracyclines, cyclophosphamide, taxanes, 5-fluorouracil, platinum compounds, trastuzumab, or bevacizumab. We observed two-dimensional and tissue Doppler echocardiographic parameters and hs-cTnT levels for a median of 360 days (IQR 162, 478) following the start of chemotherapy. Results: The generalised estimating equation (GEE) analysis revealed significant elevations in hs-cTnT levels at three months (β = 1.2; p = 0.005) and six months (β = 2.3; p = 0.02) from baseline, influenced by anthracycline treatment (p = 0.009), renal function (p = 0.003), and increased cardiotoxicity risk (high: p = 0.013; medium: p < 0.001). Elevated hs-cTnT levels independently predicted the deterioration of the LV longitudinal myocardial function, measured by the systolic tissue velocities, according to the GEE analysis. The receiver operating characteristic curve-derived hs-cTnT thresholds—of 8.23 ng/L and 8.08 ng/L—had a high negative predictive value for identifying Average and Lateral LVS′ decreases, respectively. Conclusions: Our research supports the use of baseline and continuing hs-cTnT testing in cancer patients, showing the dependence of the biomarker on renal function, cardiovascular toxicity risk level, and anthracycline treatment. The hs-cTnT cut-off value of approximately 8 ng/L may suggest a low probability of longitudinal myocardial function impairment and this observation needs further validation in larger cohorts. Full article

Background/Objectives: Ketamine, widely used for its anesthetic and analgesic properties, has been linked to cardiotoxic effects, particularly with chronic use. Prolonged ketamine exposure may impair cardiovascular function, while aerobic exercise is known to promote protective cardiovascular adaptations. This study aimed to evaluate whether aerobic training can mitigate the deleterious cardiovascular effects of chronic ketamine administration in rats. Methods: Twenty-four Wistar rats were randomly assigned to four groups: sedentary control (S), trained control (T), sedentary with ketamine (S-ket), and trained with ketamine (T-ket). Ketamine was administered intraperitoneally at a dose of 10 mg/kg, three times per week for six weeks. Aerobic training was conducted on a treadmill in the trained groups throughout the protocol. At the end of the experiment, cardiac function was assessed by echocardiography. Additionally, animals were cannulated in the carotid artery and jugular vein to measure blood pressure, baroreflex sensitivity, and heart rate variability using a data acquisition system (2 kHz, Windaq DATAQ). Results: Rats in the S-ket group showed elevated systolic arterial pressure and reduced baroreflex sensitivity compared to controls. Aerobic training attenuated these effects. Baroreflex sensitivity improved (bradycardic reflex—S: −1.7 ± 0.3; S-ket: −0.7 ± 0.1; T: −1.3 ± 0.2; T-ket: −1.3 ± 0.1), and cardiovascular autonomic function was preserved (total power—S: 45.6 ± 6.3; S-ket: 18.3 ± 2.1; T: 44.1 ± 5.7; T-ket: 38.9 ± 8.4) in trained animals. Conclusions: Aerobic exercise mitigates cardiovascular impairments caused by chronic ketamine exposure in rats, suggesting its potential as a non-pharmacological intervention to counteract ketamine-induced cardiotoxicity. These findings support incorporating exercise into treatment strategies for individuals chronically exposed to ketamine. Full article

Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome characterized by left ventricular diastolic dysfunction, exercise intolerance, low-grade chronic inflammation, and comorbidities such as hypertension, obesity, and glucose intolerance. Myocardial infiltration by activated macrophages has been proposed as a mechanism linking low-grade inflammation to increased diastolic LV stiffness in HFpEF. Changes in the relative abundance of cardiac macrophage populations may precede and promote the development of HFpEF in the aged heart. This study aimed to characterize the cardiac macrophage subsets that predominate during progression from experimental preclinical to established HFpEF. To generate the model, wild-type male C57BL/6N mice were randomized to control chow or a combination of high-fat diet plus L-NAME in drinking water for 5 weeks (asymptomatic pre-HFpEF) or 15 weeks (established HFpEF). At the end of each period, we measured body weight, running distance, metabolic biomarkers, systolic and diastolic blood pressure, myocardial function and morphology, cardiac remodeling by hypertrophic markers, morphometric analyses, fibrosis, cytokines TNF-α and IL-10, cardiac macrophage phenotype profiles (CCR2⁺ and CCR2⁻), and AMP-Activated Protein Kinase (AMPK)activity.Significant changes in myocardial macrophage populations were observed at 5 weeks (pre-HFpEF), specifically a decrease in resident reparative CCR2⁻MHCII⁻ and increase in proinflammatory CCR2⁺MHCII⁺ macrophages. These early changes were associated with higher circulating TNF-α, decreased myocardial AMPK activation, and more severe myocardial fibrosis. At 15 weeks (established HFpEF), proinflammatory CCR2⁺MHCII⁺ macrophage levels remained elevated in the myocardium; whereas the initial number of resident reparative CCR2⁻MHCII^- levels was reduced, it subsequently returned to baseline. In this model of HFpEF induced by a high-fat diet and L-NAME, which produced obesity, glucose intolerance, and hypertension, myocardial resident reparative CCR2⁻MHCII⁻ macrophages decreased and proinflammatory CCR2⁺MHCII⁺ macrophages increased during preclinical stages. These early changes in cardiac macrophage profile were associated with low-grade inflammation and myocardial remodeling and preceded the onset of HFpEF. Full article

Background: Body surface area is a key determinant of cardiac morphology and function, but it is often underestimated in the interpretation of athlete’s cardiac phenotypes. Aims: This study aimed to assess the role of anthropometric characteristics and whether particularly high vs. low body surface area (BSA) is associated with distinct morpho-functional and cardiometabolic features in elite athletes. Methods: We retrospectively included 2518 Olympic athletes. All underwent a pre-participation screening, including physical examination, ECG, blood analysis, echocardiography, and cardiopulmonary exercise testing. Participants were grouped by sex-specific BSA percentiles: Group A (<5th percentile), Group B (25th–75th), and Group C (>95th percentile). Functional, echocardiographic, and cardio-metabolic parameters were compared among groups. Results: In male athletes, Group C showed higher resting systolic blood pressure (123.8 ± 10.4 mmHg) than Group B (117.4 ± 9.6, p < 0.0001) and Group A (110.4 ± 13, p < 0.0001), and a higher prevalence of dyslipidemia (31.7% vs. 11.1% in Group B and 4% in Group A, p = 0.031). Despite greater LVEDD (59 ± 3 mm in Group C vs. 55 ± 2.9 in B and 51.1 ± 3.1 in A, p < 0.0001) and LV mass (p < 0.0001), functional performance was lower in Group C, with VO₂ max/kg of 35.2 ± 13.2 mL/min/kg vs. 44 ± 7.1 in B, and 47.8 ± 7.3 in A (p < 0.0001). Similar trends were observed in females for morpho-functional parameters, though lipid profiles did not significantly differ among groups (p > 0.05). Conclusions: Anthropometric traits significantly influence the cardiovascular and metabolic phenotype of elite athletes. Our findings support the integration of anthropometric profiling into the routine cardiovascular assessment of athletes, especially those at the extremes of body size, to better interpret physiological adaptations and risk profiles. Full article

Background: Gestational diabetes mellitus (GDM) is associated with subclinical alterations in fetal cardiac morphology and function. Ursodeoxycholic acid (UDCA), widely used in pregnancy for intrahepatic cholestasis, has demonstrated cardioprotective properties in experimental fetal models, preventing conduction abnormalities and improving myocardial function. Whether UDCA modifies fetal or neonatal cardiac adaptation in GDM pregnancies has not been previously investigated. The objective was to evaluate the effect of ursodeoxycholic acid (UDCA) on fetal and neonatal cardiac function in pregnancies complicated by gestational diabetes mellitus (GDM). Methods: In this randomized, placebo-controlled study, 113 women with GDM were enrolled, of whom 56 received UDCA and 57 the placebo. After measurement of maternal blood UDCA concentrations, 43 participants in the treatment group had levels ≥0.5 µmol/L and were included in the per-protocol analysis. Echocardiographic and Doppler-derived cardiac indices were assessed at baseline, 36 weeks’ gestation, and postpartum. Comparisons were performed using univariable tests and mixed-effects multivariable models accounting for time and treatment. Results: In the treatment group, compared to the placebo group, there were no significant differences in cardiac indices at 36 weeks’ gestation or postpartum when assessed individually. However, in the mixed-effects longitudinal analysis, a significant treatment-by-time interaction was observed. Specifically, in the postpartum period, mitral A-wave velocity (MV-A) was higher in the treatment group compared to that under the placebo (9.58, 95% CI 2.29–16.87; p = 0.010), reflecting a more pronounced increase in the atrial contribution to left ventricular filling over time. Similarly, aortic peak velocity (Ao_Vmáx) was significantly higher in the treatment group compared to that under the placebo in the postpartum period (7.97, 95% CI 0.19–15.75; p = 0.045), indicating a greater augmentation in left ventricular outflow dynamics. Conclusions: In pregnancies complicated by GDM, UDCA did not lead to significant cross-sectional differences in fetal or neonatal cardiac indices at 36 weeks or postpartum. However, longitudinal modeling indicated that UDCA was associated with a greater increase in the atrial contribution to ventricular filling (MV-A) and aortic peak velocity (Ao_Vmáx) in the postpartum period compared to that under the placebo. These findings suggest that while UDCA does not broadly alter cardiac function, it may modulate specific aspects of diastolic filling and systolic outflow dynamics during late gestation and early neonatal adaptation. Full article

Background/Objectives: Cardiovascular diseases are the most important cause of mortality in chronic obstructive pulmonary disease (COPD). Speckle-tracking echocardiography (2D-STE) can be used for assessing atrial and ventricular function, and its role in COPD is underexplored. The main objective of this study was to investigate prognostic associations in patients with COPD using 2D-STE echocardiography and laboratory biomarkers. Methods: The study included 70 participants, divided into two groups: 55 patients diagnosed with COPD and 15 healthy controls. All four cardiac chambers were analyzed with standard ultrasound and 2D-STE techniques. We measured NT-proBNP and several oxidative stress biomarkers: reduced glutathione (GSH), the GSH/GSSG ratio, malondialdehyde (MDA), and Caspase-3. Results: An NT-proBNP level above 325 pg/mL independently predicts advanced COPD stages (GOLD grades 3 and 4), with statistically significant results at a 95% confidence interval (CI) (p = 0.001). Additionally, 2D-STE identified reduced right ventricular (RV) and left ventricular (LV) strain in COPD patients before changes in LV ejection fraction. RV and LV strain measurements (RV4CLS < −16.15%, RVFWSL < −18.6%, LV GLS < −19.45%) along with PASP > 37.5 mmHg are independent predictors of advanced COPD stages, demonstrating significance at a 95% CI (p = 0.001). A positive correlation was observed between NT-proBNP, ultrasound parameters assessing RV systolic function, LV longitudinal strain impairment, and PASP. Conclusions: NT-proBNP serves as an independent biomarker of pulmonary hypertension and secondary right heart overload and independently predicts advanced COPD stages (GOLD grades 3 and 4) alongside RV and LV strain measurements. Full article

Hypertrophic cardiomyopathy (HCM) is the most common cardiomyopathy in cats and is classified as obstructive (HOCM) or non-obstructive based on anatomical differences in the left ventricular outflow tract (LVOT). In severe obstructive cases, while beta-blockers are the recommended initial treatment in humans, some patients exhibit treatment resistance. For these cases, the addition of the antiarrhythmic agent disopyramide is common. However, its use in cats has only been documented in a case report. In this study, the use of disopyramide resulted in a significant reduction in the LVOT velocity and cardiac troponin I levels. Additionally, no significant adverse effects were observed. These findings suggest that disopyramide could be a potential therapeutic option for the treatment in cats with HOCM. Full article

The relationship of diabetes mellitus (DM) with cardiovascular mortality and morbidity has been widely established. Diabetic cardiomyopathy (DBCM) has been increasingly recognized as the development of cardiac dysfunction accompanied by heart failure (HF) symptoms in the absence of obvious causes like coronary artery disease (CAD), hypertension (HTN) or valvular diseases. The objective of this review is to critically appraise the role of echocardiography in the diagnosis and prognostic stratification of DBCM. Echocardiography remains the first-line imaging modality due to its availability, repeatability, non-invasive nature and ability to assess structural and functional changes. Classical echocardiographic indices such as left ventricular hypertrophy and systolic and diastolic dysfunction assessment provide valuable information but they lack sensitivity, often remaining normal until advanced stages of DBCM. Recently developed echocardiographic modalities, including strain imaging, myocardial work indices and left atrial strain, may allow for earlier detection of subclinical myocardial dysfunction, having important prognostic implications. However, these advanced modalities require high imaging quality, expertise and standardization, being subject to technical and physio-logical limitations. Stress echocardiography, particularly exercise-based protocols, is an increasingly recognized, valuable tool for unmasking exertional abnormalities in filling pressures, myocardial reserve and pulmonary pressures that are not evident at rest. Until now, stress echocardiography requires validation in large cohorts to assess its prognostic power. This review highlights the importance of timely recognition of DBCM, underscores the advantages and disadvantages of current echocardiographic approaches and outlines future perspectives in multimodality imaging to improve patient outcomes. Full article

Background: Hypertrophic cardiomyopathy (HCM) is a heterogeneous myocardial disease in which conventional prognostic models, primarily focused on sudden cardiac death, often fail to identify patients at risk of clinically relevant events such as heart failure progression or rehospitalization. Cardiopulmonary exercise testing (CPET) quantifies functional capacity, while stress echocardiography (SE) provides mechanistic insights into exercise-induced hemodynamic changes. Their combined application (CPET–SE) may enhance risk stratification in patients with HCM. Methods: In this retrospective study, 388 patients with obstructive and non-obstructive HCM (mean age 48 ± 15 years, 63.1% male) underwent baseline CPET–SE between 2010 and 2022 and were followed for a median of 7.4 years [IQR 4.3–10.2]. Echocardiographic parameters were assessed at rest and peak exercise, and CPET indices included peak oxygen consumption (pVO₂), ventilatory efficiency, and anaerobic threshold. The primary outcome was a composite of heart failure hospitalization or progression to end-stage HCM. Results: Over a median follow-up of 7.4 years, 63 patients (16.2%) experienced an event of the primary outcome. Patients who developed a primary outcome had greater left atrial diameter (45.0 vs. 41.0 mm, p < 0.001) and indexed volume at rest (36.4 vs. 29.0 mL/m², p < 0.001), with further dilation during stress (p = 0.046); increased LV wall thickness (p = 0.001); higher average E/e′ at rest and during stress (p ≤ 0.004); and higher pulmonary artery systolic pressure at rest (p = 0.027) and during stress (p = 0.044). CPET findings included lower pVO₂ (16.0 vs. 19.5 mL/kg/min, p = 0.001), reduced % predicted pVO₂ (p = 0.006), earlier anaerobic threshold (p = 0.032), impaired ventilatory efficiency (p = 0.048), and chronotropic incompetence (p < 0.001) in patients who experienced a primary outcome. Multivariable analysis identified dyslipidemia (OR 2.58), higher E/e′ (OR 1.06), and lower pVO₂ (OR 0.92) as independently associated with the primary outcome. Conclusions: CPET–SE provided a comprehensive evaluation of patients with HCM, associating aerobic capacity to its hemodynamic determinants. Reduced pVO₂ showed the strongest association with adverse outcomes, while exercise-induced diastolic dysfunction and elevated pulmonary pressures identified a high-risk phenotype. Incorporating CPET–SE into longitudinal management of patients with HCM may enable earlier detection of physiological decompensation and guide personalized therapeutic strategies. Full article

Background: Regular endurance training induces physiological changes in cardiac structure and function. The precise epigenetic mechanisms by which cardiovascular adaptations are mediated are still unclear. This review seeks to clarify the role of epigenetic regulation in exercise-induced cardiovascular adaptation. Methods: This systematic review was conducted in accordance with the PRISMA guidelines up to 30 April 2025, using the databases PubMed, VHL, and LILACS Plus. Studies were included if they focused on microRNA expression and DNA methylation in individuals with cardiovascular disease who underwent endurance training. Results: Six articles, including 384 participants with heart failure, coronary artery disease, and hypertension, were included in the final analysis. Changes in DNA methylation and microRNA expression of specific genes involved in cardiovascular structural and functional adaptation were observed. Significant improvements were found in body composition, VO_2peak, systolic and diastolic blood pressure, and left ventricular function and structure. Conclusions: Endurance training has a positive impact on epigenetic mechanisms related to cardiovascular structural and functional adaptation. A clear causal link between epigenetic modifications and clinical outcomes remains to be established. Full article

Left ventricular (LV) hypertrabeculation is increasingly recognized as a phenotype that may reflect physiological adaptation, particularly in athletes exposed to chronic overload, although its functional relevance remains uncertain. This study evaluated the prevalence of excessive trabeculation and its physiological correlation with LV remodeling. We conducted a single-center, cross-sectional study involving 320 Olympic-level athletes without cardiovascular disease. All underwent cardiac magnetic resonance (CMR). Hypertrabeculation was defined by the Petersen criteria. Athletes meeting these criteria were classified as hypertrabeculated and compared with non-hypertrabeculated matched for age, sex, and sport category. LV morphology, function, strain parameters, and hemodynamic forces (HDFs) were analyzed. Hypertrabeculation was identified in 9% of the cohort. No significant differences were observed between groups for training exposure (p = 0.262), body surface area (p = 0.762), LV volumes (end-diastolic volume indexed p = 0.397 end-systolic volume indexed p = 0.118), ejection fraction (p = 0.101), mass (p = 0.919), sphericity index (p = 0.419), myocardial wall thickness (p = 0.394), tissue characterization (T1 mapping p = 0.366, T2 mapping p = 0.833), global longitudinal strain (GLS p = 0.898), global circumferential strain (GCS p = 0.219), or HDFs. All values were within the normal range. In our cohort, LV hypertrabeculation, evaluated by CMR, was relatively common but not associated with structural or functional abnormalities, supporting its interpretation as a benign variant in asymptomatic athletes with normal cardiac function. Full article

Introduction: Sepsis-induced cardiac dysfunction (SICD) is a transient cardiac disfunction, with variable described prevalence and uncertain prognostic. This study aimed to characterize the laboratory and microbiological findings in critically ill patients with sepsis who developed left ventricular (LV) or biventricular systolic dysfunction. Methods: Patients who required intensive care unit hospitalization for sepsis were screened retrospectively. Only patients with positive cultures and echocardiography performed within 24 h from admission were included. The exclusion criteria were infective endocarditis, acute coronary syndrome, history of cardiomyopathy, severe valve disease, end-stage organ or oncological disease. Cardiac function was appreciated on transthoracic echocardiography, using LV ejection fraction for the left ventricle and tricuspid annular plane systolic excursion (TAPSE) for the right ventricle. SICD was confirmed if the systolic dysfunction found upon admission was reversible within 7–10 days. Results: A total of 100 patients with positive cultures were included. The median age was 73 and 55% were male. SICD was diagnosed in 14% of patients. Patients with SICD were more likely to develop septic shock and had longer hospital and intensive care unit stay. In-hospital mortality was 44% with no significant difference between SICD and non-SICD patients. Laboratory markers upon hospital admission showed that SICD patients had significantly higher values of lactate and transaminases. Cardiac (troponin and NT-proBNP) and inflammation markers (leukocytes, neutrophils, NLR, C-reactive protein, procalcitonin) had higher values in patients with SICD but the difference did not reach statistical significance. Streptococcal infections and polymicrobial cultures were risk factors for developing SICD. Higher rates of infections with Enterobacterales were seen in the SICD group but the difference was not significant. Conclusions: SICD patients had higher lactate, inflammation, and cardiac biomarkers levels upon admission and significantly higher rates of streptococcal infections and polymicrobial cultures. Full article

Background: Mitral annular plane systolic excursion (MAPSE) is a simple and widely used M-mode echocardiographic marker of left-ventricular longitudinal function that correlates well with left ventricular ejection fraction (LVEF). Conventional chronic right ventricle (RV) pacing is associated with left ventricle (LV) dysfunction, inducing heart failure (HF) and leading to the development of pacing-induced cardiomyopathy (PiCM). The aim of this study is to ascertain the clinical usefulness of MAPSE in the assessment of LV function in patients with permanent RV pacing. Methods: We performed a cross-sectional association analysis, enrolling consecutive patients with pacemakers and chronic RV pacing burdens over 20% (Vp > 20%) from 2021 to 2024. All patients were assessed by standard transthoracic echocardiography (TTE) with LVEF and MAPSE among other parameters being assessed. We performed a correlation test using linear regression and plotted an ROC curve. Results: 409 patients (mean age = 68.7 year) were included, 225 men (55%) and 245 (59.9%) with dual-chamber pacemakers. The mean follow-up period was 18 ± 2 months, with HF incidence in the study group being 23.2%. The results showed that average, septal, and lateral MAPSE all correlate well with LVEF, but septal values seemed to provide the strongest correlation (r = 0.90, p < 0.001), and that a septal MAPSE cut off value of <10 mm (sensitivity 99.4, specificity 42.1, AUC = 0.89) was associated with impaired LVEF (<50%). Conclusions: MAPSE seems to corelate well with LVEF across the spectrum of HF in pts with chronic RV conventional pacing. Septal MAPSE shows the strongest correlation with LVEF, and a value of <10 mm is a cut-off for altered LVEF, making it a potentially useful marker of cardiac function in these pts. Full article

Transient receptor potential canonical channel type 6 (TRPC6), a non-selective cation channel that mediates Ca²⁺ influx, is expressed in the heart and implicated in pathological cardiac hypertrophy. However, the role of TRPC6 in regulating cardiac mitochondrial metabolism and contributing to development of HFpEF remains unclear. We examined whether TRPC6 deficiency prevents mitochondrial dysfunction and offers cardiac protection in a mouse model of HFpEF induced by high-fat diet (HFD) for 12 weeks combined with L-NAME administration during the final 8 weeks in TRPC6 knockout (KO) and wild-type (WT) control mice. Cardiac systolic and diastolic functions were assessed at baseline, 4 and 8 weeks after HFD+L-NAME. Dobutamine-induced stress test and treadmill exercise test were performed at the end of the protocol to evaluate cardiac reserve capacity and exercise tolerance. Mitochondrial oxygen consumption rate (OCR) and mitochondrial-derived reactive oxygen species (ROS) generation were examined in isolated cardiac fibers. WT mice subjected to HFD+L-NAME developed cardiac hypertrophy, diastolic dysfunction, and exercise intolerance, whereas TRPC6 KO mice, under the same conditions, maintained preserved diastolic function, exercise tolerance, and cardiac reserve. We also observed increased TRPC6 in mitochondria, as well as caspase-9 activation and impaired mitochondrial respiration in WT mice. In contrast, TRPC6 KO mice exhibited preserved mitochondrial OCR and attenuated mitochondrial ROS generation. In summary, TRPC6 deficiency prevents the development of HFpEF by mitigating diastolic dysfunction, preserving cardiac reserve capacity, and attenuating mitochondrial dysfunction. Full article

Background: Neonatal resuscitation guidelines recommend the use of the vasopressor epinephrine during neonatal cardiopulmonary resuscitation (CPR); however, vasopressin may be a potential alternative. Successful neonatal CPR requires rapid vasopressor administration, but the current guideline-recommended routes can take several minutes to establish and require substantial skill and/or training. The intramuscular (IM) route provides rapid drug administration and does not require special skills, training, or equipment. Objective: We aimed to compare two doses of IM vasopressin to intravenous (IV) vasopressin in a healthy neonatal piglet model to examine the hemodynamic and pharmacokinetic effects. Methods: Fifteen neonatal piglets (n = 5/group; 1–3 days of age) were anesthetized, intubated via a tracheostomy, and randomized to 4 IU/kg IM vasopressin, 8 IU/kg IM vasopressin, or 0.4 IU/kg IV vasopressin. Various hemodynamic and cardiac function parameters were continuously recorded throughout the experiment. Blood was collected prior to drug administration and throughout the experiment for pharmacokinetic and pharmacodynamic analysis. Results: The 4 IU/kg IM vasopressin dose was ineffective in producing systemic changes in hemodynamics or cardiac function as it was poorly absorbed. The 8 IU/kg IM vasopressin dose had comparable results to IV vasopressin and was rapidly distributed to systemic circulation. Conclusions: The higher IM vasopressin dose of 8 IU/kg is effective in increasing systolic and diastolic blood pressure. Full article