Cardiac adaptation to conditioning in horses was evaluated after empirical training based on trainers\' experience. Twelve purebred Arabian horses, aged (mean ± SD) 28.42 ± 3.75 months, which did not perform any type of exercise prior to the research, were submitted to treadmill conditioning for six weeks. The conditioning program was based on the velocity run by the horse at which the blood lactate concentration, determined in an incremental exercise test (IET), reached 2 mmol/L (V2). The velocity at which the blood lactate concentration reached 4 mmol/L (V4) was also determined. The echocardiograms were performed at rest with pulsed-wave and tissue Doppler imaging in B- and M-modes. All procedures were carried out before and after the conditioning period. The results showed increases in V2 (from 5.2 ± 0.3 to 6.7 ± 0.4 m/s) and V4 (from 5.8 ± 0.4 to 7.6 ± 0.5 m/s) (p < 0.0001). There were also increases in the left ventricle internal diameter at diastole (LVIDd), left ventricle mass (LV mass), and stroke volume (SV), while no changes were observed in the LV free wall thickness and mean and relative wall thicknesses. The conditioning protocol, which was completed by all horses, proved to be safe and efficient, as it improved the aerobic capacity of the animals. Finally, the cardiac remodeling that occurred was mainly associated with the effect of physical training.

Pre-eclampsia and fetal growth restriction (FGR) have been long related to primary placental dysfunction, caused by abnormal trophoblast invasion. Nevertheless, emerging evidence has led to a new hypothesis for the origin of pre-eclampsia and FGR. Suboptimal maternal cardiovascular adaptation has been shown to result in uteroplacental hypoperfusion, ultimately leading to placental hypoxic damage with secondary dysfunction. In this review, we summarize current evidence on maternal cardiac hemodynamics in FGR and pre-eclampsia. We also discuss the different approaches for antihypertensive treatment according to the hemodynamic phenotype observed in pre-eclampsia and FGR.

暂无摘要。

Echocardiography was combined with pulse oximetry plethysmography to investigate postnatal cardiovascular adaptation in late preterm and term infants. Median (IQR) pleth variability decreased over three days and similar, day2 15%(12-18%) preterm versus 16%(15-18%) term infants. Median (IQR) pulse transit time heart rate normalised was lower in term babies, day2 0.55(0.51-0.63) versus 0.64(0.62-0.68).

Maternal tolerance of the semiallogenic fetus necessitates conciliation of competing interests. Viviparity evolved with a placenta to mediate the needs of the fetus and maternal adaptation to the demands of pregnancy and to ensure optimal survival for both entities. The maternal-fetal interface is imagined as a 2-dimensional porous barrier between the mother and fetus, when in fact it is an intricate multidimensional array of tissues and resident and circulating factors at play, encompassing the developing fetus, the growing placenta, the changing decidua, and the dynamic maternal cardiovascular system. Pregnancy triggers dramatic changes to maternal hemodynamics to meet the growing demands of the developing fetus. Nearly a century of extensive research into the development and function of the placenta has revealed the role of placental dysfunction in the great obstetrical syndromes, among them preeclampsia. Recently, a debate has arisen questioning the primacy of the placenta in the etiology of preeclampsia, asserting that the maternal cardiovascular system is the instigator of the disorder. It was the clinical observation of the high rate of preeclampsia in hydatidiform mole that initiated the focus on the placenta in the etiology of the disease. Over many years of research, shallow trophoblast invasion with deficient remodeling of the maternal spiral arteries into vessels of higher capacitance and lower resistance has been recognized as hallmarks of the preeclamptic milieu. The lack of the normal decrease in uterine artery resistance is likewise predictive of preeclampsia. In abdominal pregnancies, however, an extrauterine pregnancy develops without remodeling of the spiral arteries, yet there is reduced resistance in the uterine arteries and distant vessels, such as the maternal ophthalmic arteries. Proponents of the maternal cardiovascular model of preeclampsia point to the observed maternal hemodynamic adaptations to pregnancy and maladaptation in gestational hypertension and preeclampsia and how the latter resembles the changes associated with cardiac disease states. Recognition of the importance of the angiogenic-antiangiogenic balance between placental-derived growth factor and its receptor soluble fms-like tyrosine kinase-1 and disturbance in this balance by an excess of a circulating isoform, soluble fms-like tyrosine kinase-1, which competes for and disrupts the proangiogenic receptor binding of the vascular endothelial growth factor and placental-derived growth factor, opened new avenues of research into the pathways to normal adaptation of the maternal cardiovascular and other systems to pregnancy and maladaptation in preeclampsia. The significance of the \"placenta vs heart\" debate goes beyond the academic: understanding the mutuality of placental and maternal cardiac etiologies of preeclampsia has far-reaching clinical implications for designing prevention strategies, such as aspirin therapy, prediction and surveillance through maternal hemodynamic studies or serum placental-derived growth factor and soluble fms-like tyrosine kinase-1 testing, and possible treatments to attenuate the effects of insipient preeclampsia on women and their fetuses, such as RNAi therapy to counteract excess soluble fms-like tyrosine kinase-1 produced by the placenta. In this review, we will present an integrated model of the maternal-placental-fetal array that delineates the commensality among the constituent parts, showing how a disruption in any component or nexus may lead to the multifaceted syndrome of preeclampsia.

Objective: The present study sought to expand upon prior investigations of the relationship between the post-exercise heart rate recovery (HRR) and the cardiac autonomic responsiveness after orthostatic stress test.Method: HRR at the 1st, 3rd, and 5th min after maximal exercise test were correlated with relative change (Δ%) of time-domain (CV, pNN50, and rMSSD) and frequency-domain (TP, LF, HF, and LF/HF ratio) indices of heart rate variability (HRV) after active orthostatic test in 46 healthy men. Statistical analysis employed non-parametric tests with a p-value set at 5%.Results: HRR at 1st min correlated with Δ%pNN50 (rs:0.36 - p = .02). In the 3rd and 5th min, these measures correlated with Δ%pNN50, Δ%rMSSD, Δ%CV, Δ%TP, and Δ%HF indices (rs:0.33, 0.59 - p ≤ .05). Coefficient of HRR at the 1st min correlated with Δ%pNN50, Δ%rMSSD, and Δ%HF (rs:0.28, 0.45 - p ≤ .05). The 3rd and 5th min showed correlation with Δ%pNN50, Δ%rMSSD, Δ%HF, Δ%CV, and Δ%TP (rs:0.37, 0.64 - p ≤ .05). No correlation was found with indices combined sympathetic-parasympathetic modulation and HRR. After the sample was divided into high and low parasympathetic responsiveness subgroups after the orthostatic test, faster HRR was associated with the degree of parasympathetic responsiveness (reduction) following postural change (p ≤ .05).Conclusion: HRR throughout the 1st to 5th min is positively correlated with parasympathetic responsiveness and overall cardiac autonomic modulation of HRV after the orthostatic stress test, and faster HRR is positively correlated with the relative degree of parasympathetic responsiveness after the active postural change at rest in healthy men.

BACKGROUND: Transition from intrauterine to extrauterine life is a critical phase during which several changes occur in cardiovascular system. In clinical practice, it is important to have a method that allows an easy, rapid and precise evaluation of hemodynamic status of a newborn for clinical management. We here propose a rapid, broadly applicable method to monitor cardiovascular function using ultrasonic cardiac output monitoring (USCOM).
METHODS: We here present data obtained from a cohort of healthy term newborns (n = 43) born by programmed cesarean section at Fondazione MBBM, Ospedale San Gerardo. Measurements were performed during the first hour of life, then at 6 + 2, at 12-24, and 48 h of life. We performed a screening echocardiography to identify a patent duct at 24 h and, if patent, it was repeated at 48 h of life.
RESULTS: We show that physiologically, during the first 48 h of life, blood pressure and systemic vascular resistance gradually increase, while there is a concomitant reduction in stroke volume, cardiac output, and cardiac index. The presence of patent ductus arteriosus significantly reduces cardiac output (p = 0.006) and stroke volume (p = 0.023). Furthermore, newborns born at 37 weeks of gestational age display significantly lower cardiac output (p < 0.001), cardiac index (p = 0.045) and stroke volume (p < 0.001) compared to newborns born at 38 and ≥ 39 weeks. Finally, birth-weight (whether adequate, small or large for gestational age) significantly affects blood pressure (p = 0.0349), stroke volume (p < 0.0001), cardiac output (p < 0.0001) and cardiac index (p = 0.0004). In particular, LGA infants display a transient increase in cardiac index, cardiac output and stroke volume up to 24 h of life; showing a different behavior from AGA and SGA infants.
CONCLUSIONS: Compared to previous studies, we expanded measurements to longer time-points and we analyzed the impact of commonly used clinical variables on hemodynamics during transition phase thus making our data clinically applicable in daily routine. We calculate reference values for each population, which can be of clinical relevance for quick bedside evaluation in neonatal intensive care unit.

BACKGROUND: In women with singleton pregnancies, maternal adaptation is considered a stress test for later life cardiovascular disease. The aim of this study was to assess maternal adaptation in women with twin pregnancies compared to women carrying singletons during and after pregnancy.
METHODS: This was a population based prospective cohort study of 91 women with twin pregnancies and 8107 women carrying singletons. The association of twin pregnancy and maternal adaptation was examined using regression analyses. In pregnancy, we measured soluble fms-like tyrosine kinase-1 (sFLT-1), placental growth (PGF) factor, systolic (SBP) and diastolic blood pressure (DBP), and the occurrence of pre-eclampsia (PE). After pregnancy, measurements were obtained on SBP and DBP, cardiac function, retinal calibres, intima media thickness and distensibility of the common carotid artery.
RESULTS: sFLT-1 and PGF concentrations were higher in early (13.4 weeks) and mid-pregnancy (20.4 weeks) in women with twin pregnancies compared to women with singleton pregnancies. Women with twin pregnancies had a different DBP pattern in pregnancy. Women with twin pregnancies were more likely to have PE (odds ratio 3.63; 95% CI [1.76 to 7.48]). Six and ten years after pregnancy, no differences in maternal adaptation were observed.
CONCLUSIONS: Women with twin pregnancies show an altered adaptation during pregnancy compared to women with singleton pregnancies. This is associated with a substantially increased incidence of PE, but does not lead to persistent altered maternal adaptation years after pregnancy.

Circulating microRNAs (miRNAs, miRs) have great potential as cardiac biomarkers and they are also being explored for their roles in intercellular communication and gene expression regulation. The analysis of circulating miRNAs in response to exercise would provide a deeper understanding of the molecular response to physical activity and valuable information for clinical practice. Here, eight male college students were recruited to participate in cardiopulmonary exercise testing (CPET) and 1 h acute exercise training (AET). Blood samples were collected and serum miRNAs involved in angiogenesis, inflammation and enriched in muscle and/or cardiac tissues were analyzed before and after cardiopulmonary exercise and acute exercise. The miRNAs we detected were miR-1, miR-20a, miR-21, miR-126, miR-133a, miR-133b, miR-146, miR155, miR-208a, miR-208b, miR-210, miR-221, miR-222, miR-328, miR-378, miR-499, and miR-940. We found that serum miR-20a was decreased significantly after CPET and serum miR-21 was increased after AET. In addition, no robust correlation was identified between the changes of these miRNAs and makers of cardiac function and exercise capacity, which indicates a distinct adaptation of these miRNAs to exercise. Future studies are highly needed to define the potential use of these circulating miRNAs as useful biomarkers of exercise training, and disclose the biological function of circulating miRNAs as physiological mediators of exercise-induced cardiovascular adaptation.

Although pregnancy has long-lasting consequences for maternal vascular health, little is known about vascular changes postpartum (PP). Focusing on the uterine circulation, which undergoes unique structural and functional adaptation during gestation, we hypothesized that most pregnancy-induced changes would return to baseline PP, with minimal hysteresis. Large (main; MUA) and small (segmental; SUA) uterine arteries from adult Sprague Dawley rats (n = 42) were evaluated 1 and 4 weeks PP (1PP, 4PP) and compared with those of late-pregnant (LP, day 21) and age-matched non-pregnant (NP) animals. Some comparisons were extended to mesenteric arteries to evaluate differences between reproductive and systemic vessels. Pregnancy-induced axial elongation regressed > 80% 1PP in MUAs and SUAs, although some minimal hysteresis remained 4PP. Circumferential growth was slower to regress, with no reductions in lumen diameter or media thickness 1PP; values returned to (MUA) or approached (SUA) NP values by 4PP. Changes in vascular smooth muscle cell cross-sectional area-a measure of hypertrophy-paralleled those in lumen diameter. Mesenteric and uterine artery compliance diverged during gestation, and continued to do so PP. Decreased MUA compliance 4PP was supported by an increased collagen:elastin ratio. Adrenergic sensitivity increased in uterine, and decreased in mesenteric arteries during pregnancy, and returned to NP values 4PP in both types of vessels. MUA α-1 adrenoceptor expression tracked along with sensitivity. Thus, postpartum adaptation varies by both parameter and vessel type. While many parameters regressed postpartum, alterations in compliance did not, suggesting that matrix changes may have long-term consequences for maternal vascular function and health.