Similar Arterial Blood Pressure Research Articles

Alterations in cardiac function in women with severe preeclampsia: return to normal in one year after delivery?

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. In peri-partum period women with preeclampsia have demonstrated signs of subtle left ventricular (LV) dysfunction. However, there is still controversy if these changes persist or improve late after delivery. Purpose. To evaluate LV dimensions and function in severe preeclamptic women and healthy controls immediately post-delivery and 1 year postpartum. Methods. The study population comprised 24 women with severe preeclampsia and 15 healthy term controls. All women underwent standard and speckle-tracking echocardiography to assess myocardial function and deformation parameters 1 day after delivery and 1 year postpartum. To examine the impact of preload and afterload on myocardial function LV end-diastolic volume and systolic blood pressure were used accordingly. Results. On day 1 post-delivery women with severe preeclampsia were exposed to increased afterload with significantly higher systolic blood pressure compared to controls (147 [136-157] in preeclamptic vs. 112 [102-118] mmHg in control group, p < 0.001). Similarly, preeclamptic women had also higher preload demonstrated with larger LV end-diastolic volume (114 [100-128] vs. 95 [92-102] ml, p = 0.003) and left atrial volume index (36 [33-38] vs. 32 [29-36] ml/m2, p = 0.02) than control group. Among other geometric parameters difference in LV mass index was observed between groups (preeclamptic group: (81 [70-96] vs. control group: 66 [61-74] g/m2, p = 0.01). Global systolic parameters (LV ejection fraction and global longitudinal strain) did not differ between groups; however, peak systolic myocardial velocity (s’) was significantly lower in preeclamptic compared to control group (7.6 [6.5-8.1] vs. 8.0 [7.5-8.9] cm/s, p = 0.02) immediately post-delivery. Diastolic function differed between groups with significantly higher E/e’ ratio in preeclamptic women than controls (8.7 [7.6-10.0] vs. 6.9 [6.4-7.8] p = 0.01) one day post-delivery. One year after delivery both groups had normal and similar arterial blood pressure and there were no differences in geometric, systolic and diastolic function parameters between groups (Figure A-D). Conclusions. Our results showed that women with severe preeclampsia had subtle cardiac dysfunction immediately post-delivery compared to healthy controls and recovered completely in one year after delivery. Subtle cardiac dysfunction in preeclampsia immediately post-delivery seemed to be related or unmasked by pronounced changes in loading conditions, which resolved in mid-term postpartum period. Long-term follow-up with larger study population is needed to identify subgroup of women who have persistent subclinical cardiac alterations and experience cardiovascular events later in life. Abstract Figure

Stretching our understanding of baroreflex control in humans: evidence of a positive feedback pulmonary baroreflex.

Stretching our understanding of baroreflex control in humans: evidence of a positive feedback pulmonary baroreflex.

Maternal Protein Restriction Increases Respiratory and Sympathetic Activities and Sensitizes Peripheral Chemoreflex in Male Rat Offspring1–3

Background: Maternal protein restriction in rats increases the risk of adult offspring arterial hypertension through unknown mechanisms.Objectives: The aims of the study were to evaluate the effects of a low-protein (LP) diet during pregnancy and lactation on baseline sympathetic and respiratory activities and peripheral chemoreflex sensitivity in the rat offspring.Methods: Wistar rat dams were fed a control [normal-protein (NP); 17% protein] or an LP (8% protein) diet during pregnancy and lactation, and their male offspring were studied at 30 d of age. Direct measurements of baseline arterial blood pressure (ABP), heart rate (HR), and respiratory frequency (Rf) as well as peripheral chemoreflex activation (potassium cyanide: 0.04%) were recorded in pups while they were awake. In addition, recordings of the phrenic nerve (PN) and thoracic sympathetic nerve (tSN) activities were obtained from the in situ preparations. Hypoxia-inducible factor 1α (HIF-1α) expression was also evaluated in carotid bifurcation through a Western blotting assay.Results: At 30 d of age, unanesthetized LP rats exhibited enhanced resting Rf (P = 0.001) and similar ABP and HR compared with the NP rats. Despite their similar baseline ABP values, LP rats exhibited augmented low-frequency variability (∼91%;P = 0.01). In addition, the unanesthetized LP rats showed enhanced pressor (P = 0.01) and tachypnoeic (P = 0.03) responses to peripheral chemoreflex activation. The LP rats displayed elevated baseline tSN activity (∼86%;P = 0.02) and PN burst frequency (45%;P = 0.01) and amplitude (53%;P = 0.001) as well as augmented sympathetic (P = 0.01) and phrenic (P = 0.04) excitatory responses to peripheral chemoreflex activation compared with the NP group. Furthermore, LP rats showed an increase of ∼100% in HIF-1α protein density in carotid bifurcation compared with NP rats.Conclusion: Sympathetic-respiratory overactivity and amplified peripheral chemoreceptor responses, potentially through HIF-1α–dependent mechanisms, precede the onset of hypertension in juvenile rats exposed to protein undernutrition during gestation and lactation.

Glucose administration during volume resuscitation using dextran-40 from hemorrhagic shock ameliorates acid/base-imbalance in fasted rats under sevoflurane anesthesia

The hyperglycemic response is an important prognostic factor for survival after hemorrhage. In this study, we investigated the effects of glucose administration during volume resuscitation from hemmorhagic shock in fasted rats under sevoflurane anesthesia on hemodynamics, acid/base-balance and glucose metabolism. Hemorrhagic shock was induced in rats by withdrawing 25 mL/kg of blood. For volume resuscitation, rats in group-Dextran[saline] and group-Dextran[glucose] underwent infusion therapy using 10% dextran-40 dissolved in physiological saline and 10% dextran-40 dissolved in 5% glucose, respectively. Arterial blood was sampled just before blood withdrawal, immediately after blood withdrawal, immediately after volume resuscitation and at 30 min after volume resuscitation for arterial gas analyses and measurement of plasma insulin levels. After volume resuscitation, group-Dextran[glucose] showed similar arterial blood pressure, significantly lower heart rate, similar arterial PO₂ and similar hematocrit in comparison with group-Dextran[saline], suggesting that there was no particular difference in oxygen demand/supply-balance between the two groups. After volume resuscitation, group-Dextran[glucose] showed significantly higher arterial pH, similar arterial PCO₂, significantly higher bicarbonate levels and significantly higher base excess in comparison with group-Dextran[saline], suggesting that metabolic acidosis is a cause of the difference in acid/ base-balance between the two groups. After volume resuscitation, group-Dextran[glucose] showed significantly higher glucose levels, significantly higher insulin levels and significantly lower lactate levels in comparison with group-Dextran[saline]. At 30 min after volume resuscitation, base excess correlated significantly with lactate levels. These results suggest that glucose administration during volume resuscitation using dextran-40 from hemorrhagic shock ameliorates acid/base-imbalance associated with hyperlactatemia in fasted rats under sevoflurane anesthesia.

Chronic mu-opioid receptor stimulation in humans decreases muscle sympathetic nerve activity.

Opioid-addicted patients undergoing detoxification provide a unique opportunity to assess the effects of chronic opioid receptor stimulation on the sympathetic nervous system. We tested the hypothesis that chronic oral methadone intake decreases resting efferent sympathetic nerve activity to muscle (MSA). Furthermore, we assessed whether this effect is reversed by mu-opioid receptor blockade during antagonist-supported detoxification under general anesthesia. Fifteen young patients (30+/-1 years old, mean+/-SEM) with a long history of mono-opioid addiction and under oral methadone substitution therapy (65+/-10 mg/d for 21+/-6 months) were selected. Peroneal MSA (microneurography) and catecholamine plasma concentrations (high-performance liquid chromatography) were assessed in the awake state and compared with those of age-matched healthy control subjects. The effects of mu-opioid receptor blockade by naloxone (12.4 mg IV) were determined during propofol anesthesia. Compared with healthy volunteers, resting MSA (4+/-2 versus 22+/-2 bursts/min, P<0.0001) and antecubital venous norepinephrine plasma concentration (100+/-64 versus 256+/-48 pg/mL, P=0.01) were markedly decreased in addicted patients despite similar arterial blood pressure and heart rate. Opioid receptor blockade markedly increased MSA (5+/-2 to 24+/-3 bursts/min) and norepinephrine (49+/-12 to 305+/-48 pg/mL) and epinephrine (13+/-2 to 482+/-67 pg/mL) arterial plasma concentrations as well as mean arterial pressure (82+/-4 to 108+/-3 mm Hg) and heart rate (70+/-3 to 86+/-4 beats/min). Chronic mu-opioid receptor stimulation by methadone decreases resting MSA in humans.