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The Journal of Maternal-fetal &... Dec 2023Baroreflex is a regulatory mechanism that slows the fetal heart rate. This study aimed to investigate the effects of lipopolysaccharide (LPS)-induced endotoxemia on...
OBJECTIVE
Baroreflex is a regulatory mechanism that slows the fetal heart rate. This study aimed to investigate the effects of lipopolysaccharide (LPS)-induced endotoxemia on fetal baroreceptor sensitivity in preterm fetal sheep.
METHODS
The changes in fetal baroreceptor sensitivity were measured in seven chronically instrumented preterm fetal sheep. Fetal baroreceptor sensitivity was measured in three phases: (A) control phase, defined as the 24 h before the first injection of LPS; (B) acute phase, defined as the 24 h between the first and second injections of LPS; and (C) fetal acidosis phase, defined as the time from the second LPS injection until intrauterine fetal death. Histological examinations of the fetal membrane and umbilical cord were also conducted.
RESULTS
Each fetus developed metabolic acidosis after the second injection of LPS. The fetuses died 24.7 (SD = 6.1) hours after the second injection of LPS. Both the umbilical cord and fetal membranes showed histological evidence of severe inflammation. In total, 163 fetal baroreceptor measurements were performed in this experiment (A, = 77 times; B, = 60 times; C, = 26 times). Fetal baroreceptor sensitivity showed significant differences in all three phases (A: 2.7 [SD = 0.2]; B: 2.5 [SD = 0.2]; and C: 1.5 [SD = 0.2]). Post hoc tests showed that baroreceptor sensitivity in the acidosis phase had decreased significantly compared to that in the control and acute phases (<.001 and =.002, respectively).
CONCLUSIONS
Fetal baroreceptor sensitivity decreased during fetal acidosis induced by LPSs.
Topics: Pregnancy; Female; Humans; Sheep; Animals; Lipopolysaccharides; Pressoreceptors; Fetus; Inflammation; Fetal Diseases; Acidosis; Heart Rate, Fetal
PubMed: 36443245
DOI: 10.1080/14767058.2022.2150392 -
Experimental Physiology Jul 2004
Review
Topics: Animals; Blood Pressure; Humans; Pressoreceptors; Time Factors
PubMed: 15238501
DOI: 10.1111/j.1469-445x.2004.00053.x -
Brain Research Bulletin Jan 2000In this study, we examine the utility of computational modeling in understanding nervous system function. We start by examining the reasons for, and major approaches to,... (Review)
Review
In this study, we examine the utility of computational modeling in understanding nervous system function. We start by examining the reasons for, and major approaches to, computational modeling. We then chose a modeling approach and applied different variations to understanding nucleus tractus solitarius (NTS) neuronal responses to various baroreceptive stimuli. We examine the results in light of our objectives and with regard to the known parameters of the system under investigation. Our results demonstrate that modeling can be a useful tool in analysis of (and examination of underlying mechanisms for) NTS behavior on many levels.
Topics: Animals; Baroreflex; Models, Neurological; Neurons; Pressoreceptors; Solitary Nucleus
PubMed: 10709960
DOI: 10.1016/s0361-9230(99)00242-7 -
Acta Biologica Et Medica Germanica 1972
Topics: Animals; Blood Pressure; Carotid Sinus; Chronic Disease; Dogs; Homeostasis; Hypertension, Renal; Pressoreceptors; Vasomotor System
PubMed: 4653301
DOI: No ID Found -
Brain Research Bulletin Jan 2000
Review
Topics: Baroreflex; Medulla Oblongata; Neural Pathways; Neuropeptides; Neurotransmitter Agents; Pressoreceptors
PubMed: 10709954
DOI: 10.1016/s0361-9230(99)00236-1 -
Cardiology 1976
Review
Topics: Adult; Aged; Animals; Blood Pressure; Carotid Sinus; Dogs; Electric Stimulation; Heart Rate; Humans; Hypertension, Renal; Middle Aged; Myocardial Contraction; Neurons, Afferent; Pressoreceptors; Vascular Resistance
PubMed: 788909
DOI: 10.1159/000169790 -
American Journal of Physiology. Heart... Jul 2014We intended to determine if acute baroreflex activation therapy (BAT) increases venous capacitance and aortic conductance. BAT is effective in resistant hypertension,...
We intended to determine if acute baroreflex activation therapy (BAT) increases venous capacitance and aortic conductance. BAT is effective in resistant hypertension, but its effect on the systemic vasculature is poorly understood. Left ventricular (LV) and aortic pressures and subdiaphragmatic aortic and caval flows (ultrasonic) were measured in six anesthetized dogs. Changes in abdominal blood volume (Vabdominal) were estimated as the integrated difference in abdominal aortic inflow and caval outflow. An electrode was implanted on the right carotid sinus. Data were measured during control and BAT. Next, sodium nitroprusside (SNP) was infused and BAT was subsequently added. Finally, angiotensin II (ANG II) was infused, and three increased BAT currents were added. We found that BAT decreased mean aortic pressure (PAo) by 22.5 ± 1.3 mmHg (P < 0.001) and increased aortic conductance by 16.2 ± 4.9% (P < 0.01) and Vabdominal at a rate of 2.2 ± 0.6 ml·kg(-1)·min(-1) (P < 0.01). SNP decreased PAo by 17.4 ± 0.7 mmHg (P < 0.001) and increased Vabdominal at a rate of 2.2 ± 0.7 ml·kg(-1)·min(-1) (P < 0.05). During the SNP infusion, BAT decreased PAo further, by 26.0 ± 2.1 mmHg (P < 0.001). ANG II increased PAo by 40.4 ± 3.5 mmHg (P = 0.001). When an increased BAT current was added, PAo decreased to baseline (P < 0.01) while aortic conductance increased from 62.3 ± 5.2% to 80.2 ± 3.3% (P < 0.05) of control. Vabdominal increased at a rate of 1.8 ± 0.9 ml·kg(-1)·min(-1) (P < 0.01), reversing the ANG II effects. In conclusion, BAT increases arterial conductance, decreases PAo, and increases venous capacitance even in the presence of powerful vasoactive drugs. Increasing venous capacitance may be an important effect of BAT in hypertension.
Topics: Animals; Aorta, Abdominal; Arterial Pressure; Baroreflex; Blood Flow Velocity; Dogs; Electric Stimulation; Female; Hemodynamics; Male; Models, Animal; Pressoreceptors; Regional Blood Flow; Time Factors; Vascular Capacitance; Vasoconstrictor Agents; Vasodilator Agents; Vena Cava, Inferior; Ventricular Function, Left; Ventricular Pressure
PubMed: 24816258
DOI: 10.1152/ajpheart.00422.2013 -
Annual Review of Pharmacology and... 1994The recognition that the wall tone of most arteries and veins can change in response to shear stress has several implications for our understanding of the effects of... (Review)
Review
The recognition that the wall tone of most arteries and veins can change in response to shear stress has several implications for our understanding of the effects of drugs on the circulation. By a primary action on the heart and vasculature, drugs can cause changes in cardiac output and blood pressure that lead to changes in blood flow. These changes in blood flow can secondarily change vascular diameter, thus complicating the basic response. Furthermore, drugs can modify the local flow-sensitive mechanism directly. The flow-initiated effect seems to depend, both qualitatively and quantitatively, on the level of wall tone and is not entirely endothelium-dependent. If the primary action of a drug is to alter the tone level of vascular smooth muscle directly or if tone changes as a result of a change in blood pressure (and thus in local myogenic control), then it follows that these changes in turn influence the flow response, both quantitatively and qualitatively. The vascular response to flow is complex both in its site of origin and the functional changes initiated. It is not synonymous with the endothelial-dependent action of acetylcholine.
Topics: Animals; Humans; Muscle Contraction; Muscle Tonus; Muscle, Smooth, Vascular; Pressoreceptors; Regional Blood Flow
PubMed: 8042850
DOI: 10.1146/annurev.pa.34.040194.001133 -
Naunyn-Schmiedebergs Archiv Fur... 1955
Topics: Action Potentials; Baroreflex; Blood Pressure; Blood Pressure Determination; Chlorpromazine; Humans; Pressoreceptors
PubMed: 14394160
DOI: No ID Found -
Zeitschrift Fur Kreislaufforschung Jul 1972
Topics: Air; Animals; Blood Pressure; Carbon Dioxide; Carotid Sinus; Heart Rate; Pressoreceptors; Rabbits; Respiration; Vagus Nerve
PubMed: 5055578
DOI: No ID Found