scholarly journals Role of Mean Arterial Pressure in Mid-trimester Pregnancy for the Prediction of Gestational Hypertension and Pre-eclampsia

2021 ◽  
Vol 13 (3) ◽  
pp. 151-155
Author(s):  
Mamta Gupta ◽  
Ojasvi Shanker
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Gestational Hypertension ◽  
Trimester Pregnancy

DESIGN AN “IN HOUSE” SOFTWARE FOR SCREENING PREECLAMPSIA BY MATERNAL FACTORS AND MEAN ARTERIAL PRESSURE AT 11 – 13 WEEKS IN COMMUNE HEALTH CENTERS.

2015 ◽  
pp. 115-126
Author(s):  
Viet Nhan Nguyen ◽  
Ngoc Thanh Cao ◽  
Thi Minh Thi Ha ◽  
Van Duc Vo ◽  
Quang Vinh Truong ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Gestational Hypertension ◽  
Area Under The Curve ◽  
Health Centers ◽  
Maternal Factors ◽  
Good Tool ◽  
Uterine Artery Doppler ◽  
Study Results ◽  
In Pregnancy

Objective: Design an “in house” software for screening preeclampsia by maternal factors and mean arterial pressure at 11 – 13 gestational weeks in commune health centers. Methods: Based on the algorithms for calculating the risk of preeclampsia (PE) by maternal factors and mean artirial pressure at 11 - 13 gestational weeks in the study results of the authors, an “in house” software was deigned in Excel. The results of prediction preeclampsia by The Fetal Medicine Foundation (FMF)(version 2.3) were compared with the results by “in house” software in 1110 singleton pregnant women. Results: The “in house” software met the requirements for calculating the risks of PE and save data. FMF risk for gestational hypertension disorder in pregnancy by maternal factors, mean arterial pressure,uterine artery Doppler and PAPP-A has an area under the curve of 0.68 (95%CI: 0.59 – 0.78). The “in house” software risk for gestational hypertension in pregnancy by maternal factors, mean arterial pressure has an area under the curve of 0.643 (0.55 – 0.73) There was no statistically significant different between two programs (p:0.52). The risk cut-off 1:50 in the prediction of gestational hypertension of the “in house” software was used to identify the group of high risk with detetion rate (DR) 28.6% (95%CI: 14.9-42.2) comparing to 40.5% (95%CI:25.6-55.3) of FMF. Conclusion: The FMF version 2.3 is better but in the absence of Doppler ultrasound and PAPP-A test in the commune health cares, the “in house” software for screening PE is a good tool for councelling, following up and early intervention for PE.

scholarly journals Placental ischemia-stimulated T-helper 17 cells induce preeclampsia-associated cytolytic natural killer cells during pregnancy

2018 ◽  
Vol 315 (2) ◽  
pp. R336-R343 ◽  
Author(s):  
Corbin A. Shields ◽  
Maggie McCalmon ◽  
Tarek Ibrahim ◽  
Dakota L. White ◽  
Jan M. Williams ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Natural Killer ◽  
Cell Activation ◽  
Fetal Weight ◽  
T Helper ◽  
T Helper 17 ◽  
Placental Ischemia ◽  
In Pregnancy

Previous studies have demonstrated that T-helper 17 (TH17) cells and cytolytic natural killer (cNK) cells are increased in women with preeclampsia. In this study we investigated the role of placental ischemia-stimulated TH17 cells in induction of cNK cells in pregnancy. We further assessed the role of TH17 cell-mediated oxidative stress in facilitation of cNK cell activation in pregnancy by treating rats with the SOD mimetic tempol. CD4+/CD25− cells were isolated from reduced uterine perfusion pressure (RUPP) rats and differentiated into TH17 cells in vitro. On day 12 of gestation ( GD12), 1 × 106 placental ischemia-stimulated TH17 cells were injected into normal pregnant (NP) rats (NP + RUPP TH17 rats), and a subset of rats were treated with tempol (30 mg·kg−1·day−1) from GD12 to GD19 (NP + RUPP TH17 + tempol rats). On GD19, cNK cells, mean arterial pressure, fetal weight, and cNK cell-associated cytokines and proteins were measured. Placental cNK cells were 2.9 ± 1, 14.9 ± 4, and 2.8 ± 1.0% gated in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Mean arterial pressure increased from 96 ± 5 mmHg in NP rats to 118 ± 2 mmHg in NP + RUPP TH17 rats and was 102 ± 3 mmHg in NP + RUPP TH17 + tempol rats. Fetal weight was 2.37 ± 0.04, 1.95 ± 0.14, and 2.3 ± 0.05 g in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Placental IFNγ increased from 1.1 ± 0.6 pg/mg in NP rats to 3.9 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental perforin increased from 0.18 ± 0.18 pg/mg in NP rats to 2.4 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental levels of granzymes A and B followed a similar pattern. Treatment with tempol did not lower placental cNK cytokines or proteins. The results of the present study identify TH17 cells as a mediator of aberrant NK cell activation that is associated with preeclampsia.

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Mechanism of decreased cardiac output during ANP infusion in conscious anephric dogs

1992 ◽  
Vol 262 (1) ◽  
pp. R120-R125
Author(s):  
H. L. Mizelle ◽  
C. A. Gaillard ◽  
R. D. Manning ◽  
J. E. Hall
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Blood Cells ◽  
Venous Return ◽  
Control Period ◽  
Peripheral Resistance ◽  
Circulating Blood Volume

Atrial natriuretic peptide (ANP) may decrease cardiac output (CO) by lowering circulating blood volume (BV) or by altering the vasculature in a manner that would decrease venous return. The purpose of this study was to determine the role of decreased BV in mediating the decrease in CO during acute infusion of ANP. BV was measured by dilution of 51Cr-labeled red blood cells in seven trained conscious splenectomized dogs studied after unilateral (UNX) and total (TNX) nephrectomy. BV, hematocrit (Hct), CO, mean arterial pressure (MAP), and total peripheral resistance (TPR) were determined during a 90-min control period and 270 min of infusion of ANP (20 ng.kg-1.min-1 iv). In UNX dogs, ANP decreased BV from 60.9 +/- 1.4 to 58.6 +/- 1.4 ml/kg and increased Hct from 39.3 +/- 1.8% to 41.1 +/- 1.8% (P less than 0.05). MAP was not changed and CO fell to a low that was 86 +/- 2% of control (P less than 0.05) 240 min after starting ANP. TPR increased significantly during ANP infusion. All variables returned to control after ANP was stopped. In the same dogs studied 24 h after TNX, MAP averaged 111 +/- 5 mmHg during control and did not change during ANP infusion. CO fell to a low of 82 +/- 3% of control (P less than 0.05) after 120 min of infusion and remained reduced until after the ANP was stopped.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The role of magnesium in the treatment of alcohol withdrawal with delirium

2021 ◽  
Vol 17 (8) ◽  
pp. 47-50
Author(s):  
O.O. Havrylov ◽  
M.L. Gomon
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Magnesium Sulfate ◽  
Research Group ◽  
Alcohol Withdrawal ◽  
Serum Cortisol ◽  
Control Group ◽  
The Third ◽  
Significant Difference

Background. The role of magnesium in the treatment of alcohol withdrawal with delirium is indefinite, although it is well known about its participation in the pathogenesis of this severe condition. The study was aimed to reveal the benefits and disadvantages of the sedation with added magnesium sulfate in comparison with traditional sedative therapy. Materials and methods. In our study, we tested 40 treated patients, which were randomized in two groups. We controlled the level of sedation by the Richmond agitation-sedation scale. The target level of sedation was between 0 and –2 points. We maintained this level in all the patients. In all groups, we evaluated the following values: duration of delirium, mean arterial pressure, pulse, the level of serum magnesium, cortisol and serotonin, laboratory indicators of kidneys, and liver condition. In the control group, we carried out the sedation with 10–20 mg of diazepam every 4–6 hours with infusion of barbiturates as needed. The treatment in the research group was identical with addition of magnesium sulfate 50 mg/kg every 8 hours. Results. The results of the study demonstrated that the duration of delirium is significantly lower in the research group in comparison with the control (p < 0.05). We found hypomagnesemia in almost half of the patients. The indicators of haemodynamics such as mean arterial pressure and pulse were significantly lower in both groups on the third day (p < 0.05). We found 4 cases (20 %) of hypotension in the research group and 2 cases (10 %) in the control group. The study of the dynamics of serum cortisol and serotonin showed the significant difference on the third day in both groups (p < 0.05). We found no difference in these laboratory parameters on the third day between groups (p ≥ 0.05). There was no significant difference between the laboratory indicators of kidneys and liver condition in both groups (p ≥ 0.05). Conclusions. The use of magnesium sulfate allowed decreasing the duration of delirium but had an excessive effect on haemodynamics. Such biomarkers as serum cortisol and serotonin didn’t verify the effect of magnesium sulfate.

scholarly journals MEAN ARTERIAL PRESSURE AS A PREDICTOR OF GESTATIONAL HYPERTENSION AND PREECLAMPSIA

2016 ◽  
Vol 3 (68) ◽  
pp. 3715-3720
Author(s):  
Vidhya Ravi ◽  
Sivaranjani Panneer Selvam P ◽  
Bama S Ramesh
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Gestational Hypertension

Area postrema: essential for support of arterial pressure after hemorrhage in rats

1990 ◽  
Vol 258 (6) ◽  
pp. R1472-R1478 ◽  
Author(s):  
K. M. Skoog ◽  
M. L. Blair ◽  
C. D. Sladek ◽  
W. M. Williams ◽  
M. L. Mangiapane
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Data Acquisition ◽  
Area Postrema ◽  
Plasma Renin ◽  
Base Line ◽  
Sprague Dawley ◽  
Time Period ◽  
Sprague Dawley Rats

Previous studies have indicated that the area postrema (AP) of the rat is necessary for the development of chronic angiotensin-dependent hypertension. The present study assesses the role of the AP in the maintenance of arterial pressure during hemorrhage. Sprague-Dawley rats were given sham or AP lesions 1 wk before the experiment. They were instrumented with femoral arterial and venous catheters 2 days before the experiment. On the day of the experiment, base-line mean arterial pressure (MAP) was measured for 1 h before hemorrhage. During the following 45 min, each rat was subjected to one 7-ml/kg hemorrhage every 15 min for a total of three hemorrhages. MAP was monitored by computerized data acquisition. As shown previously, MAP was slightly but significantly lower in AP-lesion rats compared with sham-lesion rats before the hemorrhage procedure. In AP-lesion rats, hemorrhage resulted in a significantly greater fall in arterial pressure than in sham-lesion rats. In spite of larger drops in pressure in AP-lesion rats, hemorrhage caused equivalent increases in plasma renin and vasopressin in both groups. In AP-lesion rats compared with sham-lesion rats, significant bradycardia was present before hemorrhage. Hemorrhage caused bradycardia in both sham- and AP-lesion rats relative to the prehemorrhage heart rates, but AP-lesion rats showed greater bradycardia than did sham-lesion rats during every time period. We conclude that the AP may play an important role in the defense of arterial pressure against hemorrhage.

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