Fuzzy control of mean arterial pressure in postsurgical patients with sodium nitroprusside infusion

1992 ◽  
Vol 39 (10) ◽  
pp. 1060-1070 ◽  
Author(s):  
H. Ying ◽  
M. McEachern ◽  
D.W. Eddleman ◽  
L.C. Sheppard
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Fuzzy Control ◽  
Sodium Nitroprusside ◽  
Nitroprusside Infusion

Effects of angiotensin II on plasma atrial natriuretic factor in nonpregnant and pregnant ewes

1995 ◽  
Vol 73 (5) ◽  
pp. 644-650 ◽  
Author(s):  
L. Fan ◽  
D. Javeshghani ◽  
S. Mukaddam-Daher ◽  
Z. Guan ◽  
B. S. Nuwayhid ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Pregnant Sheep ◽  
Nitroprusside Infusion ◽  
Atrial Natriuretic

The release of atrial natriuretic factor (ANF) is primarily determined by atrial stretch, but may also be modulated by circulating angiotensin II (AngII). During pregnancy, the circulating concentrations of both ANF and AngII are increased. To further define possible effects of AngII on ANF release, four doses of AngII (0.5, 5, 20, 40 ng∙kg−1∙min−1) were intravenously infused into five nonpregnant and five pregnant (105–140 days of gestation) ewes alone and during the simultaneous infusion of sodium nitroprusside at doses sufficient to abolish the pressor effects of AngII. Mean arterial pressure (MAP) was increased from 80 ± 2 to a maximum of 121 ± 5 mmHg (1 mmHg = 133.3 Pa) in nonpregnant ewes (p < 0.01) and from 79 ± 2 to 116 ± 4 mmHg in pregnant ewes (p < 0.01) over the range of AngII infusion. MAP was unaltered during AngII plus nitroprusside infusion, averaging 78 ± 3 mmHg in nonpregnant ewes and 80 ± 2 mmHg in pregnant ewes. Basal ANF was higher (p < 0.01) in pregnant sheep than in nonpregnant sheep. With AngII infusion alone, plasma ANF was increased from 13 ± 2 to 42 ± 4 fmol/mL in nonpregnant ewes (p < 0.01) and from 23 ± 5 to 72 ± 16 fmol/mL in pregnant ewes (p < 0.01). However, during AngII plus nitroprusside infusion, the increases in plasma ANF observed were completely abolished in both nonpregnant and pregnant ewes. These results suggest that AngII does not have a direct stimulatory effect on ANF release but rather that the increase in plasma ANF is a consequence of the pressor effects of AngII. This response does not appear to be altered during ovine pregnancy.Key words: angiotensin II, atrial natriuretic factor, nitroprusside, mean arterial pressure.

Characterization of acute reversible systemic hypertension in a model of heme protein-induced renal injury

1999 ◽  
Vol 277 (1) ◽  
pp. F58-F65 ◽  
Author(s):  
David H. Warden ◽  
Anthony J. Croatt ◽  
Zvonimir S. Katusic ◽  
Karl A. Nath
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Vessel Wall ◽  
Heme Proteins ◽  
Blood Vessel Wall ◽  
Vasodilatory Response

In the glycerol model of renal injury we describe an acute rise in systemic arterial pressure which is attended by a reduced vasodilatory response to acetylcholine in vivo; vasodilatory responses to verapamil, however, were not impaired. Neither arginine nor sodium nitroprusside diminished this rise in blood pressure; N ω-nitro-l-arginine methyl ester (l-NAME) elevated basal mean arterial pressure and markedly blunted the rise in mean arterial pressure following the administration of glycerol. Aortic rings from the glycerol-treated rat demonstrate an impaired vasodilatory response to acetylcholine, an effect not repaired by arginine; the vasodilatory responses to nitric oxide donors, sodium nitroprusside and SIN-1, were also impaired; 8-bromo-cGMP, at higher doses, evinced a vasodilatory response comparable to that observed in the control rings. This pattern of responses was not a nonspecific effect of aortic injury, since aortic rings treated with mercuric chloride, a potent oxidant, displayed an impaired vasodilatory response to acetylcholine but not to sodium nitroprusside. We conclude that in the glycerol model of heme protein-induced tissue injury, there is an acute elevation in mean arterial pressure attended by impaired endothelium-dependent vasodilatation in vitro and in vivo. We suggest that the acute scavenging of nitric oxide by heme proteins depletes the blood vessel wall of its endogenous vasodilator and permeation of heme proteins into the blood vessel wall may contribute to such sustained effects as observed in vitro.

scholarly journals A brief report on the effects of vasoactive agents on peripheral venous waveforms in a porcine model

2020 ◽  
Vol 9 ◽  
pp. 204800402094085
Author(s):  
Monica Polcz ◽  
Kyle M Hocking ◽  
Devin Chang ◽  
Philip Leisy ◽  
Jenna H Sobey ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Piezoelectric Sensor ◽  
Waveform Analysis ◽  
Volume Status ◽  
Vasoactive Agents ◽  
Non Invasive ◽  
Pulmonary Capillary ◽  
Wedge Pressure

Objectives Non-invasive venous waveform analysis (NIVA) is a recently described, novel technique to assess intravascular volume status. Waveforms are captured with a piezoelectric sensor; analysis in the frequency domain allows for calculation of a “NIVA value” that represents volume status. The aim of this report was to determine the effects of vasoactive agents on the venous waveform and calculated NIVA values. Design Porcine experimental model. Setting Operating theatre. Participants A piezoelectric sensor was secured over the surgically exposed saphenous vein in eight anesthetized pigs. Main outcome measures NIVA value, pulmonary capillary wedge pressure (PCWP), and mean arterial pressure prior to and post intravenous administration of 150–180 µg of phenylephrine or 100 µg of sodium nitroprusside. Results Phenylephrine led to a decrease in NIVA value (mean 9.2 vs. 4.6, p < 0.05), while sodium nitroprusside led to an increase in NIVA value (mean 9.5 vs. 11.9, p < 0.05). Mean arterial pressure increased after phenylephrine ( p < 0.05) and decreased after sodium nitroprusside ( p < 0.05). PCWP did not change significantly after phenylephrine ( p = 0.25) or sodium nitroprusside ( p = 0.06). Conclusions Vasoactive agents lead to changes in non-invasively obtained venous waveforms in euvolemic pigs, highlighting a potential limitation in the ability to NIVA to estimate static volume in this setting. Further studies are indicated to understand the effects of vasoactive agents in the setting of hypovolemia and hypervolemia.

Differential baroreceptor reflex modulation by centrally infused angiotensin peptides

1992 ◽  
Vol 263 (1) ◽  
pp. R89-R94 ◽  
Author(s):  
M. J. Campagnole-Santos ◽  
S. B. Heringer ◽  
E. N. Batista ◽  
M. C. Khosla ◽  
R. A. Santos
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Baroreceptor Reflex ◽  
Reflex Modulation ◽  
Ang Ii ◽  
Average Ratio ◽  
Angiotensin Peptides ◽  
Reflex Bradycardia

The present study was designed to investigate the effect of intracerebroventricular (icv) and intravenous (iv) infusion of angiotensin (ANG)-(1-7), ANG III, and ANG II on the baroreceptor control of heart rate (BHR) in conscious rats. Reflex changes in HR were elicited by bolus iv injection of either phenylephrine or sodium nitroprusside before and within 1 and 3 h of icv infusion of ANG II (n = 10), ANG III (n = 9), ANG-(1-7) (n = 9), or saline (n = 9) at a rate of 3 nmol.7.5 microliter-1.h-1. In another group of animals (n = 23), iv infusion of the same amount of ANG peptides was carried out at a rate of 0.7 ml/h. The average ratio of changes in HR in beats per minute and changes in mean arterial pressure (MAP, mmHg) was used as an index of BHR sensitivity. ANG II and ANG III produced a significant increase in the basal levels of MAP, but only during the first hour of infusion (iv or icv). No significant changes in baseline HR were observed. ANG-(1-7) and saline infusion did not change basal levels of HR or MAP (iv or icv). ANG II (iv and icv) and ANG III (icv) caused a significant decrease in the BHR sensitivity for reflex bradycardia. In contrast, icv infusion of ANG-(1-7) induced a significant increase in BHR sensitivity for reflex bradycardia (-3.0 +/- 0.3, 1 h, and -2.8 +/- 0.1 beats.min-1.mmHg-1, 3 h vs. -2.1 +/- 0.2 beats.min-1.mmHg-1, before infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Intra-strain variations of baroreflex sensitivity in young Wistar-Kyoto rats

2009 ◽  
Vol 32 (6) ◽  
pp. 251 ◽  
Author(s):  
Vitor E Valenti ◽  
Caio Imaizumi ◽  
Luiz Carlos De Abreu ◽  
Eduardo Colombari ◽  
Monica A Sato ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Femoral Artery ◽  
Baroreflex Sensitivity ◽  
Abdominal Aortic ◽  
Aortic Artery ◽  
Wistar Kyoto ◽  
The Right

Purpose: To compare baroreflex sensitivity among conscious rats of the same strain. Methods: Male WKY rats (eight weeks old) were studied. Cannulas were inserted into the abdominal aortic artery through the right femoral artery to measure mean arterial pressure (MAP) and heart rate (HR). Baroreflex gain was calculated as the ratio between variation of HR in function of the MAP variation (?HR/?MAP) tested with a depressor dose of sodium nitroprusside (SNP, 50µg/kg, iv) and with a pressor dose of phenylephrine (PE, 8µg/kg, iv). We divided the rats into four groups: 1) Low bradycardic baroreflex (LB), BG between -1 and -2 bpm/mmHg tested with PE; 2) High bradycardic baroreflex (HB), BG < -2 bpm/mmHg tested with PE; 3) Low tachycardic baroreflex (LT), BG between -1 and -2 bpm/mmHg tested with SNP and; 4) High tachycardic baroreflex (HT), BG < -2 bpm/mmHg tested with SNP. Significant differences were considered for p < 0.05. Results: Approximately 82% of the rats presented reduced bradycardic reflex while 22 showed attenuated tachycardic reflex. No alterations were noted regarding basal MAP and HR, tachycardic and bradycardic peak and HR range. Conclusions: There was alteration in baroreflex sensitivity among rats of the same strain. Care should be taken when interpreting studies employing WKY as a control for the SHR.

ACTH, cortisol, and renin responses to arterial hypotension in sheep

1986 ◽  
Vol 251 (1) ◽  
pp. R18-R22
Author(s):  
C. E. Wood
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin ◽  
Renin Activity ◽  
Jugular Veins ◽  
Induced Hypotension ◽  
Posteriori Analysis ◽  
Carotid Arterial ◽  
Nitroprusside Infusion ◽  
A Posteriori Analysis

This study was designed to investigate adrenocorticotropin (ACTH), cortisol, and renin responses to nitroprusside-induced hypotension in adult sheep. Five sheep were surgically prepared with carotid arterial skin loops at least 1 yr before these experiments. After catheterization of the carotid arteries and external jugular veins the sheep were infused with nitroprusside intravenously at rates of 0, 10, 15, or 20 micrograms . kg-1 . min-1 for 10 min. Nitroprusside produced significantly dose-related decreases in mean arterial pressure and increases in heart rate, plasma ACTH and cortisol concentrations, and plasma renin activity. Hematocrit was significantly increased in the 10- and 20-micrograms . kg-1 . min-1 groups during nitroprusside, probably reflecting contraction of the spleen. After the end of the period of hypotension, hematocrit was significantly decreased in all nitroprusside infusion groups, probably reflecting transcapillary movement of fluid into the vascular space. A posteriori analysis of the data suggests that the ACTH response to nitroprusside infusion was better predicted by the nadir in mean arterial pressure and that the renin activity response was better predicted by the initial rate of decrease of mean arterial pressure during nitroprusside infusion.

Microcirculatory Basis for Nonuniform Flow Delivery with Intravenous Nitroprusside 

1999 ◽  
Vol 91 (3) ◽  
pp. 723-723 ◽  
Author(s):  
Shahzad S. Mustafa ◽  
Richard J. Rivers ◽  
Mary D. S. Frame
Keyword(s):  
Shear Stress ◽  
Mean Arterial Pressure ◽  
Wall Shear Stress ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Flow Distribution ◽  
Sprague Dawley ◽  
Wall Shear ◽  
Arteriolar Diameter

Background The purpose of this study was to determine the effects of systemic infusions of nitroglycerin and sodium nitroprusside on flow distribution and wall shear stress in the microcirculation. Methods With university approval, the cremaster muscle of 28 anesthetized (70 mg/kg pentobarbital given intraperitoneally) hamsters (Harlan Sprague Dawley: Syrian; weight, 121+/-11 g [mean +/- SDD) was observed using in vivo fluorescence microscopy. Arteriolar diameter, erythrocyte flux, and velocity were measured for a feed arteriole and its sequential branches. Observations were made during control (mean arterial pressure, 88+/-4 mm Hg) and after 30 min of intravenous delivery of sodium nitroprusside or nitroglycerin, titrated to decrease mean arterial pressure by 20 mm Hg. Results Sodium nitroprusside significantly dilated select upstream portions of the network (23+/-2.6 to 29+/-2.6 microm); no arterioles were dilated with nitroglycerin. Erythrocyte flux into the feed (i.e., inflow into the arteriolar network) and into the sequential branches (i.e., distribution within the network) were evaluated. With nitroglycerin, inflow decreased significantly from 1,560+/-335 to 855+/-171 cells/s, and flux into the branches decreased evenly. With sodium nitroprusside, inflow increased significantly to 2,600+/-918 cells/s, yet cells were "stolen" from upstream branches (a decrease from 425+/-67 to 309+/-87 cells/s in the first branch). Excess flow passed into a downstream "thorough-fare channel," significantly increasing flux from 347+/-111 to 761+/-246 cells/s. Wall shear stress decreased uniformly with nitroglycerin infusion, with a decrease in the feed from 8.8+/-2.5 to 6+/-1.7 dyn/cm2. With sodium nitroprusside, variable changes occurred that were location specific within the network. For instance, at the inflow point to the network, wall shear stress changed from 8.3+/-2.5 to 4.2+/-3.3 dyn/cm2. Conclusions Nitroglycerin infusion promoted homogeneity of flow. Sodium nitroprusside significantly increased the heterogeneity of flow within this arteriolar network; an anatomic location for steal induced by sodium nitroprusside is identified.

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