Adaptive fuzzy neural control of mean arterial pressure through sodium nitroprusside infusion

Author(s):  
Yang Gao ◽  
Aleng Joo Er
1995 ◽  
Vol 73 (5) ◽  
pp. 644-650 ◽  
Author(s):  
L. Fan ◽  
D. Javeshghani ◽  
S. Mukaddam-Daher ◽  
Z. Guan ◽  
B. S. Nuwayhid ◽  
...  

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.


2004 ◽  
Vol 53 (12) ◽  
pp. 4087
Author(s):  
Tan Wen ◽  
Wang Yao-Nan

1999 ◽  
Vol 277 (1) ◽  
pp. F58-F65 ◽  
Author(s):  
David H. Warden ◽  
Anthony J. Croatt ◽  
Zvonimir S. Katusic ◽  
Karl A. Nath

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.


2020 ◽  
Vol 9 ◽  
pp. 204800402094085
Author(s):  
Monica Polcz ◽  
Kyle M Hocking ◽  
Devin Chang ◽  
Philip Leisy ◽  
Jenna H Sobey ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document