Effects of Sodium Nitroprusside (Nipruss) in Addition to Volume Administration in Shock States Associated with Increased Total Peripheral Vascular Resistance

Nitrates III ◽  
1981 ◽  
pp. 577-581
Author(s):  
F. W. Schmahl ◽  
M. Frank ◽  
H. Heckers ◽  
B. Urbaschek
Keyword(s):  
Sodium Nitroprusside ◽  
Vascular Resistance ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Total Peripheral Vascular Resistance

Cardiovascular actions of beta-phenylethylamine

1979 ◽  
Vol 236 (4) ◽  
pp. H592-H595
Author(s):  
C. S. Liang ◽  
D. Sprecher
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Peripheral Vascular Resistance ◽  
Adrenergic Nerve ◽  
Peripheral Vascular ◽  
Vascular Effects ◽  
Aortic Blood ◽  
Total Peripheral Vascular Resistance ◽  
Aortic Blood Pressure

beta-Phenylethylamine increased mean aortic blood pressure, total peripheral vascular resistance, left ventricular dP/dt, and (dP/dt)/P in chloralose-anesthetized dogs. Pretreatment with phentolamine reduced the increases in aortic blood pressure and total peripheral vascular resistance produced by beta-phenylethylamine, whereas, the effects of beta-phenylethylamine on left ventricular dP/dt and (dP/dt)/P were abolished by propranolol. beta-Phenylethylamine pretreatment, but increased both after phentolamine pretreatment. Furthermore, both the cardiac and vascular effects of beta-phenylethylamine were abolished by desipramine. These results indicate that beta-phenylethylamine exerts both positive inotropic and vasoconstrictory effects, probably by releasing endogenous norepinephrine from the adrenergic nerve endings.

scholarly journals Features of changes in volume-impedance hemodynamic indicators during the tilt test in young males with a history of vasovagal syncopes

Kardiologiia ◽  
2019 ◽  
Vol 59 (11) ◽  
pp. 31-38
Author(s):  
A. V. Barsukov ◽  
O. G. Chepcheruk ◽  
D. V. Glukhovskoi ◽  
V. V. Yakovlev ◽  
A. V. Gordienko
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Negative Response ◽  
Peripheral Vascular Resistance ◽  
Tilt Test ◽  
Peripheral Vascular ◽  
Total Peripheral Vascular Resistance ◽  
History Of ◽  
Group 3 ◽  
Group 1

Background. The direction of changes in hemodynamic parameters during the tilt test (TT) nin individuals with history of vasovagal syncope (VVS) is a subject of discussion. Objective: to study changes of volume-impedance hemodynamic indicators in the process of tilt test in somatically healthy young men with history of VVS. Materials and methods. A total of 102 men aged 18–30 years were divided into 4 groups, taking into account the specific features of fainting history and response to TT. Persons of group 1 (n=14) had history of VVS and positive response to TT (syncope). Subjects of group 2 (n=14) had history of VVS and a pattern of postural tachycardia without fainting during TT. Persons of group 3 (n=42) had history of VVS and negative response to TT. Subjects of group 4 (n=32) had no history of VVS and negative response to TT. During TT, we studied dynamics of some indicators, including cardiac output (CO) and total peripheral vascular resistance (TPVR). Results. In individuals of all groups in the initial horizontal phase of TT values of CO and TPVR corresponded to the norm. Subjects of group 1 had significantly lower CO compared with subjects of groups 2, 3, 4 (p<0.05, p<0.01, p<0.05, respectively). Values of TPVR in subjects of group 1 were significantly higher than in subjects of groups 2, 3, 4 (p<0.05; p<0.05; p<0.05, respectively). In response to orthostasis CO values increased in groups 1, 2, 4 (by 18%, 10%, 5%, respectively) and did not change in group 3; TPVR values decreased in groups 1, 2 (by 8%, 0.5%, respectively), and increased in groups 3, 4 (by 8%, 4% respectively). In the final horizontal phase of TT, CO values in group 1 were significantly lower than in groups 3, 4 (p<0.05), while TPVR values did not significantly differ between all groups (p>0.05). Conclusions. In tilt-positive and tilt-negative subjects with history of VVS, standardized postural stress leads to unidirectional changes in cardiac output, but to multidirectional changes in total peripheral vascular resistance.

scholarly journals Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients

2001 ◽  
pp. 339-346 ◽  
Author(s):  
MJ Diekman ◽  
MP Harms ◽  
E Endert ◽  
W Wieling ◽  
WM Wiersinga
Keyword(s):  
Vascular Resistance ◽  
Linear Regression Analysis ◽  
Plasma Concentrations ◽  
Peripheral Vascular Resistance ◽  
Thyroid Function Tests ◽  
Peripheral Vascular ◽  
Endothelin 1 ◽  
Euthyroid State ◽  
Total Peripheral Vascular Resistance ◽  
Hypothyroid Patients

OBJECTIVE: Total peripheral vascular resistance (TPR) decreases in thyrotoxicosis and increases in hypothyroidism. Several mechanisms may be involved, including adaptation to changes in heat production and direct non-genomic effects of tri-iodothyronine (T3) on vascular smooth muscle cells. The aim of this study was to see if changes in TPR are related to changes in plasma concentrations of the endothelial hormones adrenomedullin and endothelin-1 as well as other hormones affecting vasculature. DESIGN: A prospective study. SUBJECTS: Eleven hypothyroid patients (pretreatment: thyroid-stimulating hormone (TSH) 68 (38-201) mU/l, T3 0.7 (0.35-1.5) nmol/l, fT4 3.0 (2.0-5.9) pmol/l, median (range)) and 14 with hyperthyroidism (pretreatment: TSH 0.02 (<0.01-0.06) mU/l, T3 6.4 (2.3-13.0) nmol/l, fT4 56.1 (22.9-70.0) pmol/l) were studied before treatment and 3 months after reaching the euthyroid state. Blood collection was carried out simultaneously with the recording of finger arterial pressure (FINAP). Cardiac output and TPR were derived from stroke volume computations by modelling flow from the FINAP signal. RESULTS: Thyroid-function tests of hypothyroid and thyrotoxic patients did not differ after restoration of the euthyroid state. TPR, expressed in arbitrary units (AU), decreased after correction of hypothyroidism (from 1.32+/-0.65 to 0.96+/-0.36 AU, P=0.04) and increased after correction of hyperthyroidism (from 0.75+/-0.18 to 1.10+/-0.35 AU, P=0.007). Adrenomedullin concentrations did not change during the transition from the hypothyroid state 3.2(0.9-11.0) pmol/l to the euthyroid state 4.9(0.9-8.6) pmol/l, but decreased after treatment of hyperthyroidism, from 5.2(0.9-11.0) pmol/l to 2.2(0.9-5.4) pmol/l. Plasma endothelin-1 was undetectable in all samples. Changes in TPR upon treatment correlated with log DeltafT4 (r=-0.65, P=0.001), log DeltaT3, (r=-0.57, P=0.006), Delta noradrenaline (r=0.54, P=0.02) and Delta ANP (atrial natriuretic peptide) (r=-0.59, P=0.004). Multiple linear regression analysis indicated that only T3 was an independent determinant of TPR. Changes in T3 accounted for 46% of the variability in the changes in TPR. CONCLUSIONS: TPR is reduced in thyrotoxicosis and increased in hypothyroidism. Restoration of the euthyroid state normalizes TPR. Changes in TPR are not related to plasma adrenomedullin concentrations, but 46% could be explained by changes in T3. Altered ANP secretion and adrenergic tone may contribute to the T3-induced changes in TPR.

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