The effects of noradrenaline, B‐HT 920, methoxamine, angiotensin II and vasopressin on mean circulatory filling pressure in conscious rats

Pang, Catherine C.Y.; Tabrizchi, Reza

doi:10.1111/j.1476-5381.1986.tb10272.x

Cited by 59 publications

(24 citation statements)

References 23 publications

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“…It has previously been shown by Guyton et al that infusion of epinephrine significantly increases Pmsf to a plateau value around 16 mmHg (8). This has been confirmed experimentally by numerous authors who have shown in animals that norepinephrine and other ␣-adrenoreceptor agonists increase Pmsf (18,21,29). The reason why we found a slight inverted relation between age and Pmsf is unclear but remains to be confirmed since only 19 patients of our cohort were Ͻ50 years old.…”

Section: Discussionsupporting

confidence: 71%

Value and determinants of the mean systemic filling pressure in critically ill patients

Repessé

Charron

Fink

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Mean systemic filling pressure (Pmsf) is a major determinant of venous return. Its value is unknown in critically ill patients (ICU). Our objectives were to report Pmsf in critically ill patients and to look for its clinical determinants, if any. We performed a prospective study in 202 patients who died in the ICU with a central venous and/or arterial catheter. One minute after the heart stopped beating, intravascular pressures were recorded in the supine position after ventilator disconnection. Parameters at admission, during the ICU stay, and at the time of death were prospectively collected. One-minute Pmsf was 12.8 ± 5.6 mmHg. It did not differ according to gender, severity score, diagnosis at admission, fluid balance, need for and duration of mechanical ventilation, or length of stay. Nor was there any difference according to suspected cause of death, classified as shock (cardiogenic, septic, and hemorrhagic) and nonshock, although a large variability of values was observed. The presence of norepinephrine at the time of death (102 patients) was associated with a higher 1-min Pmsf (14 ± 6 vs. 11.4 ± 4.5 mmHg), whereas the decision to forgo life-sustaining therapy (34 patients) was associated with a lower 1-min Pmsf (10.9 ± 3.8 vs. 13.1 ± 5.3 mmHg). In a multiple-regression analysis, norepinephrine (β = 2.67, P = 0.0004) and age (β = −0.061, P = 0.022) were associated with 1-min Pmsf. One-minute Pmsf appeared highly variable without any difference according to the kind of shock and fluid balance, but was higher with norepinephrine.

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Section: Discussionsupporting

confidence: 71%

Value and determinants of the mean systemic filling pressure in critically ill patients

Repessé

Charron

Fink

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…noradrenaline, angiotensin II as well as angiotensin III (Pang & Tabrizchi, 1986;Tabrizchi & Pang, 1987; were found in similar studies in our laboratory to raise MAP and MCFP dose-dependently. Therefore, the absence of a rise in MCFP in the present study is not due to a lack of sensitivity of the technique to detect changes.…”

Section: Discussionsupporting

confidence: 50%

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Wang

Lim

Pang

1995

British J Pharmacology

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1 The effects of the nitric oxide (NO) synthase inhibitor, N0-nitro-L-arginine methyl ester (L-NAME), on mean circulatory filling pressure (MCFP), total peripheral resistance (TPR), cardiac output (CO) and resistance to venous return (Rv) were studied in rats.2 In conscious, unrestrained rats, L-NAME (0.5-16mgkg-') dose-dependently increased mean arterial pressure (MAP) but not MCFP, an inverse index of venous compliance, either in the absence or presence of the ganglionic blocker mecamylamine (10mgkg-'). 3 In pentobarbitone-anaesthetized rats, L-NAME (2, 4, 8 mg kg-') increased MAP and reduced CO in a dose-related manner but did not change MCFP. TPR (+ 84, + 140 and + 192%) as well as R, (+ 62, +72, +110%) were dose-dependently increased by L-NAME. 4 Our results show that L-NAME reduces CO by increasing arterial as well as venous resistances. L-NAME does not affect MCFP.

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“…Prazosin was also found to reduce MCFP in an anesthetized, open-chest dog preparation, but only during infusion of norepinephrine (Ito and Hirakawa, 1984). Selective ␣ 1 -adrenergic agonists produce little increase in MCFP when infused into intact rats, whereas norepinephrine produces a potent, dose-dependent increase in MCFP (Pang and Tabrizchi, 1986). Studies in isolated mesenteric veins confirm that activation of ␣ 1 -adrenergic receptors may be necessary to observe a venoconstrictor effect of ␣ 2 -adrenergic receptors in some vascular beds.…”

mentioning

confidence: 54%

The Serotonin 5-Hydroxytryptaphan_1A Receptor Agonist, (+)8-Hydroxy-2-(di-n-propylamino)-tetralin, Stimulates Sympathetic-Dependent Increases in Venous Tone during Hypovolemic Shock

Tiniakov¹,

Scrogin²

2006

J Pharmacol Exp Ther

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Adjuvant treatment of hypovolemic shock with vasoconstrictors is controversial due to their propensity to raise arterial resistance and exacerbate ischemia. A more advantageous therapeutic approach would use agents that also promote venoconstriction to augment perfusion pressure through increased venous return. Recent studies indicate that 5-hydroxytryptophan (5-HT) 1A receptor agonists increase blood pressure by stimulating sympathetic drive when administered after acute hypotensive hemorrhage. Given that venous tone is highly dependent upon sympathetic activation of ␣ 2 -adrenergic receptors, we hypothesized that the 5-HT 1A receptor agonist, (ϩ)8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), would increase venous tone in rats subject to hypovolemic shock through sympathetic activation of ␣ 2 -adrenergic receptors. Systemic administration of 8-OH-DPAT produced a sustained rise in blood pressure (ϩ44 Ϯ 3 mm Hg 35 min after injection, P Ͻ 0.01 versus saline) and mean circulatory filling pressure (ϩ4.2 Ϯ 0.7 mm Hg, P Ͻ 0.01 versus saline) in conscious rats subjected to hypovolemic shock. An equipressor infusion of epinephrine failed to influence mean circulatory filling pressure (MCFP). Ganglionic blockade, ␣ 1 -, or peripheral ␣ 2 -adrenergic receptor blockade prevented the rise in MCFP observed with 8-OH-DPAT, but only ␣ 1 -adrenergic receptor blockade diminished the pressor effect of the drug (P Ͻ 0.01). 8-OH-DPAT raises blood pressure in rats in hypovolemic shock through both direct vascular activation and sympathetic activation of ␣ 1 -adrenergic receptors. The sympathoexcitatory effect of 8-OH-DPAT contributes to elevated venous tone through concurrent activation of both ␣ 1 -and ␣ 2 -adrenergic receptors. The data suggest that 5-HT 1A receptor agonists may provide an advantageous alternative to currently therapeutic interventions used to raise perfusion pressure in hypovolemic shock.

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The effects of noradrenaline, B‐HT 920, methoxamine, angiotensin II and vasopressin on mean circulatory filling pressure in conscious rats

Cited by 59 publications

References 23 publications

Value and determinants of the mean systemic filling pressure in critically ill patients

Value and determinants of the mean systemic filling pressure in critically ill patients

Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

The Serotonin 5-Hydroxytryptaphan_1A Receptor Agonist, (+)8-Hydroxy-2-(di-n-propylamino)-tetralin, Stimulates Sympathetic-Dependent Increases in Venous Tone during Hypovolemic Shock

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The effects of noradrenaline, B‐HT 920, methoxamine, angiotensin II and vasopressin on mean circulatory filling pressure in conscious rats

Cited by 59 publications

References 23 publications

Value and determinants of the mean systemic filling pressure in critically ill patients

Value and determinants of the mean systemic filling pressure in critically ill patients

Increase by NG‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

The Serotonin 5-Hydroxytryptaphan1A Receptor Agonist, (+)8-Hydroxy-2-(di-n-propylamino)-tetralin, Stimulates Sympathetic-Dependent Increases in Venous Tone during Hypovolemic Shock

Contact Info

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Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

The Serotonin 5-Hydroxytryptaphan_1A Receptor Agonist, (+)8-Hydroxy-2-(di-n-propylamino)-tetralin, Stimulates Sympathetic-Dependent Increases in Venous Tone during Hypovolemic Shock