Vasoactive Intestinal Peptide in Shock and Heart Failure

The physiological properties of VIP suggest that the increased plasma concentrations in patients with heart failure contribute to restore the compromised haemodynamic balance either by improving myocardial performance or by counteracting the harmful effects related to simultaneous activation of other neuroendocrine systems, i.e. the sympathetic and renin-angiotensin systems. Decreased VIP concentrations are related to progressive worsening of heart failure. The higher VIP concentrations in elderly patients compared with healthy controls suggest that the capacity to increase VIP production is preserved in older people.

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“…, 2000). Clark et al . (1983) found an increase of plasma VIP in eight patients with severe cardiac failure secondary to ischaemic heart disease.…”

Section: Discussionmentioning

confidence: 99%

“…, 1978; Francis et al ., 1988; Francis, 1991; Packer, 1992). The physiological properties of VIP have suggested that this peptide could also contribute to improvement of the compromised haemodynamic balance (Clark et al ., 1983; Edvinsson et al. , 1990; Nicholls et al ., 1992; Onuoha et al.…”

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confidence: 99%

Vasoactive intestinal peptide (VIP): a new neuroendocrine marker of clinical progression in chronic heart failure?

Lucia

Caiola

Coppola

et al. 2003

Clinical Endocrinology

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“…Therefore, VIP may have a beneficial effect in the treat ment of hemorrhagic shock, either by modu lating mast cell degranulation, or through its cardiovascular effects. Clark et al [1983] and Ottesen et al [1985] have reported that VIP has systemic vasodilator and positive inotropic actions, and that its infusion into dogs enhances cardiac output by up to 40%. These properties of VIP may be very impor tant for the restoration of tissue blood flow and of arterial blood pressure, especially when the sympathetic reflexes are maximally activated, as in severe hemorrhage.…”

Section: Discussionmentioning

confidence: 99%

Mast Cell Degranulation in Hemorrhagic Shock in Rats and the Effects of Vasoactive Intestinal Peptide, Aprotinin and H<sub>1</sub> and H<sub>2</sub>-Receptor Blockers on Degranulation

Tıkız¹,

Tunçel²,

Gürer

et al. 1991

Pharmacology

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Various stressful stimuli cause mast cell degranulation. Hemorrhagic shock is one such stressful stimulus which may cause mast cell degranulation and histamine release. Histamine may be involved in the pathophysiology of hemorrhage. It was reported that there are large amounts of histamine in the anterior and posterior lobes of the pituitary and the adjacent median eminence of the hypothalamus. Most of the histamine in the posterior pituitary is in mast cells. In addition, both vasoactive intestinal peptide (VIP) and histamine-containing neurons are available in the hypothalamus. It therefore seems reasonable to suppose that these three systems (i.e., mast cells, VIP-containing neurons, and histamine-containing neurons) may play an important role in the progression of hemorrhagic shock. 66 albino rats (200–250 g) of either sex were used. The presence of mast cells was examined by light microscopy. Hemorrhage caused mast cell degranulation in a correlation with the amount of blood loss. In all cases, the most intense degranulation was observed in the hypothalamus, especially the nucleus arcuatus, and in the subcutaneous tissue. The intensity of degranulation gradually decreased in the peripheral blood vessel, peritoneum and omentum, in this order. VIP prevented degranulation, but aprotinin and H₁ and H₂ receptor blockers did not.

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“…Plasma concentrations of VIP were increased in severe hepatic failure23 and cardiac failure2425 but unchanged in patients with circulatory shock24 or myocardial infarction. 24 Patients with heart transplants show abnormal circulating concentrations or circadian rhythmicity or both of the hormones responsible for the regulation of the cardiovascular system.26…”

Section: Introductionmentioning

confidence: 99%

Lack of circadian rhythm of plasma concentrations of vasoactive intestinal peptide in patients with orthotopic heart transplants.

Cugini

Lucia²,

Scibilia³

et al. 1993

Heart

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Objective-To study the circadian pattern of plasma concentrations of vasoactive intestinal peptide (VIP) in patients with orthotopic heart transplants. Circulating VIP is known to have neural and immunological sources. Patients and methods-13 patients with orthotopic heart transplants were studied 12-53 months (mean 318 months) after operation. All were haemodynamically compensated and had no histological evidence of rejection. They were being treated with cyclosporin, azathioprine, and prednisone. Ten healthy individuals were studied as controls. Circulating VIP was assayed six times within a 24h period. Time qualified data were analysed by ANOVA and the cosinor method. Student's t test for unpaired data and Bingham's test for cosinorderived parameters were used for statistical comparisons. Results-Plasma concentrations of VIP were lower in the patients with orthotopic heart transplants than in the controls (p < 0.001). ANOVA and the cosinor method respectively showed a statistically significant within-day variability and circadian rhythm in the controls but not in the patients with heart transplants.Discussion-The low plasma concentrations of VIP in the patients with heart transplants could be the result of the lack of contribution by the cardiac VlPergic fibres, a reduction of VIP release by the pharmacologically suppressed immune system, the inhibitory effects of cyclosporin on neural fimction and humoral secretions, and the effects of negative feedback on VIP release of high concentrations of atrial natriuretic peptide. The lack of the circadian rhythm suggests a structural disorder, which should be firther investigated. (Br HeartrJ 1993;70:363-365) Vasoactive intestinal peptide (VIP) is widely distributed throughout the central and peripheral nervous system where it acts as a neurotransmitter or neuromodulator or both.1-11 The cardiovascular system of various mammalian species is innervated by VIP fibres, which are more dense in the sinoatrial node, atrioventricular node, atrial myocardium, and epicardial coronary arteries and less dense in the ventricular myo-cardium.12-"5 The physiological role of endo-genous VIP in the cardiovascular system has not been clearly established. In adult animals and humans intravenous VIP causes vasodilatation of the systemic and coronary arteries and has positive inotropic and chronotropic effects.l6-22VIP is assumed to be a neurotransmitter rather than a bloodborne hormone and its circulating concentrations probably represent an overflow of the neuronal release. Plasma concentrations of VIP were increased in severe hepatic failure23 and cardiac failure2425 but unchanged in patients with circulatory shock24 or myocardial infarction.24Patients with heart transplants show abnormal circulating concentrations or circadian rhythmicity or both of the hormones responsible for the regulation of the cardiovascular system.26In the present study we investigated the hypothesis that, like other vasoactive peptides, VIP release is also impaired. We used a chronobiological prot...

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Vasoactive Intestinal Peptide in Shock and Heart Failure

Cited by 18 publications

References 4 publications

Vasoactive intestinal peptide (VIP): a new neuroendocrine marker of clinical progression in chronic heart failure?

Vasoactive intestinal peptide (VIP): a new neuroendocrine marker of clinical progression in chronic heart failure?

Mast Cell Degranulation in Hemorrhagic Shock in Rats and the Effects of Vasoactive Intestinal Peptide, Aprotinin and H<sub>1</sub> and H<sub>2</sub>-Receptor Blockers on Degranulation

Lack of circadian rhythm of plasma concentrations of vasoactive intestinal peptide in patients with orthotopic heart transplants.

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