neuropeptide-y and Shock

Topics: Animals; Atrial Natriuretic Factor; Calcitonin Gene-Related Peptide; Endothelins; Humans; Neuropeptide Y; Shock; Vasoactive Intestinal Peptide

We recently showed that intravenous sodium nitroprusside treatment (SNP) could relieve the pulmonary vasospasm of pulmonary embolism (PE) and non-pulmonary embolism (non-PE) regions in a rabbit massive pulmonary embolism (MPE) model associated with shock. The present study explored the potential role of cardiopulmonary sympathetic activity on the pathogenesis and the impact of vasodilators on cardiopulmonary sympathetic activity in this model.. Rabbits were randomly divided into sham operation group (S group, n = 8), model group (M, equal volume of saline intravenously, n = 11), SNP group (3.5 μg/kg/min intravenously, n = 10) and diltiazem group (DLZ, 6.0 μg/kg/min intravenously, n = 10).. MPE resulted in reduced mean arterial pressure and increased mean pulmonary arterial pressure as well as reduced PaO. Present results indicate that upregulation of the sympathetic medium transmitters TH and NPY in whole lung tissues serves one of the pathological features of MPE. The vasodilators SNP and DLZ could relieve pulmonary vasospasm in both embolization and non-embolization regions and reverse circulatory shock, thereby indirectly downregulating the sympathetic activation of the whole lung tissues and breaking a vicious cycle related to sympathetic activation in this model.

Topics: Animals; Neuropeptide Y; Pulmonary Embolism; Rabbits; Random Allocation; Shock; Sympathetic Nervous System; Tyrosine 3-Monooxygenase; Vasodilator Agents

Topics: Animals; beta-Endorphin; Calcitonin; Calcium; Guinea Pigs; Histamine; Immunoenzyme Techniques; Male; Neuropeptide Y; Neurotensin; Shock; Substance P; Thyroid Gland; Vasoactive Intestinal Peptide

Neuropeptide Y is co-stored with noradrenaline in peripheral sympathetic nerves, but is not present in the adrenal chromaffin cells in the pig. Plasma levels of neuropeptide Y-like immunoreactivity and catecholamines were studied upon haemorrhagic shock in the anaesthetized pig. The animals were bled in two successive steps (30 and 10 ml kg-1), resulting in a reduction of the mean arterial blood pressure by 44% and 53%, respectively. Plasma levels of noradrenaline increased abruptly after the first bleeding from 1.21 +/- 0.27 to 26.5 +/- 6.3 nmol l-1. Plasma neuropeptide Y showed a progressive increase from 62 +/- 8 pmol l-1 in the basal state to 365 +/- 98 pmol l-1 at 60 min after the first bleeding. After the second bleeding plasma neuropeptide Y and noradrenaline showed a largely parallel increase and finally reached levels of 2524 +/- 580 pmol l-1 and 316 +/- 117 nmol l-1, respectively. A veno-arterial gradient of neuropeptide Y and noradrenaline indicating local release was present over the spleen after both bleeding steps. The overflow of neuropeptide Y was delayed about 15 min compared to noradrenaline after the initial bleeding. Depletion of the neuropeptide Y content after shock in the heart and skeletal muscle supported local release also from these organs. Infusions of neuropeptide Y to obtain similar plasma concentrations as during shock (nM range) caused reduction in blood flow as determined by the radionuclide-labelled microsphere technique in several organs including spleen and skeletal muscle (threshold response at 319 +/- 22 pmol l-1) but not in heart and brain. In conclusion, both neuropeptide Y and noradrenaline were markedly elevated in plasma upon haemorrhagic shock, suggesting release from sympathetic nerve terminals. Neuropeptide Y could therefore have a role as a sympathetic neurotransmitter, and during severe stress, circulating plasma levels are in the range where vasoconstriction is evoked by exogenous NPY.

Topics: Animals; Epinephrine; Heart Rate; Neuropeptide Y; Norepinephrine; Shock; Swine; Sympathetic Nervous System; Vascular Resistance; Vasoconstriction