5 hydroxytryptamine/hemorrhage

Peri-aneurysmal CSF was obtained at operation from 13 patients with subarachnoid haemorrhage from ruptured intracranial aneurysms. The 5-hydroxytryptamine antagonist ketanserin inhibited contractions of isolated human intracranial arteries, elicited by this CSF. The presence of 5-HT in CSF was

The reactivity of rabbit basilar artery to norepinephrine and 5-hydroxytryptamine was tested in vitro three days following cisternal injection of 1.0 ml autologous blood to simulate subarachnoid hemorrhage. Following this treatment the artery became three to five times more sensitive to

The circular contractile responses to various stimuli have been measured in segments of cerebral arteries (both middle cerebral and basilar) taken from dogs either 3 or 7 days following the cisternal injection of autologous blood under anaesthesia. The maximum contractile response to

The biogenic amine, radioactive 5-hydroxytryptamine, is removed from the blood during passage through the pulmonary vasculature. After one hour of hemorrhagic shock, the extraction rate increased from 74 to 89 per cent. One and two hours after resuscitation, the lung extracted only 30 per cent of

BACKGROUND Chloroquine inhibits platelet aggregation in vitro and in vivo. Because inhibition of platelet aggregation may prolong bleeding time, the effect of chloroquine administration on bleeding time and disappearance of platelet serotonin, which may affect bleeding time, were

Concentrations of monoamines and metabolites and uric acid were measured in sequential 15-min microdialysis samples taken from the area of the supraoptic nucleus (SON) in 9 urethane-anaesthetized rats. A decrease in blood pressure of 40 mm Hg was induced by withdrawing 3-4 ml of blood from an

OBJECTIVE Endothelial dysfunction is claimed to play a role in the pathogenesis of delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). We have examined the effect of experimental SAH on the modulatory action of endothelial and nonendothelial nitric oxide (NO) in the contractile response

OBJECTIVE Delayed cerebral ischemia after subarachnoid hemorrhage (SAH) remains a major cause of death and disability. It has been hypothesized that cerebrovascular upregulation of vasoconstrictor receptors is a key step in the development of delayed cerebral ischemia. Upregulation of endothelin-B

In the present work we studied the levels of 5-HT in the pericardial fluid of 160 cadavers according to cause of death; such as myocardial infarction, violent asphyxia, pulmonary embolism, infections, bronchopulmonary diseases, traumatic and hemorrhagic diseases in the CNS, and multiple traumatism.