pituitrin has been researched along with Vasospasm--Intracranial* in 3 studies
1 review(s) available for pituitrin and Vasospasm--Intracranial
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Hyponatremia as a risk factor for microvascular spasm following subarachnoid hemorrhage.
Hyponatremia is a water-electrolyte balance disorder diagnosed in about 30% of patients after subarachnoid hemorrhage (SAH). The main factors responsible for hyponatremia in these patients are increased plasma concentrations of either vasopressin (leading to water retention and dilutional hyponatremia) or natriuretic peptides (leading to plasma sodium ions deficiency). Data demonstrates that the leading causes of post-SAH disability - delayed cerebrovascular spasm (CVS) and delayed cerebral ischemia (DCI) - are more often diagnosed in patients who develop hyponatremia than in normonatremic patients with SAH. Data also indicates that reducing sodium ion concentration in the blood/perfusate affects the tone and regulation of cerebral blood vessels in a manner that depends on the vessel's location in a vascular tree (intraparenchymal arterioles vs. large vessels on the brain surface) and environmental conditions. In the present article, we review possible mechanisms underlying the effects of hyponatremia on cerebral blood vessels and discuss the potential role of hyponatremia in the development of large vessels and microvascular spasm, taking into consideration the presence of vasopressin and natriuretic peptides. Topics: Brain Ischemia; Humans; Hyponatremia; Natriuretic Peptides; Risk Factors; Sodium; Spasm; Subarachnoid Hemorrhage; Vasopressins; Vasospasm, Intracranial | 2022 |
2 other study(ies) available for pituitrin and Vasospasm--Intracranial
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Failure of Induced Hypertension for Symptomatic Vasospasm in the Setting of Clozapine Therapy.
Hemodynamic augmentation is utilized as a treatment in the setting of symptomatic cerebral vasospasm. This approach includes the use of vasopressors to induce hypertension with the aim of improved cerebral blood flow. Agents with potent alpha-1 antagonism properties, including clozapine, can inhibit or blunt the response of several vasopressor agents.. Case report.. A 54-year-old schizophrenic male with an aneurysmal subarachnoid hemorrhage required hemodynamic augmentation in which several vasopressor trials resulted in no or poor response. The addition of epinephrine resulted in a decrease of mean arterial pressure. Vasopressin initiation demonstrated an immediate vasopressor effect.. Vasopressors are an important treatment modality in symptomatic cerebral vasospasm. This case highlights the potential for clozapine to blunt the effects of vasopressors; or in the case of epinephrine, it causes a reversal effect. Vasopressin may be considered an agent of choice in patients who have recently taken clozapine and require hemodynamic augmentation. Topics: Clozapine; Drug Interactions; Epinephrine; GABA Antagonists; Humans; Hypertension; Intracranial Aneurysm; Male; Middle Aged; Schizophrenia; Subarachnoid Hemorrhage; Vasoconstrictor Agents; Vasopressins; Vasospasm, Intracranial | 2015 |
Enhanced reactivity to vasopressin in rat basilar arteries during vasospasm after subarachnoid hemorrhage.
Subarachnoid hemorrhage increases the plasma level of vasopressin, a well-known vasoconstrictor. We examined the sensitivity to vasopressin in rat basilar artery after subarachnoid hemorrhage using a rat subarachnoid hemorrhage model. Vasospasm was observed 1-2 days after subarachnoid hemorrhage induction, and the contractile response to vasopressin in rat basilar arteries was assessed. The concentration-response curve for vasopressin in subarachnoid hemorrhage (1 day) rats shifted leftward compared with that of control rats. The concentration-response curve for vasopressin V(1) receptor agonist also shifted leftward and upward compared with that of control rats. The concentration-response curve for vasopressin was inhibited not by vasopressin V(2) receptor antagonist but by vasopressin V(1) receptor antagonist. Thus, it was demonstrated that the vasoconstricting effect of vasopressin was significantly enhanced in the vasospasm phase after subarachnoid hemorrhage. Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Basilar Artery; Dose-Response Relationship, Drug; Endothelium, Vascular; In Vitro Techniques; Male; Morpholines; Oxytocin; Potassium Chloride; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Spiro Compounds; Subarachnoid Hemorrhage; Time Factors; Vasoconstriction; Vasoconstrictor Agents; Vasopressins; Vasospasm, Intracranial | 2005 |