pituitrin and Spasm

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

After its reintroduction as an arterial graft in coronary artery surgery, the radial artery is now established as an alternative arterial conduit, with good early and midterm patency. However, because of the concern about its vasospasticity, numerous vasodilator strategies have been used. Recently the use of the irreversible alpha-adrenergic antagonist phenoxybenzamine has been proposed. Although this treatment is effective in eliminating the vasoconstriction mediated by noradrenaline, the contribution of other circulating vasoconstrictors to vasospasm could be as important. This study investigates the response of radial arteries treated with phenoxybenzamine to vasoconstrictor stimuli and possible preventative strategies.. In vitro, sections of radial artery, pretreated with phenoxybenzamine after harvesting, were stimulated with maximal concentrations of the vasoconstrictors noradrenaline, vasopressin, angiotensin II, KCl, and endothelin-1. In matched segments of artery, vasoconstrictor responses were recorded in the presence of diltiazem, glyceryl trinitrate, and papaverine and compared with phenoxybenzamine-treated samples.. Phenoxybenzamine-treated radial artery failed to respond to noradrenaline but did respond to vasopressin, angiotensin II, endothelin-1, and KCl. Diltiazem was largely ineffective against contractile stimuli apart from KCl. Glyceryl trinitrate and papaverine significantly reduced responses to all of the vasoconstrictors tested.. In phenoxybenzamine-treated sections of radial artery, circulating vasoconstrictor agonists may still contribute to the induction of spasm. Additional vasodilator strategies may be required to completely prevent vasospasm.

Topics: Adrenergic alpha-Agonists; Aged; Angiotensin II; Coronary Artery Bypass; Diltiazem; Dose-Response Relationship, Drug; Endothelin-1; Humans; Middle Aged; Nitroglycerin; Norepinephrine; Papaverine; Peripheral Vascular Diseases; Phenoxybenzamine; Phosphodiesterase Inhibitors; Radial Artery; Spasm; Time Factors; Treatment Outcome; Vasoconstriction; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

One hundred patients affected by S.A.H. have been studied, evaluating the possible correlations between clinical findings and hyponatremia. For a better understanding of hyponatremia during S.A.H., the hematic concentration of A.D.H. and A.N.P. have been determined and correlated with hyponatremia.

Topics: Atrial Natriuretic Factor; Cerebral Arterial Diseases; Female; Humans; Hyponatremia; Male; Prognosis; Spasm; Subarachnoid Hemorrhage; Vasopressins

1. Prostaglandin E(1) (PGE(1)) increased the responses of guinea-pig myometrium in a low calcium medium to added Ca(2+), acetylcholine, vasopressin, Ba(2+) and Sr(2+). The concentration of PGE(1) used (50 pg/ml) was clearly below the threshold for direct spasmogenesis. In the presence of PGE(1) the doses necessary for half-maximal contractions were decreased by factors of 2.6 for Ca(2+), 2.4 for acetylcholine, and 3.7 for vasopressin. The responses to Ba(2+) or Sr(2+), though studied less extensively, were found to be affected in much the same manner.2. The K(+) depolarized myometrium in a low Ca(2+) medium contracts in response to added Ca(2+). These responses also were increased by low concentrations of PGE(1), but the effective concentration of PGE(1) was indistinguishable from that for direct spasmogenesis.3. Possible mechanisms for the interaction of PGE(1) and Ca(2+) in the myometrium are discussed. It is tentatively suggested that these findings may be relevant to the physiological control of human myometrium.

Topics: Acetylcholine; Animals; Barium; Calcium; Female; Guinea Pigs; In Vitro Techniques; Muscle Contraction; Muscle, Smooth; Potassium; Prostaglandins; Spasm; Strontium; Uterus; Vasopressins

Topics: Arterioles; Caffeine; Cats; Epinephrine; Histamine; Neostigmine; Niacinamide; Norepinephrine; Papaverine; Pharmacology; Phenoxybenzamine; Phentolamine; Research; Retinal Vessels; Spasm; Tolazoline; Vasopressins

Topics: Emergencies; Heart Arrest; Heart Massage; Histamine H1 Antagonists; Humans; Hypotension; Infusions, Parenteral; Podiatry; Seizures; Spasm; Tachycardia; Vasopressins; Vocal Cord Paralysis

Topics: Arginine Vasopressin; Coronary Vessels; Humans; Spasm; Vasopressins