pituitrin and Ischemic-Attack--Transient

Resistance of large arteries appears to be greater in the cerebral circulation than in other vascular beds. Large arteries contribute importantly to total cerebral vascular resistance and are major determinants of local microvascular pressure. Recent studies have shown that resistance of large arteries and cerebral microvascular pressure are affected by several physiological stimuli, including changes in systemic blood pressure, increases in cerebral metabolism, activity of sympathetic nerves, and humoral stimuli such as circulating vasopressin and angiotensin. Stimuli such as sympathetic stimulation and vasopressin produce selective responses of large arteries and, thereby, regulate microvascular pressure without a significant change in cerebral blood flow. These findings lead to the new hypothesis that the brain may be sensitive to changes in cerebral microvascular pressure, resulting in activation of compensatory neurohumoral mechanisms. Important changes occur in large cerebral arteries under pathophysiological conditions. Chronic hypertension increases resistance of large cerebral arteries, which protects the microcirculation against hypertension. Atherosclerosis potentiates constrictor responses of large cerebral arteries to serotonin and thromboxane, which may contribute to vasospasm and transient ischemic attacks.

Topics: Angiotensin II; Arterioles; Arteriosclerosis; Blood Pressure; Brain; Cerebral Arteries; Cerebrovascular Circulation; Humans; Hypertension; Ischemic Attack, Transient; Microcirculation; Sympathetic Nervous System; Thromboxanes; Vascular Resistance; Vasopressins

A causal or supportive relationship between 1,2-diacylglycerol (DAG) content and the maintenance of tonic vasoconstriction was sought in canine basilar arteries treated in vitro with various agents reported to increase DAG levels in other tissues (platelet-derived growth factor, vasopressin, angiotensin II, and endothelin-1) and, conversely, with agents known to activate sustained constriction (high K+, phorbol ester, hemolysate, and endothelin-1). Multiple segments from individual isolated arteries were prepared. Some segments were immediately frozen as controls and others incubated in physiological saline solution at 37 degrees C for either 5 minutes or 30 minutes in the presence or absence of different concentrations of the test materials. Segments were then quickly frozen until homogenized for lipid extraction and DAG assay. The DAG content of samples incubated up to 2 hours in physiological saline solution alone did not significantly differ from that of immediately frozen control samples. Resting DAG content expressed relative to total protein measured in each sample averaged 3.82 +/- 0.26 (standard error of the mean) pmol DAG/microgram of protein (74 samples from 37 arteries). Endothelin at 2 x 10(-7) mol/L led to a statistically significant increase in DAG content of approximately 40% of basal content at 5 and 30 minutes. A smaller increase in DAG attributable to hemolysate (approximately 25%) was statistically significant at 30 minutes, whereas vasopressin provoked a notable decrease in DAG content. The other agents had no effect. No differences in these results were noted between normal canine basilar arteries and arteries constricted in vivo by subarachnoid blood clot before isolation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Basilar Artery; Culture Techniques; Diglycerides; Dogs; Dose-Response Relationship, Drug; Endothelins; Female; Ischemic Attack, Transient; Isometric Contraction; Male; Phorbol 12,13-Dibutyrate; Platelet-Derived Growth Factor; Subarachnoid Hemorrhage; Vasoconstrictor Agents; Vasopressins

In Mongolian gerbils, the content of vasopressin in the cerebral cortex, the striatum, and the hypothalamus is increased after induction of acute cerebral ischemia. We used an iodinated vasopressin analogue and light microscopic autoradiography to study the distribution of vasopressin V1 receptors in the brain of adult male gerbils and to evaluate the effects of a transient bilateral cerebral ischemia (6 minutes) on the density of this receptor population. The animals were killed immediately or 10, 30, or 100 hours after transient bilateral occlusion of the common carotid arteries. In control animals, specific [125I]-VPA binding sites were present in various structures of the brain (olfactory bulb, anterior olfactory nucleus, lateral septum, bed nucleus of the stria terminalis, median preoptic area, ventral pallidum, substantia innominata, amygdala, thalamus, hypothalamic mammillary nuclei, superior colliculus, subiculum, central gray, nucleus of the solitary tract, hypoglossal nucleus). The strongest labeling was detected in the cerebral cortex, layers 5-6. After 30-100 hours of survival time following ischemia there was a marked decrease in [125I]-VPA binding site density in these cerebral cortex layers. To a lesser degree, a decrease was also detected in the lateral septal nucleus. In contrast, labeling in other noncortical structures remained unchanged. All animals with 100 hours recovery showed a loss of cells in hippocampus (CA1 layer) and striatum. In addition, ischemia induced concomitant and proliferative changes in cortical and hippocampal astrocytes assessed by glial fibrillary acid protein immunoreactivity. These observations indicate a role for vasopressin in the cerebral cortex either on neurons or on glial cells and the modulation of vasopressin receptor expression by transient cerebral ischemia.

Topics: Animals; Autoradiography; Binding Sites; Cerebral Cortex; Corpus Striatum; Gerbillinae; Hippocampus; Hypothalamus; Immunohistochemistry; Ischemic Attack, Transient; Male; Radioligand Assay; Vasopressins

The function of nitric oxide in spastic cerebral arteries after subarachnoid hemorrhage (SAH) was angiographically investigated in dogs. On days 4 and 7, after two intracisternal injections of autologous blood, higher concentrations of L-arginine than those of endogenous L-arginine in the cerebrospinal fluid produced a transient vasodilation of the spastic basilar artery, whereas NG-monomethyl-L-arginine (L-NMMA) produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on day 4 than day 7, but less than that in intact dogs. Vasopressin, which is known to activate the endothelial L-arginine pathway, could induce a vasodilation only after the treatment with L-arginine. Intracisternal injection of superoxide dismutase (SOD), which caused no effect by itself, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on day 4 and both the magnitude and duration of that effect on day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. Enhancement of L-arginine's effect by SOD suggested that the inactivation of nitric oxide by superoxide anion contributed to the development of vasospasm.

Topics: Animals; Arginine; Basilar Artery; Blood Pressure; Cerebral Angiography; Cisterna Magna; Dogs; Injections; Ischemic Attack, Transient; Nitric Oxide; omega-N-Methylarginine; Subarachnoid Hemorrhage; Superoxide Dismutase; Vasodilation; Vasopressins

The relationship between plasma atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) both of which show high values after subarachnoid hemorrhage and cerebral vasospasm was studied. The subjects were 23 patients who were admitted because of aneurysmal subarachnoid hemorrhage during three years from March, 1989 to March, 1992 and in whom plasma ANP and ADH levels could be determined over time. Cerebral vasospasm was evaluated by the finding of cerebral angiography, clinical symptoms, and presence or not of low density areas on CT. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less for two days or more. Angiographical vasospasm was found in 17 patients (85%), symptomatic vasospasm in 15 patients (65.2%), low density areas on CT in 9 patients (40.9%) and hyponatremia in 8 patients (34.8%). Symptomatic vasospasm was noted in 7 of the 8 patients (87.5%) with hyponatremia, low density areas on CT in 4 patients (50%), the detection rate being high. The plasma ANP and ADH levels were 76.7 +/- 32.1 pg/ml and 2.2 +/- 0.7 pg/ml respectively in the patients with symptomatic vasospasm against 38.3 +/- 21.3 pg/ml and 2.4 +/- 0.6 pg/ml respectively without symptomatic vasospasm, the plasma ANP level being significantly high in the patients with symptomatic vasospasm (p < 0.01). The plasma ANP and ADH were 71.2 +/- 33.8 pg/ml and 2.0 +/- 1.1 pg/ml respectively in the patients with low density areas on CT against 51.2 +/- 31.3 pg/ml and 1.8 +/- 0.5 pg/ml respectively without low density areas on CT.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Humans; Hyponatremia; Intracranial Aneurysm; Ischemic Attack, Transient; Rupture, Spontaneous; Subarachnoid Hemorrhage; Vasopressins

Topics: Angiography; Catheterization; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Intestine, Large; Ischemia; Ischemic Attack, Transient; Thrombosis; Vasodilator Agents; Vasopressins

Topics: Blood Volume; Erythrocyte Volume; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Plasma Volume; Postoperative Period; Subarachnoid Hemorrhage; Vasopressins

Topics: Acetylcholine; Angiotensin II; Animals; Basilar Artery; Bradykinin; Cerebral Arteries; Dogs; Dose-Response Relationship, Drug; Epinephrine; Female; Histamine; In Vitro Techniques; Ischemic Attack, Transient; Isoproterenol; Male; Methods; Muscle Contraction; Norepinephrine; Prostaglandins; Serotonin; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Animals; Cerebral Angiography; Cerebral Cortex; Cisterna Magna; Disease Models, Animal; Dogs; Hypothalamus; Ischemic Attack, Transient; Male; Oxytocin; Subarachnoid Space; Tissue Extracts; Vasopressins