pituitrin and Cerebrovascular-Disorders

It is well known that vasopressin participates in the regulation of the cardiovascular system, water electrolyte balance and many functions of the central nervous system. Receptors for vasopressin are widely distributed throughout the brain. They are present in neurons, in astrocytes and their perivascular processes, in endothelial and smooth muscle cells of blood vessels and in choroid plexus. Such a location suggests that vasopressin may participate in the regulation of vascular resistance in cerebral circulation and water homeostasis in the brain. Present review of the data published on this subject suggests that endogenous vasopressin is involved in brain pathology rather than in physiological regulations. Numerous studies have shown increased release of vasopressin and expression of vasopressin receptors in the brain following ischemia, trauma or subarachnoid hemorrhage in patients and in animal models of these diseases. Moreover, it has been demonstrated that antagonists of vasopressin V(1a) receptors are able to alleviate brain edema and spastic changes in blood vessels after subarachnoid hemorrhage. Vasopressin is also implicated in brain edema and in impairment of cerebral vasculature in hypo-osmotic states. The discussed results suggest that vasopressin V(1a) receptors antagonists may be a useful tool for the treatment of some states associated with cerebrovascular pathology.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Brain; Cerebrovascular Disorders; Disease Models, Animal; Gene Expression Regulation; Humans; Receptors, Vasopressin; Vascular Resistance; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Cortex Hormones; Arrhythmias, Cardiac; Cardiovascular Diseases; Catecholamines; Cerebrovascular Disorders; Humans; Hyperglycemia; Hypertension; Hyponatremia; Models, Biological; Pulmonary Edema; Vasopressins

Topics: Adrenocorticotropic Hormone; Arginine Vasopressin; Brain Edema; Cerebrovascular Disorders; Cortisone; Drug Therapy; Humans; Hydrocortisone; Stroke; Vasopressins

Abnormal patterns of diurnal blood pressure variation have been reported to be related to advanced target organ damage and poor cardiovascular prognosis. We studied silent cerebrovascular disease and stroke events in older Japanese patients with different nocturnal blood pressure dipping. There was a J-shaped relationship of nocturnal dipping status with silent cerebral infarcts detected by brain magnetic resonance imaging at baseline, and with stroke incidence during the follow-up period. The extreme-dippers (with marked nocturnal blood pressure dipping) and the risers (with higher nocturnal blood pressure than awake blood pressure) had a higher prevalence of silent cerebral infarcts and a poorer stroke prognosis than those with appropriate nocturnal blood pressure dipping (dippers). The extreme-dippers tended to have predominant systolic hypertension and increased blood pressure variability. Several factors affect the diurnal blood pressure variation pattern. The non-dipping pattern is associated with autonomic nervous dysfunction and poor sleep quality due to nocturnal behavior and sleep apnea. The extreme-dippers might have increased arterial stiffness with reduced circulating blood volume in addition to an excessive morning surge due to alpha-adrenergic hyperactivity. Anti-hypertensive medication that normalizes the diurnal blood pressure variation might improve the cardiovascular prognosis in high-risk hypertensive patients.

Topics: Aged; Aged, 80 and over; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Cerebrovascular Disorders; Circadian Rhythm; Follow-Up Studies; Humans; Hypertension; Hypotension; Middle Aged; Stroke; Vasopressins

Dahl salt-sensitive (DSS) rats fed an 8.7% sodium chloride diet from weaning spontaneously developed hypertension and a 50% mortality rate by 5 weeks. Before death the rats exhibited behavioural signs of stroke and disruption of the blood-brain barrier.. To test the hypothesis that rats exhibiting stroke had middle cerebral arteries (MCAs) that had lost the ability to constrict in response to pressure, and to assess whether this defect was associated with abnormalities in protein kinase C (PKC)-mediated constriction.. MCAs were sampled from DSS rats before and after stroke and from Dahl salt-resistant (DSR) rats fed 8.7% NaCl. Constrictions in response to a 100 mmHg pressure step and to PKC activation by phorbol dibutyrate (PDB) (0.1 micromol/l) in the presence of nifedipine (3 micromol/l) were measured.. MCAs from DSS rats after stroke constricted in response to vasopressin but were unable to constrict in response to pressure or PDB in the presence of nifedipine, whereas those from DSS rats before stroke and from DSR rats constricted in response to all the stimuli. The PKC inhibitors, chelerythrine (12 micromol/l) and bisindolylmaleimide (5 micromol/l) inhibited constrictions in response to pressure and to PDB in the presence of nifedipine.. Constriction of the MCA in response to pressure is dependent on functional PKC signalling. Development of stroke in DSS rats fed a high-salt diet is associated with an inability of the MCAs to constrict in response to pressure, possibly because of the presence of an incompetent PKC system. The inability to constrict in response to pressure may cause blood flow abnormalities that contribute to disruption of the blood-brain barrier in these rats.

Topics: Animals; Blood Pressure; Calcium Channel Blockers; Cerebrovascular Disorders; Disease Models, Animal; Dose-Response Relationship, Drug; Hypertension; Middle Cerebral Artery; Models, Cardiovascular; Nifedipine; Protein Kinase C; Rats; Rats, Inbred Dahl; Sodium Chloride, Dietary; Stroke; Survival Analysis; Time Factors; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

We sought to determine the effects of vasopressin and saline placebo in comparison with epinephrine on neurologic recovery and possible cerebral pathology in an established porcine model of prolonged cardiopulmonary resuscitation (CPR).. It is unknown whether increased cerebral blood flow during CPR with vasopressin is beneficial with regard to neurologic recovery or detrimental owing to complications such as cerebral edema after return of spontaneous circulation.. After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive every 5 min either vasopressin (0.4, 0.4 and 0.8 U/kg; n = 6), epinephrine (45, 45 and 200 microg/kg; n = 6) or saline placebo (n = 5). The mean value +/- SEM of aortic diastolic pressure was significantly (p < 0.05) higher 90 s after each of three vasopressin versus epinephrine versus saline placebo injections (60 +/- 3 vs. 45 +/- 3 vs. 29 +/- 2 mm Hg; 49 +/- 5 vs. 27 +/- 3 vs. 23 +/- 1 mm Hg; and 50 +/- 6 vs. 21 +/- 3 vs. 16 +/- 3 mm Hg, respectively). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve return of spontaneous circulation.. All the pigs that received epinephrine and saline placebo died, whereas all pigs on vasopressin survived (p < 0.05). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology.. During prolonged CPR, repeated vasopressin administration, but not epinephrine or saline placebo, ensured long-term survival with full neurologic recovery and no cerebral pathology in this porcine CPR model.

Topics: Animals; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Cerebrovascular Disorders; Disease Models, Animal; Electric Countershock; Epinephrine; Magnetic Resonance Imaging; Swine; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

The effect of therapy for hyponatremia with central origin (cerebrovascular disease and head injury) was investigated in order to examine contributing factors. Out of a total of 58 subjects admitted to the hospital during the previous three years with cerebrovascular disease (49 cases), and head injuries (9 cases), hyponatremia with central origin occurred within 2 weeks. Special treatment for hyponatremia was not given in 30 of the 58 cases (control group). The group (28 cases) which underwent therapy was optionally selected in terms of the following-SIADH, natriuretic polypeptide involvement and sick cells resulting from Na-K pump disorder. These 28 cases were classified into subgroups: water restricted (7 cases), hypertonic NaCl load (9 cases), glucose/insulin/potassium (GIK) therapy (4 cases), phenytoin administration (8 cases). In all of the 58 patients, the serum sodium, potassium and osmolarity and urinary sodium and potassium were measured daily. The balance of water, sodium and potassium were calculated on hyponatremic phase. Plasma levels of such hormones as antidiuretic hormone, aldosterone and cortisol were measured on hyponatremic phase. For each group, onset day and duration of hyponatremia and lowest sodium value were investigated for the sake of comparison. No significant difference for onset day and lowest sodium value was found between each group. Duration was as follows: control group 9.4 +/- 3.3 days, water restricted 7.4 +/- 2.1 days, hypertonic NaCl load 3.3 +/- 1.4 days, GIK therapy 7.3 +/- 2.9 days and phenytoin administration 8.9 +/- 3.7 days. Hypertonic NaCl load indicated a significantly shorter duration compared with the other groups. Hypertonic NaCl load was found to be most effective for hyponatremia with central origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aldosterone; Cerebrovascular Disorders; Craniocerebral Trauma; Glucose; Humans; Hydrocortisone; Hyponatremia; Inappropriate ADH Syndrome; Insulin; Phenytoin; Potassium; Saline Solution, Hypertonic; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Aldosterone; Blood Urea Nitrogen; Cerebrovascular Disorders; Humans; Hyponatremia; Middle Aged; Potassium; Vasopressins

In order to investigate the vasopressor role of ADH in the regulation of blood pressure, passive immunization experiments with an antibody to AVP were carried out in experimentally hypertensive rats. In hypertensive rats treated with deoxycorticosterone acetate (DOCA), spontaneously hypertensive rats (SHR) and spontaneously hypertensive stroke-prone rats (SHR-sp), the intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood pressure of 11 approximately 25mmHg, while in rats with two-kidney Goldblatt hypertension and normal rats, the blood pressure was not affected. This strongly suggests that ADH contributed to systemic vaso-constriction in DOCA hypertension and spontaneous hypertension in rats.

Topics: Animals; Blood Pressure; Cerebrovascular Disorders; Desoxycorticosterone; Hypertension; Hypothalamus; Immune Sera; Male; Pituitary Gland; Rats; Vasopressins

A laboratory model was developed in the dog to quantitate the effects of cerebral venous hypertension on inappropriate antidiuretic hormone (ADH) secretion. When cerebral venous pressure was abruptly increased during continuous water loading, there was a sharp rise in urine osmolality within 30 minutes. Urine osmolality continued to increase during, and ten minutes after, the period of hypertension. On lowering cerebral venous pressure, the osmolality returned to baseline within 60 minutes. The effects could be extended for at least three hours and presumably longer. A 50% response threshold for this ADH effect occurred at a cerebral venous pressure between 18 and 19 cm of water. The effect correlated with plasma ADH levels. The study paralled documented clinical observations. The results are discussed in light of the recognition and management of surgical states where increased cerebral venous pressure might produce a severe antidiuretic effect.

Topics: Animals; Arginine Vasopressin; Brain; Cerebrovascular Disorders; Disease Models, Animal; Dogs; Hypertension; Hypothalamus; Osmolar Concentration; Time Factors; Vasopressins; Venous Pressure

Topics: Bronchopneumonia; Cerebrovascular Disorders; Humans; Inappropriate ADH Syndrome; Lithium; Male; Middle Aged; Vasopressins

In 100 patients with different forms of cerebral strokes the author studied the general water content. Its distribution in the organism. Na and K concentration in the plasma and erythrocytes and the general electrolyte content in spaces of the body. It was established that the most frequent syndromes of water-electrolyte disorders in the acute period of strokes is intracellular or general hydratation (81%). In parenchymatous-subarachnoidal hemorrhages the general dehydratation was combined with a hyperhydratation of the extracellular space, while in sichemic strokes there was an anhydridemia up to 10-18 days. A disturbance of the electrolyte metabolism was also expressed in a transmineralization with a drop of the general Na and K content due to intracellular losses. The K deficit was averagely 29% and the Na--15.5% and should be taken into consideration in a substitutive hydro-electrolyte therapy. Solutions with an increased K content should be used in order to compensate its deficit.

Topics: Acute Disease; Adrenal Cortex; Body Water; Cerebral Hemorrhage; Cerebrovascular Disorders; Extracellular Space; Humans; Hypothalamus; Mineralocorticoids; Plasma Volume; Potassium; Sodium; Time Factors; Vasopressins; Water-Electrolyte Imbalance

The paper analyses the results of a study of the clinical peculiarities of the course of essential hypertension with crises, of the changes in the functional state of the central nervous system, and of some neuro-humoral systems of the human body. In most of the patients tending to develope frequent crises distinct changes were noted in the EEG that indicate dysfunction of the hypothalamic zone and of the reticular formation of the brain stem, their clinical course being characterized by significant astheno-neurotic disorders with autonomous dysfunction and cerebral angiodistonic disturbances. For the prevention of crises it is essential to conduct a pathogenetically substantiated and highly differentiated systematic therapy, as well as special measures aimed at increasing the endurance of the central nervous system, improving the circulation and metabolic processes in the brain, decreasing tnd hypothalamic structures of the brain, and correcting the dishormonal disorders.

Topics: Adult; Antihypertensive Agents; Brain; Cerebral Arteries; Cerebrovascular Disorders; Diencephalon; Humans; Hypertension; Middle Aged; Physical Therapy Modalities; Reticular Formation; Vasopressins

Topics: Cerebrovascular Disorders; Humans; Hypertension; Hypothalamus; Pituitary Gland, Posterior; Vasopressins

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.

Topics: Adult; Aged; Carcinoma, Bronchogenic; Cerebrovascular Disorders; Esophageal Neoplasms; Female; Hormones, Ectopic; Humans; Hyponatremia; Hypothyroidism; Lung Neoplasms; Male; Middle Aged; Myxedema; Neurologic Manifestations; Vasopressins; Water Intoxication

Topics: Adult; Aged; Aging; Animals; Arrhythmias, Cardiac; Cardiovascular Diseases; Cerebrovascular Disorders; Coronary Disease; Humans; Hypertension; Middle Aged; Rabbits; Rats; Vasopressins

Topics: Cerebrovascular Disorders; Humans; Vasopressins

Topics: Aged; Cerebrovascular Disorders; Coma; Female; Humans; Hyponatremia; Hypopituitarism; Potassium Deficiency; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adult; Aged; Cerebrovascular Disorders; Circadian Rhythm; Creatinine; Diffuse Cerebral Sclerosis of Schilder; Encephalitis; Female; Humans; Middle Aged; Potassium; Sodium; Tuberculosis, Meningeal; Urination Disorders; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Adult; Aged; Angiography; Brain Edema; Cerebrovascular Disorders; Craniocerebral Trauma; Echoencephalography; Electroencephalography; Electrooculography; Female; Humans; Male; Middle Aged; Oxytocin; Perfusion; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Blood Volume Determination; Cardiovascular Diseases; Cerebrovascular Disorders; Chromium Isotopes; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Hematocrit; Hemoglobinometry; Humans; Hydrocortisone; Iodine Isotopes; Metaraminol; Methylphenidate; Phenoxybenzamine; Respiratory Tract Diseases; Shock, Hemorrhagic; Urologic Diseases; Vasopressins

Topics: Adrenocorticotropic Hormone; Aged; Brain Edema; Cerebrovascular Disorders; Female; Humans; Male; Vasopressins

Topics: Adrenocorticotropic Hormone; Aged; Brain Edema; Cerebrovascular Disorders; Female; Humans; Male; Middle Aged; Vasopressins; Water-Electrolyte Balance