pituitrin and Syncope

The vasovagal response is the development of inappropriate cardiac slowing and arteriolar dilatation. Vasovagal responses reflect autonomic neural changes: bradycardia results from sudden augmentation of efferent vagal activity, and hypotension results from sudden reduction or cessation of sympathetic activity and relaxation of arterial resistance vessels. Two different neural pathways are thought to be involved, one originating in the hypothalamus, the other in the heart. Direct hypothalamic activation of the medullary cardiovascular centres triggered by emotional stress or pain causes a vasovagal response (central type). The combination of a reduced central blood volume secondary to venous pooling or blood loss, and an increased inotropic state of the heart, may stimulate ventricular mechanoreceptors and provoke vasodilatation and bradycardia (peripheral type). Cardiovascular afferents originating from stretch receptors in various parts of the vascular tree sometimes induce opposite reflexes when compared with those from ventricular afferents. The depressor reflex involved in the peripheral type of vasovagal response originates in the heart itself and overrides normal baroreflex circulatory control; an antagonism between the control of volume and pressure on the filling side of the heart and the control system of arterial pressure becomes apparent. Vasovagal responses are not necessarily abnormal; the neural pathways involved in the vasovagal response are probably present in all healthy subjects who individually mainly differ in susceptibility.

Topics: Arterioles; Blood Pressure; Heart Rate; Hemodynamics; Humans; Male; Neural Pathways; Reflex; Shock; Stress, Psychological; Syncope; Vagus Nerve; Vasodilation; Vasopressins

Topics: Aldosterone; Atmospheric Pressure; Blood Pressure; Blood Volume; Carbon Dioxide; Cardiac Output; Central Venous Pressure; Cerebrovascular Circulation; Forearm; Hemodynamics; Humans; Kidney; Leg; Lung Compliance; Neck; Oxygen; Posture; Pulmonary Circulation; Pulse; Regional Blood Flow; Renin; Respiration; Syncope; Vascular Resistance; Vasopressins; Ventricular Function

An attenuated baroreflex response and orthostatic intolerance have been reported in endurance-trained male athletes; however, it is still unknown whether this occurs also in females. The purpose of the present study was to examine whether endurance exercise-trained women had a predisposition to orthostatic compromise, and if so, what causative factor(s) may induce orthostatic intolerance.. We studied cardiovascular and hormonal responses to graded lower body negative pressure (LBNP) (0 to -60 mm Hg) in 26 middle-distance female runners (18.6 +/- 0.1 yr) as the exercise-trained (ET) subjects and 23 age-matched untrained (UT) control subjects. On the basis of the occurrence of syncope episodes during LBNP, ET and UT subjects were further allocated to two groups; ET with presyncope (ET+syncope) and without presyncope (ET-syncope) and UT with presyncope (UT+syncope) and without presyncope (UT-syncope).. Occurrence of presyncope episodes during LBNP was higher in ET (65.4%, P < 0.05) than that for UT (34.8%). Leg compliance was higher (P < 0.05) in ET than in UT. LBNP reduced stroke volume (SV) more (P < 0.05), increased heart rate (HR) higher (P < 0.05), and increased forearm vascular resistance (FVR) more in ET+syncope as compared with the other groups. Response of vasoactive hormones to LBNP was higher in ET+syncope (P < 0.05) than that of the other groups except for norepinephrine (NE); high in both ET+syncope and UT+syncope. The relationship between SV and NE, an index of sympathetic neuronal response, had no training-related changes during LBNP.. We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP.

Topics: Adolescent; Adult; Baroreflex; Female; Humans; Hypotension, Orthostatic; Hypovolemia; Lower Body Negative Pressure; Norepinephrine; Physical Endurance; Renin; Running; Sex Factors; Stroke Volume; Syncope; Vasopressins

Nausea is a common prodromal symptom of neurally mediated syncope, but the biological factors linking nausea with syncope have not been studied. We aimed to characterize nausea during tilt-induced syncope by exploring related changes in gastric myoelectrical activity and plasma epinephrine, norepinephrine, and vasopressin concentrations across study phases of recumbency, tilt, syncope, and recovery.. Electrogastrographic and plasma hormone changes were compared between patients with tilt-induced syncope and nausea (n = 18) and control subjects (n = 6) without symptoms or hemodynamic changes during tilt-table testing.. Over a 4-minute period preceding syncope, sequential electrogastrography epochs demonstrated an increase over time in bradygastria (P = .003) and tachygastria (P = .014) power ratios, while the dominant frequency (P < .001) and the percent normogastria (P = .004) decreased. Syncope led to significant differences between cases and controls in electrogastrographic power ratios in each frequency range: bradygastria (P = .001), tachygastria (P = .005), and normogastria (P = .03). Nausea always followed electrogastrographic changes, and nausea resolution always preceded electrogastrographic normalization. Plasma vasopressin (676.5 ± 122.8 vs 91.2 ± 15.3 pg/mL, P = .012) and epinephrine (434 ± 91.3 vs 48.7 ± 2.5 pg/mL, P = .03), but not norepinephrine (P > .05), also differed with syncope between cases and controls.. The nausea related to tilt-induced syncope is temporally associated with changes in gastric myoelectrical activity and increases in plasma vasopressin and epinephrine. The biological mechanisms that induce syncope are physiologically distinct from other experimental models of nausea such as illusory self-motion, yet nausea with syncope appears to have similarly associated electrogastrographic and hormone changes. Thus, tilt-induced syncope could serve as an informative experimental model for nausea research.

Topics: Adolescent; Electromyography; Epinephrine; Female; Humans; Nausea; Norepinephrine; Stomach; Syncope; Tilt-Table Test; Vasopressins

Studies of adults with orthostatic intolerance (OI) have revealed altered neurohumoral responses to orthostasis, which provide mechanistic insights into the dysregulation of blood pressure control. Similar studies in children with OI providing a thorough neurohumoral profile are lacking. The objective of the present study was to determine the cardiovascular and neurohumoral profile in adolescent subjects presenting with OI. Subjects at 10-18 yr of age were prospectively recruited if they exhibited two or more traditional OI symptoms and were referred for head-up tilt (HUT) testing. Circulating catecholamines, vasopressin, aldosterone, renin, and angiotensins were measured in the supine position and after 15 min of 70° tilt. Heart rate and blood pressure were continuously measured. Of the 48 patients, 30 patients had an abnormal tilt. Subjects with an abnormal tilt had lower systolic, diastolic, and mean arterial blood pressures during tilt, significantly higher levels of vasopressin during HUT, and relatively higher catecholamines and ANG II during HUT than subjects with a normal tilt. Distinct neurohumoral profiles were observed when OI subjects were placed into the following groups defined by the hemodynamic response: postural orthostatic tachycardia syndrome (POTS), orthostatic hypotension (OH), syncope, and POTS/syncope. Key characteristics included higher HUT-induced norepinephrine in POTS subjects, higher vasopressin in OH and syncope subjects, and higher supine and HUT aldosterone in OH subjects. In conclusion, children with OI and an abnormal response to tilt exhibit distinct neurohumoral profiles associated with the type of the hemodynamic response during orthostatic challenge. Elevated arginine vasopressin levels in syncope and OH groups are likely an exaggerated response to decreased blood flow not compensated by higher norepinephrine levels, as observed in POTS subjects. These different compensatory mechanisms support the role of measuring neurohumoral profiles toward the goal of selecting more focused and mechanistic-based treatment options for pediatric patients with OI.

Topics: Adolescent; Aldosterone; Angiotensin I; Angiotensin II; Angiotensins; Arterial Pressure; Blood Pressure; Catecholamines; Child; Diastole; Dopamine; Epinephrine; Female; Heart Rate; Humans; Hypotension, Orthostatic; Male; Norepinephrine; Orthostatic Intolerance; Postural Orthostatic Tachycardia Syndrome; Prospective Studies; Renin; Syncope; Systole; Tilt-Table Test; Vasopressins

The aim of the study was to investigate the resting levels of novel cardiovascular biomarkers in common types of noncardiac syncope.. An observational study was conducted including 255 patients (mean age 60 years, range 15-93; 45% men) with unexplained syncopal attacks. Subjects underwent an expanded head-up tilt test including carotid sinus massage, and nitroglycerin provocation if indicated. Using logistic regression, we explored the associations between specific diagnoses of syncope and resting levels of circulating biomarkers: C-terminal pro-arginine vasopressin (CT-proAVP), C-terminal endothelin-1 precursor fragment (CT-proET-1), midregional fragments of pro-atrial natriuretic peptide (MR-proANP) and pro-adrenomedullin (MR-proADM).. A total of 142 (56%) patients were diagnosed with vasovagal syncope (VVS), 85 (33%) with orthostatic hypotension (OH) and 47 (18%) with carotid sinus hypersensitivity (CSH); in addition, 74 (29%) patients had more than one diagnosis. Thirty-five patients (14%) demonstrated a cardioinhibitory reflex. The probability of VVS was highest in the first quartile of MR-proANP [Q1 vs. Q4: odds ratio (OR) 5.57, 95% confidence interval (CI) 1.86-16.74; P < 0.001] and CT-proET-1 (OR 7.17, 95% CI 2.43-21.13; P < 0.001). By contrast, the probability of OH was highest in the fourth quartile of CT-proET-1 (Q4 vs. Q1: OR 8.66, 95% CI 2.49-30.17; P < 0.001). Furthermore, CSH was most frequently observed in the first quartile of MR-proANP (Q1 vs. Q4: OR 6.57, 95% CI 1.62-26.62; P = 0.008) among those over 60 years of age, whereas the cardioinhibitory reflex was strongly associated with low CT-proET-1 levels (Q1 vs. Q4: OR 69.7, 95% CI 6.97-696.6; P < 0.001). Moreover, in patients with VVS, a high concentration of CT-proET-1 was predictive of OH (OR per 1 SD 2.4, 95% CI 1.15-5.02; P = 0.02), whereas low CT-proET-1 suggested involvement of the cardioinhibitory reflex (OR per 1SD 0.42, 95% CI 0.25-0.70; P = 0.001).. The levels of MR-proANP and CT-proET-1 are markedly changed in common forms of syncope, suggesting the involvement of novel neurohormonal mechanisms in syncopal attacks.

Topics: Adolescent; Adrenomedullin; Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Biomarkers; Electrocardiography; Endothelin-1; Female; Humans; Male; Middle Aged; Peptide Fragments; Retrospective Studies; Syncope; Vasopressins; Young Adult

Aim of this study was to test the hypothesis that after presyncope, some blood hormone pools increase while others decrease.. In twelve healthy male adults, we determined plasma volume changes with plasma mass densitometry and hormone levels. The following were compared: supine rest, presyncope and 20-min post-presyncopal supine rest. We determined plasma renin activity (PRA), aldosterone, adrenocorticotropic hormone (ACTH), adrenomedullin and vasopressin (AVP) from venous blood samples.. Using passive 4-min 70° head-up tilt followed by 4-min sequences of additional lower body negative pressure of increasing intensity (15 mmHg steps), presyncope occurred after 11·6 ± 2·8 min, at which time plasma volume was reduced by 15·5 ± 7·4%, aldosterone increased by 37%, ACTH by 75%, PRA by 187% and AVP about 16-fold in average (all P < 0·01); no significant changes in adrenomedullin were seen. Twenty-min post-presyncope, ACTH increased above presyncopal levels (+36%, P < 0·05), aldosterone by 35% (P = 0·07). PRA (-47%, P < 0·01) and AVP (-84%, P < 0·05) decreased below presyncopal but were still above supine control (P < 0·01); similarly, plasma density fell by 2·17 ± 0·97 g L(-1) below presyncopal (P < 0·01), but above supine control (P < 0·05), indicating rapid recovery (83% of initial plasma volume).. We conclude that during the 20-min supine post-syncopal period, plasma volume, PRA and AVP return closer to baseline but aldosterone and ACTH continue increasing. The magnitude of observed concentration changes cannot be explained by haemoconcentration/haemodilution, rather it appears that the observed changes are indicative of hormone-specific endocrine activation patterns in the recovery phase.

Topics: Adrenocorticotropic Hormone; Adrenomedullin; Adult; Aldosterone; Head-Down Tilt; Humans; Male; Plasma Volume; Renin; Syncope; Tilt-Table Test; Vasopressins; Young Adult

To get a more complete picture of cardiovascular regulation after postural changes, this investigation directly monitored volume-related, hemodynamic, and endocrine variables during and after 30 min of passive head-up tilt (HUT) of various degrees. It was hypothesized that the return of variables to pre-tilt control level is of system-specific duration and different from what is found after lower body negative pressure (LBNP).. We tested 7 persons on 5 different days using, in random order, no (HUT0) or different intensity (12 degrees , 30 degrees , 53 degrees , and 70 degrees ) of passive orthostasis (HUT12, HUT30, HUT53, HUT70). Data were collected before (supine), during, and after (supine) HUT and compared with synchronous data from HUT0.. There was graded alteration with the sine of tilt angle for all hormones and directly volume-related variables. The effects of HUT70 were of the same magnitude as previously documented by others. After HUT, hemodynamic variables and catecholamines returned to control levels most rapidly. Heart rate depression, as observed in a companion LBNP study in the same subjects, did not occur. Vasopressin, PRA, plasma volume and Z0 returned to nominal values more slowly. Plasma aldosterone was still elevated 50 min after reassuming supine posture.. Besides specific dose-responses within hemodynamic, volume-dependent, and hormonal variables after orthostatic loading of different degree, the return to control levels after HUT occurs with distinctly different time-courses, which are not identical with those seen after LBNP-simulated orthostasis.

Topics: Adult; Aldosterone; Dizziness; Epinephrine; Gravitation; Hemodynamics; Humans; Hydrocortisone; Lower Body Negative Pressure; Male; Renin-Angiotensin System; Syncope; Tilt-Table Test; Vasopressins

Topics: Arginine Vasopressin; Cardiac Catheterization; Humans; Renin; Syncope; Vasopressins

1. Syncopal or near syncopal episodes have been observed in five subjects who stood or were tilted and in whom blood samples were being taken. 2. In all subjects bradycardia and hypotension developed before the onset of symptoms. Increases in plasma adrenaline concentrations occurred in all subjects, beginning before the faint. Changes in plasma noradrenaline concentrations were variable: in three subjects there was a marked fall and in the other two subjects an increase. Plasma vasopressin increased in all subjects. 3. Increase in plasma adrenaline may be contributing to the vasodilatation and arterial hypotension which occur during syncope.

Topics: Adult; Blood Pressure; Epinephrine; Female; Humans; Hydrocortisone; Male; Middle Aged; Norepinephrine; Posture; Syncope; Vasodilation; Vasopressins

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Blood Pressure; Blood Volume; Cardiovascular Physiological Phenomena; Electrolytes; Female; Gravity Suits; Humans; Male; Middle Aged; Osmolar Concentration; Pulse; Renin; Syncope; Vasopressins

Lower body negative pressure (9-12 kPa) was applied to ten normal subjects. Large increases in plasma arginine vasopression concentration occurred only in subjects that experienced syncopal symptoms and developed hypotension. Blood samples obtained from the superior vena cava at 1/2 min intervals during application of negative pressure showed that maximal plasma vasopressin concentrations occurred with hypotension. Chromatography of the presyncopal plasma on Sephadex G-25 gave a large peak which eluted in the position of synthetic arginine vasopressin.

Topics: Adult; Arginine Vasopressin; Blood Pressure; Heart Rate; Humans; Male; Pressure; Syncope; Vasopressins

Plasma arginine vasopressin concentrations were measured in five healthy volunteers during postural change under conditions of dehydration and normal hydration. A rise in plasma arginine vasopressin was observed only after dehydration and standing for 40 min. Five further volunteers who developed presyncopal symptoms during orthostasis had exceedingly high plasma arginine vasopressin levels. Changes in plasma arginine vasopressin concentration occurred with no signficant alterations in plasma osmolality.

Topics: Arginine Vasopressin; Dehydration; Female; Humans; Male; Posture; Syncope; Time Factors; Vasopressins

1. Fourteen mildly hydropenic normal volunteers were slowly tilted at a constant rate from the horizontal to the 85 degrees head-up position in order to study the interrelationship between plasma arginine vasopressin concentration, plasma renin activity and the change of plasma volume. 2. Nine subjects did not develop vaso-vagal symptoms and were studied for 45-60 min. Arginine vasopressin rose biphasically in all subjects: a small initial rise, which was seen at 3 min and persisted for 30 min, was followed by a striking rise between 30 and 45 min, when the fall of plasma volume had reached its maximum (17%). 3. Plasma renin activity reached a maximum at 30 min but fell by 45 min, as plasma concentration of arginine vasopressin rose. 4. Five subjects developed vaso-vagal symptoms 4-24 min after reaching 85 degrees when the study was terminated. A striking increase of arginine vasopressin concentration was seen within 4 min of syncope, but there was no change of plasma osmolality, cortisol concentration or renin activity.

Topics: Adult; Arginine Vasopressin; Blood Pressure; Female; Heart Rate; Humans; Male; Plasma Volume; Posture; Renin; Syncope; Time Factors; Vasopressins

Topics: Adult; Arginine Vasopressin; Blood Pressure; Female; Heart Rate; Hematocrit; Humans; Male; Posture; Syncope; Vasopressins

Topics: Adult; Anesthesia, Dental; Humans; Hyperventilation; Male; Prilocaine; Smoking; Syncope; Tachycardia; Tranylcypromine; Vasopressins

Topics: Clinical Laboratory Techniques; Diagnosis; Drug Therapy; Endoscopy; Esophageal and Gastric Varices; Gastrectomy; Gastric Hypothermia; Gastrointestinal Hemorrhage; Humans; Hypothermia, Induced; Peptic Ulcer Hemorrhage; Radiography; Syncope; Vasopressins