pituitrin and Bradycardia

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Advanced Cardiac Life Support; Algorithms; Anti-Arrhythmia Agents; Bicarbonates; Bradycardia; Calcium Channel Blockers; Cardiac Pacing, Artificial; Cardiotonic Agents; Dobutamine; Dopamine; Electric Countershock; Electrocardiography; Epinephrine; Heart Arrest; Humans; Injections, Intravenous; Isoproterenol; Sympathomimetics; Tachycardia; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation; Verapamil

The present article contains a brief review on the role of vasopressinergic projections to the nucleus tractus solitarii in the genesis of reflex bradycardia and in the modulation of heart rate control during exercise. The effects of vasopressin on exercise tachycardia are discussed on the basis of both the endogenous peptide content changes and the heart rate response changes observed during running in sedentary and trained rats. Dynamic exercise caused a specific vasopressin content increase in dorsal and ventral brainstem areas. In accordance, rats pretreated with the peptide or the V1 blocker into the nucleus tractus solitarii showed a significant potentiation or a marked blunting of the exercise tachycardia, respectively, without any change in the pressure response to exercise. It is proposed that the long-descending vasopressinergic pathway to the nucleus tractus solitarii serves as one link between the two main neural controllers of circulation, i.e., the central command and feedback control mechanisms driven by the peripheral receptors. Therefore, vasopressinergic input could contribute to the adjustment of heart rate response (and cardiac output) to the circulatory demand during exercise.

Topics: Animals; Baroreflex; Blood Pressure; Bradycardia; Brain Stem; Heart Rate; Rats; Solitary Nucleus; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Binding, Competitive; Blood Pressure; Bradycardia; Central Nervous System; Humans; Hypertension; Receptors, Serotonin; Serotonin Antagonists; Serotonin Receptor Agonists; Vasopressins

Various rhythm disturbances occur in the postoperative patient. Proper management requires an awareness of clinical circumstances in which they are most likely to happen. Often, the appearance of new arrhythmias in the postoperative period is a manifestation of underlying remediable medical problems. Direct antiarrhythmic therapy is unnecessary in many patients when these precipitating conditions are properly treated.

Topics: Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Bradycardia; Bundle-Branch Block; Electrocardiography; Heart Diseases; Humans; Surgical Procedures, Operative; Tachycardia; Tachycardia, Paroxysmal; Vasopressins

Topics: Acceleration; Adaptation, Physiological; Atrial Function; Blood Volume; Bradycardia; Cardiac Output; Decalcification, Pathologic; Electrocardiography; Exercise Test; Fludrocortisone; Gravitation; Humans; Kidney; Nutrition Disorders; Physical Education and Training; Posture; Pulmonary Atelectasis; Regional Blood Flow; Respiration; Space Flight; Stress, Physiological; Thorax; Vasopressins; Venous Pressure; Ventilation-Perfusion Ratio; Weightlessness

Topics: Bradycardia; Female; Humans; Uterine Myomectomy; Uterine Neoplasms; Vasopressins

Here, we report the participation of N-methyl-D-aspartate (NMDA) glutamate receptor in the mediation of cardiovascular and circulating vasopressin responses evoked by a hemorrhagic stimulus. In addition, once NMDA receptor activation is a prominent mechanism involved in nitric oxide (NO) synthesis in the brain, we investigated whether control of hemorrhagic shock by NMDA glutamate receptor was followed by changes in NO synthesis in brain supramedullary structures involved in cardiovascular and neuroendocrine control. Thus, we observed that intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK801, 0.3 mg/kg) delayed and reduced the magnitude of hemorrhage-induced hypotension. Besides, hemorrhage induced a tachycardia response in the posthemorrhage period (i.e., recovery period) in control animals, and systemic treatment with MK801 caused a bradycardia response during hemorrhagic shock. Hemorrhagic stimulus increased plasma vasopressin levels during the recovery period and NMDA receptor antagonism increased concentration of this hormone during both the hemorrhage and postbleeding periods in relation to control animals. Moreover, hemorrhagic shock caused a decrease in NOx levels in the paraventricular nucleus of the hypothalamus (PVN), amygdala, bed nucleus of the stria terminalis (BNST), and ventral periaqueductal gray matter (vPAG). Nevertheless, treatment with MK801 did not affect these effects. Taken together, these results indicate that the NMDA glutamate receptor is involved in the hemorrhagic shock by inhibiting circulating vasopressin release. Our data also suggest a role of the NMDA receptor in tachycardia, but not in the decreased NO synthesis in the brain evoked by hemorrhage.

Topics: Animals; Bradycardia; Brain; Cardiovascular System; Disease Models, Animal; Dizocilpine Maleate; Injections, Intraperitoneal; Male; Neurosecretory Systems; Nitric Oxide; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Shock, Hemorrhagic; Vasopressins

A 34-year-old patient underwent a laparoscopic myomectomy, complicated by a profound episode of bradycardia and hypotension following intramyometrial infiltration of vasopressin (20 IU), promptly corrected with intravenous ephedrine (6 mg) and glycopyrrolate (200 µg). At extubation, pink frothy fluid was noted in the endotracheal tube; she was visibly distressed, desaturated to 89% in air and was coughing up pink stained fluid. Acute pulmonary oedema secondary to vasopressin was suspected. A tight-fitting oxygen mask (100%) with positive end expiratory pressure was applied and intravenous furosemide (20 mg) and diamorphine (4 mg, 1 mg increments) were administered to facilitate diuresis and oxygenation. Chest X-ray confirmed acute pulmonary oedema. Arterial blood gas demonstrated type 2 respiratory failure. Over 12 hours, the oxygen was weaned to 1 L/min. She demonstrated excellent diuresis. Troponin and brain-natriuretic peptide were elevated, but echocardiogram was normal. The cardiology diagnosis was vasopressin-induced coronary vasospasm, precipitating acute pulmonary oedema. She was discharged home on day 5.

Topics: Adult; Airway Extubation; Bradycardia; Dose-Response Relationship, Drug; Female; Humans; Positive-Pressure Respiration; Pulmonary Edema; Uterine Myomectomy; Vasoconstrictor Agents; Vasopressins

This study investigated the cardiovascular effects of nesfatin-1 in normotensive rats and animals subjected to hypotensive hemorrhage. Hemorrhagic hypotension was induced by withdrawal 2 mL blood/100 g body weight over a period of 10 min. Acute hemorrhage led to a severe and long-lasting decrease in mean arterial pressure (MAP) and heart rate (HR). Intracerebroventricularly (i.c.v.) administered nesfatin-1 (100 pmol) increased MAP in both normotensive and hemorrhaged rats. Nesfatin-1 also caused bradycardia in normotensive and tachycardia in hemorrhaged rats. Centrally injected nesfatin-1 (100 pmol, i.c.v.) also increased plasma catecholamine, vasopressin and renin concentrations in control animals and potentiated the rise in all three cardiovascular mediators produced by hemorrhage. These findings indicate that centrally administered nesfatin-1 causes a pressor response in conscious normotensive and hemorrhaged rats and suggest that enhanced sympathetic activity and elevated vasopressin and renin concentrations mediate the cardiovascular effects of the peptide.

Topics: Animals; Blood Pressure; Bradycardia; Calcium-Binding Proteins; Catecholamines; Central Nervous System Agents; Disease Models, Animal; DNA-Binding Proteins; Heart Rate; Hemorrhage; Hypotension; Male; Nerve Tissue Proteins; Nucleobindins; Rats, Sprague-Dawley; Renin; Vasopressins

Vasopressin is often used locally to reduce blood loss during surgery. The use of a local infiltration of a low concentration of vasopressin, less than 0.05-0.3 units/mL, has been considered to be safe. The use of low-dose vasopressin is not free of side effects, and it can also sometimes cause lethal complications.. In a healthy woman with multiple uterine myomas, we experienced a case of sudden cardiac arrest immediately after the intramyometrial injection of vasopressin at a total dose of 11 units (0.2 units/mL). The patient was successfully resuscitated.. Local intramyometrial infiltration of low-dose vasopressin may cause lethal cardiopulmonary complications.

Topics: Blood Loss, Surgical; Bradycardia; Dose-Response Relationship, Drug; Female; Heart Arrest; Hemostatics; Humans; Injections, Intramuscular; Laparoscopy; Leiomyomatosis; Vasopressins

Labetalol is an effective antihypertensive medication frequently used to treat systemic hypertension in acute care settings, including the management of hypertension associated with a subarachnoid hemorrhage. We present a case of profound hypotension, refractory to inotropic and vasopressor therapy following an iv infusion of labetalol.. Initiation of an iv labetalol infusion resulted in good blood pressure control in a patient suffering from a Fisher grade 3 subarachnoid hemorrhage with an initial Glascow coma scale of 14/15 and mild hydrocephalus. Progressive deterioration of neurological symptoms and evidence of worsening hydrocephalus preceded the sudden development of profound hypotension (60/35 mmHg) and bradycardia with a minimum heart rate of 40 beats.min(-1). Initial resuscitative efforts included administration of intravascular fluid, hypertonic saline, atropine, adrenalin (more than 10 mg in divided doses) and noradrenalin. These measures restored the blood pressure to 80/45 with a HR of 98 beats.min(-1). Intraoperative placement of an intraventricular drain released cerebrospinal fluid under pressure with an initial intracranial pressure of 15 cm H(2)O. A combination of adrenalin, noradrenalin, dopamine and vasopressin infusions were required to restore the blood pressure to 130/65 mmHg after an additional two hours. All inotropic and vasopressor support was weaned off after the 14th hr (about two drug half-lives). The patient was awake and responsive the following day, with no obvious neurological consequences. No evidence of neurological injury, drug administration error or myocardial dysfunction was documented.. The episode of profound hypotension which occurred after initiating a labetolol infusion required maximal combined vasopressor therapy to restore the blood pressure suggesting that this patient demonstrated an extreme sensitivity to labetalol. Combination therapy with adrenergic and nonadrenergic agonists may be required for optimal treatment of profound hypotension associated with labetalol-induced vasoplegia.

Topics: Antihypertensive Agents; Bradycardia; Cardiotonic Agents; Dopamine; Epinephrine; Female; Humans; Hypotension; Intracranial Aneurysm; Labetalol; Middle Aged; Norepinephrine; Subarachnoid Hemorrhage; Time Factors; Vasoconstrictor Agents; Vasopressins

Vasopressin has been documented to effectively reduce blood loss in gynecologic practice. However, local infiltration of vasopressin may cause lethal cardiopulmonary complications in spite of rarity of reported cases. Severe bradycardia and cardiac arrest were encountered after intramyometrial injection of vasopressin in our two healthy patients undergoing open uterine myomectomy. We herewith discuss the associated complications and the anesthetic considerations.

Topics: Adult; Baroreflex; Bradycardia; Female; Heart Arrest; Hemostatics; Humans; Injections; Myometrium; Pulmonary Edema; Vasopressins

Vasopressin is an alternative drug to adrenaline in intractable ventricular fibrillation. However, vasopressin can cause significant bradycardia, resulting in reduced cardiac output. We investigated whether pre-treatment with atropine abrogates vasopressin-induced bradycardia in a beating-heart canine model.. Five adult mongrel dogs received endotracheal vasopressin (1.0 U/kg) with or without endotracheal atropine (0.02 mg/kg) or a placebo (10 ml saline) after being anesthetized and ventilated. Hemodynamic variables and arterial blood gases were determined. Each dog (studied 3 times, one week apart) served as its own control.. Endotracheal vasopressin produced early and significant (p<0.05) bradycardia (from 55+/-7 mmHg to 35+/-5 beats/min) compared with controls, starting one minute post-injection and lasting one hour. In contrast, in atropine-pretreated animals the heart rate increased significantly (p<0.05) for as long as one hour post-atropine and vasopressin administration. In addition, animals treated with vasopressin with or without atropine exhibited a significant rise in diastolic blood pressure (from 83+/-5 to 160+/-15 and from 83+/-3 to 108+/-10 mmHg, respectively). Systolic and mean blood pressures also increased significantly compared with controls. Blood gases remained unchanged in all groups.. Endotracheal administration of vasopressin can cause protracted bradycardia. Pretreatment with atropine can abrogate this effect. We suggest that atropine administration be considered when vasopressin is administered during cardio-pulmonary resuscitation. Further studies are warranted to evaluate the effect of vasopressin and atropine in a closed-chest model of cardio-pulmonary resuscitation.

Topics: Administration, Inhalation; Animals; Atropine; Blood Pressure; Bradycardia; Dogs; Female; Heart Rate; Intubation, Intratracheal; Male; Vasopressins

Severe hypotensive haemorrhage results in a biphasic response, characterized by an initial increase in heart rate and sympathetic vasomotor activity (phase I) followed by a life-threatening hypotension, accompanied by profound sympathoinhibition and bradycardia (phase II). The phase II response is believed to be dependent on inputs from cardiopulmonary receptors, and may be triggered by the reduction in venous return and cardiac filling associated with severe haemorrhage. In this study, we tested the hypothesis that the phase II response could be reversed by venoconstriction, which is known to enhance venous return and cardiac filling, by comparing the effects of phenylephrine (which constricts veins as well as arterioles) with that of vasopressin (which constricts arterioles but not veins). In sodium pentobarbitone-anaesthetised rats, haemorrhage evoked an initial increase in heart rate (HR) and renal sympathetic activity (RSNA) followed by a large decrease in both variables to levels below the pre-haemorrhage baseline levels (phase II response). During the phase II response, an intravenous injection of phenylephrine, sufficient to restore mean arterial pressure to the pre-haemorrhage level, resulted in a gradually developing increase (over 3-4 min) in HR and RSNA back to the baseline levels. In contrast, intravenous injection of an equipressor dose of vasopressin did not result in any increase in RSNA and only a transient increase in HR. Injection of phenylephrine, but not vasopressin, also increased the pulsatile component of central venous pressure, indicative of reduced venous capacitance. The findings indicate that venoconstriction reverses the phase II sympathoinhibition and bradycardia.

Topics: Animals; Blood Pressure; Bradycardia; Heart Rate; Hemorrhage; Hypotension; Male; Phenylephrine; Rats; Rats, Sprague-Dawley; Sympathetic Nervous System; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

Centrally acting cholinergic agents are currently reported to increase blood pressure in various species through the stimulation of muscarinic cholinoceptors. Moreover, several cardiovascular adverse effects have been reported from clinical studies. The aim of this study was to investigate the effects of tacrine, an acetylcholinesterase inhibitor which has been reported to have therapeutic potential in Alzheimer's disease, on blood pressure and two vasopressor systems (sympathetic and vasopressinergic) in Beagle dogs. Intravenous (i.v.) tacrine (2 mg kg(-1)) induced, in conscious and anesthetized dogs, an increase in systolic and diastolic blood pressure, accompanied by bradycardia. This increase was dose-dependent with a peak effect at 1.5 min following administration. Tacrine also induced an increase in noradrenaline, adrenaline and vasopressin plasma levels. Pretreatment with the muscarinic receptor antagonist, atropine (2 mg kg(-1), i.v.), abolished the pressor response to i.v. injection of tacrine while pretreatment with the peripheral muscarinic receptor antagonist, methylscopolamine (0.2 mg kg(-1), i.v.), did not alter the increase in blood pressure. Similarly, noradrenaline and adrenaline changes in plasma levels were not modified by methylscopolamine but were abolished by atropine pretreatment. A similar tendency although not significant was observed for vasopressin plasma levels. The present results demonstrate that in dogs, tacrine (2 mg kg(-1), i.v.) stimulates central muscarinic cholinoceptors to increase blood pressure through activation of the two components of the sympathetic nervous system (i.e., neuroneuronal noradrenergic and the neurohormonal adrenergic pathways) as well as through increasing noradrenaline, adrenaline and vasopressin plasma levels.

Topics: Animals; Atropine; Blood Pressure; Bradycardia; Cholinesterase Inhibitors; Dogs; Dose-Response Relationship, Drug; Epinephrine; Female; Injections, Intravenous; Male; Muscarinic Antagonists; N-Methylscopolamine; Norepinephrine; Parasympathomimetics; Receptors, Muscarinic; Tacrine; Vasopressins

To report a case of pulmonary edema after local injection of vasopressin at laparoscopy.. University teaching hospital.. A 24-year-old woman who underwent a laparoscopic myomectomy.. Injection of vasopressin (10 mL of 0.5 U/mL) into the uterine wall overlying the myoma.. Bradycardia, atrioventricular block, and pulmonary edema.. The use of vasopressin can be associated with severe cardiopulmonary complications.

Topics: Adult; Blood Pressure; Bradycardia; Female; Heart Rate; Humans; Injections; Laparoscopy; Leiomyoma; Myometrium; Pulmonary Edema; Uterine Neoplasms; Vasoconstrictor Agents; Vasopressins

Vasopressin is now commonly used to control bleeding during surgery of the cervix. In larger intravenous doses, vasopressin can cause coronary artery vasoconstriction and increase systemic vascular resistance. Nicotine has a similar effect on the coronary circulation. The effects of combining both these drugs has not been studied. We describe a 22-year-old woman who developed severe hypotension and bradycardia after receiving a small dose of paracervical vasopressin. She was using a transdermal nicotine patch at the time of her surgery. We suspect her cardiac problems, and recently reported cardiac events in other women receiving small doses of paracervical vasopressin, could be caused by a synergism of the vasoconstrictive properties of nicotine and vasopressin. Caution is urged when vasopressin is to be administered to patients who smoke or use nicotine transdermal patches.

Topics: Administration, Cutaneous; Adult; Bradycardia; Cervix Uteri; Conization; Drug Synergism; Female; Heart Rate; Humans; Hypotension; Nicotine; Smoking Cessation; Tobacco Use Disorder; Uterine Cervical Dysplasia; Vasopressins; Vulvar Diseases

Topics: Bradycardia; Cervix Uteri; Female; Hemostatics; Humans; Injections; Pulmonary Edema; Vasopressins

Topics: Adult; Bradycardia; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Hyponatremia; Pregnancy; Pregnancy Complications, Cardiovascular; Vasopressins

Vasopressin may be associated with systemic hemodynamic changes, including severe myocardial ischemia, even in healthy patients. A 36-year-old woman underwent laparoscopy for the treatment of a uterine leiomyoma. After intravascular injection of vasopressin, she experienced life-threatening hypotension, and the procedure was subsequently aborted. After she recovered, she underwent successful laparoscopy without the use of vasopressin, and no complications occurred. As endogenous vasopressin levels sometimes rise during laparoscopy, patients may become susceptible to the drug's effects, and appropriate precautions must be taken.

Topics: Adult; Blood Pressure; Bradycardia; Female; Follow-Up Studies; Hemostatics; Humans; Hypotension; Injections; Intraoperative Complications; Laparoscopy; Leiomyoma; Reoperation; Uterine Neoplasms; Vasoconstrictor Agents; Vasopressins

Continuous infusion of IV vasopressin have been widely used to lower portal pressure and reduce bleeding from esophageal varices. Recently, the combination of vasopressin and nitroglycerin has been noted to be superior to vasopressin alone. This is due to the ability of nitroglycerin to reduce the detrimental effects of vasopressin while preserving its beneficial effects. In September 1989 the authors initiated a protocol in the medical intensive care unit of a large university teaching center that directed caregivers in the simultaneous use of vasopressin and nitroglycerin for use in variceal bleeding.. To determine whether the protocol was being used correctly and whether the addition of nitroglycerin produced the desired cardiovascular effects.. Nineteen patients (25 separate episodes) assigned to the vasopressin/nitroglycerin protocol were monitored retrospectively over a 20-month period for a total of 1068 hours of vasopressin/nitroglycerin infusion. Twenty-four patients received nitroglycerin at 10 to 50 micrograms per minute, 13 at 50 to 100 micrograms per minute and 6 at 100 to 400 micrograms per minute.. Nitroglycerin dosage was not advanced appropriately in 78% of episodes despite evidence of bradycardia, hypertension and peripheral vasoconstriction.. Revision of the protocol, giving additional guidance to clinicians on assessment and nitroglycerin advancement, was necessary and was accomplished.

Topics: Bradycardia; Clinical Protocols; Constriction, Pathologic; Drug Monitoring; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Heart Rate; Hemodynamics; Humans; Hypertension; Infusions, Intravenous; Nitroglycerin; Nursing Assessment; Nursing Evaluation Research; Nursing Records; Patient Care Planning; Practice Patterns, Physicians'; Retrospective Studies; Vasopressins

Intracerebroventricular administration of serotonin (5-HT) to conscious rats increases mean arterial pressure (MAP) and decreases heart rate. To determine the mechanisms involved, 5-HT (2.5 micrograms) was injected intracerebroventricularly into conscious rats pretreated with various neurotransmitter and hormone antagonists. The selective 5-HT2 antagonist LY 53857 abolished the increase in MAP and the bradycardia elicited by 5-HT. The increase in MAP produced by 5-HT was potentiated by chlorisondamine (a ganglionic antagonist), unaffected by prazosin (an alpha 1-antagonist) or a vasopressin V1 antagonist alone, but eliminated by the combined pretreatment with prazosin plus the vasopressin antagonist. In contrast, the bradycardia was eliminated by either the vasopressin V1 antagonist or chlorisondamine. In conclusion, 5-HT injected into the lateral cerebral ventricle of conscious rats induces sympathoexcitation and the release of vasopressin, which results in an increase in MAP; 5-HT also elicits a bradycardia mediated through an interaction of the autonomic nervous system with circulating vasopressin.

Topics: Animals; Autonomic Nervous System; Blood Pressure; Bradycardia; Chlorisondamine; Ergolines; Heart Rate; Hypertension; Injections, Intraventricular; Male; Prazosin; Rats; Rats, Inbred Strains; Serotonin; Serotonin Antagonists; Vasopressins

Plasma atrial natriuretic factor, aldosterone, renin activity, and antidiuretic hormone were studied in low output heart failure syndromes: cardiogenic shock in ten patients with acute myocardial infarction of the anterior wall (first group), hypovolemic shock after melena from peptic ulcer in ten subjects (second group), and hypotension with bradycardia syndrome in ten patients with acute myocardial infarction of the inferior wall (third group). Circulating atrial natriuretic factor in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) was significantly higher than in healthy volunteers matched for sex and age (8.4 +/- 0.3 pg/ml). In these patients there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the second and third groups were within normal range. Plasma aldosterone was high in all groups, plasma renin activity was elevated in the first and third groups, and high antidiuretic hormone was observed in the first and second groups. These findings indicate that in low output heart failure syndromes only hemodynamic changes affecting the atria stimulate atrial natriuretic factor release. No correlations were found between plasma atrial natriuretic factor and other hormones. In particular, high atrial natriuretic factor levels in the patients with cardiogenic shock did not inhibit release of aldosterone, renin, or antidiuretic hormone. It may be surmised that in these patients the hemodynamic effects override the inhibitory effects of atrial natriuretic factor.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Blood Volume; Bradycardia; Cardiac Output, Low; Female; Heart Failure; Humans; Male; Melena; Middle Aged; Myocardial Contraction; Myocardial Infarction; Peptic Ulcer Hemorrhage; Renin; Shock, Cardiogenic; Vascular Resistance; Vasopressins; Venous Pressure

Topics: Aged; Bradycardia; Esophageal and Gastric Varices; Humans; Male; Nursing Assessment; Vasopressins

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Bradycardia; Cardiac Output, Low; Female; Hemodynamics; Humans; Hypotension; Male; Middle Aged; Myocardial Infarction; Renin; Shock; Shock, Cardiogenic; Vasopressins

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.

Topics: Adrenocorticotropic Hormone; Animals; Blood Pressure; Bradycardia; Glutamates; Glutamic Acid; Heart Rate; Male; Microinjections; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland; Rats; Rats, Inbred Strains; Vasopressins

The cardiovascular effects of centrally administered cholinomimetics were examined in conscious Long-Evans and Brattleboro rats. Carbachol (1 microgram/kg) or physostigmine (50 micrograms/kg) induced a long-lasting increase in blood pressure and a decrease in heart rate in Long-Evans rats whereas no bradycardia was observed in Brattleboro rats, and the pressor response was significantly less than that in Long-Evans rats. The cardiovascular responses to nicotine (30 micrograms/kg) in Brattleboro rats were not different from those in Long-Evans rats. Intravenous vasopressin antagonist, d(CH2)5Tyr(Me) arginine vasopressin, significantly attenuated the pressor response and eliminated the bradycardic response to carbachol in Long-Evans rats. However, the pressor response to carbachol in Brattleboro rats was still significantly less than that in Long-Evans rats treated with vasopressin antagonist. Intravenous phentolamine partially inhibited the pressor response to carbachol in Long-Evans rats and completely eliminated it in Brattleboro rats. Combined intravenous treatment with phentolamine and vasopressin antagonist completely eliminated the pressor response to carbachol in Long-Evans rats. Centrally administered methylatropine eliminated either the hypertensive or bradycardic response to carbachol in Long-Evans rats. These results indicate that the pressor and bradycardic response to carbachol or physostigmine is mediated by the central muscarinic receptor mechanism. Hypertensive response to intracerebroventricularly administered carbachol in normal rats is mediated both by an increase in central sympathetic outflow and in circulating vasopressin. The bradycardia seems to be mediated mainly by vasopressin.

Topics: Animals; Arginine Vasopressin; Atropine Derivatives; Autonomic Nervous System; Blood Pressure; Bradycardia; Carbachol; Cardiovascular Physiological Phenomena; Cardiovascular System; Deamino Arginine Vasopressin; Hypertension; Injections, Intraventricular; Male; Nicotine; Parasympatholytics; Phentolamine; Physostigmine; Rats; Rats, Brattleboro; Vasopressins

A 59-year-old man with severe variceal bleeding received therapy with intravenously administered vasopressin and cimetidine. Inappropriate bradycardia, sinoatrial and atrioventricular blocks, and terminal bradycardia leading to asystole, occurred during bleeding, with the greatest number of rhythm abnormalities occurring during combined cimetidine and vasopressin therapy. The results of post-mortem examination showed only mild coronary artery disease. The hazards of combined vasopressin and cimetidine therapy are reviewed.

Topics: Arrhythmias, Cardiac; Bradycardia; Cimetidine; Coronary Disease; Drug Therapy, Combination; Electrocardiography; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Guanidines; Heart Block; Humans; Male; Middle Aged; Vasopressins

Rats subjected to various levels of +Gz acceleration exhibited an increased blood concentration of noradrenalin and adrenalin, indicative of a sympatho-adrenergic reaction. Under the same conditions, from plasma determinations, and by histochemical examination of the supra-optic nucleus, an increased antidiuretic response was noted. This response was reduced in cold environment.

Topics: Animals; Bradycardia; Centrifugation; Cold Temperature; Epinephrine; Heart Rate; Hypergravity; Male; Noise; Norepinephrine; Rats; Rats, Wistar; Supraoptic Nucleus; Tachycardia; Vasopressins

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Animals; Arrhythmias, Cardiac; Bradycardia; Dextrans; Electrocardiography; Energy Metabolism; Flavin-Adenine Dinucleotide; Glycogen; Lysine; Microcirculation; Mitochondria, Muscle; Molecular Weight; Myocardium; NAD; Oxidative Phosphorylation; Oxygen Consumption; Phosphorus; Phosphorylases; Rabbits; Stimulation, Chemical; Succinates; Vasopressins

Topics: Adrenal Glands; Adrenal Insufficiency; Blindness; Bradycardia; Brain; Electrolytes; Female; Glucagon; Glucose; Glucose Tolerance Test; Growth Hormone; Humans; Hypoglycemia; Hypopituitarism; Infant; Infant, Newborn; Infant, Newborn, Diseases; Insulin; Intellectual Disability; Male; Pituitary Gland; Seizures; Vasopressins

Topics: Adenosine Triphosphate; Animals; Arrhythmias, Cardiac; Bradycardia; Coronary Circulation; Dextrans; Electrocardiography; Erythrocyte Aggregation; Glucosyltransferases; Glycogen; Heart; Hypoxia; Microcirculation; Mitochondria, Muscle; Myocardium; Oxidative Phosphorylation; Phosphocreatine; Rabbits; Rats; Vasopressins

1. Injection of 0.5-2.0 units of vasopressin or 25-100 mug of adrenaline into the peritoneal cavity of pregnant rats produced a transient slowing of the foetal heart. The bradycardia could be induced in foetuses after 15-21 days of gestation. Foetal heart rates dropped from normal values of 140-180 beats/min, often to less than 20 beats/minute. The period of bradycardia was dose dependent and ranged from 30 to 65 minutes.2. Maternal injection of the hormones produced a fall in foetal blood pressure from an average of 54, often to less than 20 mm of water, in 17-day foetuses. Direct injection of the hormones into the pericardial sac of the foetuses had the opposite effect and pressures rose an average of 15 mm of water 1 min after the injection.3. During the period of bradycardia, the potassium concentrations in foetal serum rose from an average value of 8.9 mequiv/1. to an average of 17.3 mequiv/litre. Concentrations of serum sodium fell from 126.2 to 121.4 mequiv/1. during the bradycardia. No changes were detected in the concentrations of either calcium or chloride. Foetal P(O2) levels fell from 25 to 15, P(CO2) rose from 61 to 89 or more, and pH fell from 7.19 to 6.86 during the bradycardia.4. Maternal death and uterine clamping caused foetal bradycardia and a rise in foetal serum potassium to an average of 20.2 mequiv/litre.5. It is concluded that interruption of normal uterine blood flow by vasoconstruction (adrenaline or vasopressin) or direct blockage (uterine clamping) results in a transient hypoxia, bradycardia, and serum ion changes in foetuses.

Topics: Animals; Blood Pressure; Bradycardia; Calcium; Carbon Dioxide; Chlorides; Clinical Trials as Topic; Epinephrine; Female; Fetal Heart; Fetus; Heart Rate; Injections, Intraperitoneal; Maternal-Fetal Exchange; Oxygen Consumption; Potassium; Pregnancy; Rats; Sodium; Time Factors; Vasopressins

Topics: Animals; Blood Pressure; Bradycardia; Cerebral Ventricles; Dogs; Injections; Injections, Intravenous; Vasopressins

Topics: Anesthesia, Inhalation; Atrial Fibrillation; Bradycardia; Female; Halothane; Heart Arrest; Humans; Uterine Prolapse; Vasopressins

Topics: Animals; Blood Pressure; Blood Pressure Determination; Bradycardia; Cardiac Output; Cardiovascular System; Dogs; Heart; Heart Rate; Hemodynamics; Hypoxia; Injections, Intravenous; Lactates; Myocardium; Oxygen; Oxygen Consumption; Respiration; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

Topics: Adenosine Triphosphate; Animals; Blood; Blood Pressure; Bradycardia; Carotid Arteries; Hypotension; Pyrophosphatases; Rats; Sympatholytics; Vasopressins; Water

Topics: Animals; Arginine Vasopressin; Arrhythmias, Cardiac; Atropine; Bradycardia; Coronary Vessels; Dipyridamole; Electrocardiography; Pharmacology; Rabbits; Rauwolfia; Research; Vasodilator Agents; Vasopressins

Topics: Blood Pressure; Bradycardia; Cats; Heart Conduction System; Hypoxia; Physiology; Research; Spinal Cord Compression; Vasopressins