Significant Release Of Catecholamines Research Articles

Takotsubo syndrome: unravelling the enigma of the broken heart syndrome?-a narrative review.

Takotsubo syndrome (TTS) is a condition characterized by transient ventricular regional wall motion abnormalities, without causative coronary artery disease, typically triggered by emotional or physical stress. TTS is more common in post-menopausal women, closely resembling acute coronary syndrome (ACS) in its clinical presentation, with multiple proposed underlying pathophysiological mechanisms and no evidence-based treatments. This review aims to provide a comprehensive summary of the latest research, encompassing the pathophysiology, diagnostic findings, prognosis, and treatment options for TTS patients. Relevant literature from 1990 to June 2023 on TTS epidemiology, physiopathology, diagnosis, clinical manifestations, treatment, and prognosis was retrieved through PubMed research. Only English publications were included. TTS is an increasingly recognized cardiovascular disorder, a significant release of catecholamines is thought to be a key contributing element, yet its exact mechanism remains unclear. Notably, TTS poses significant short and long-term risks akin to ACS. Initial treatment should focus on ruling out ACS and providing standard care for subsequent left ventricular dysfunction and complications. Research hints at a potential role for Angiotensin-converting enzyme inhibitors and Angiotensin II receptor blockers in improving long-term prognosis in TTS patients. Significant knowledge gaps still exist in our understanding of the pathophysiology, treatment options, and areas for improvement in diagnosing and prognosticating this intriguing condition. Further research is therefore needed.

Myocardial effects of desflurane in hamsters with hypertrophic cardiomyopathy.

The effects of desflurane on myocardial contraction and relaxation in diseased myocardium have not been completely understood. The effects of desflurane (1.8 to 9.4 vol%) in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C, pH 7.40, Ca2+ 2.5 mM; stimulation frequency, 3/min) under low (isotony) and high (isometry) load. Data are mean percentages of baseline +/- SD. Desflurane induced no significant inotropic effect in healthy muscles (maximum unloaded shortening velocity and isometric active force at 9.4 vol%: 97 +/- 9% and 92 +/- 20%, respectively). In contrast, in cardiomyopathic muscles, desflurane induced a moderate negative inotropic effect (maximum unloaded shortening velocity and active force at 9.4 vol%: 84 +/- 19% and 75 +/- 25%, respectively). The negative inotropic effect was more pronounced than that in healthy muscles under low (P < 0.05) but not high load, and even when concentrations were corrected for minimum alveolar concentrations in each strain. Adrenoceptor blockade or pretreatment with reserpine did not modify the inotropic effect of desflurane, suggesting the absence of intramyocardial catecholamine release. However, tyramine also did not induce any significant catecholamine release in hamster myocardium. In both strains, desflurane induced no significant lusitropic effect under low or high load. Desflurane had no inotropic effect in healthy muscles and a moderate negative inotropic effect in cardiomyopathic muscles. The absence of desflurane-induced intramyocardial catecholamine release was related to hamster myocardium characteristics.

Does hormonal function of the tumor influence the outcome of laparoscopic adrenalectomy?

Patients with hypertension, with catecholamine hypersecretion, and with cortisol excess may associate intraoperative cardiovascular instability and postoperative complications. To compare the outcome of laparoscopic adrenalectomy (LpA) in patients with aldosterone adenoma (11), Cushing's adenoma (six), Cushing's disease (four), pheochromocytoma (Pheo) (11), and nonfunctioning tumor (five). Intra- and postoperative parameters were studied and in patients with Pheo intraoperative catecholamine plasma levels were correlated with cardiovascular derangements. Operative time, estimated blood loss, hospital stay, analgesic requirements, and time to return to normal activity were significantly higher in patients undergoing total bilateral adrenalectomy for Cushing's syndrome compared with other groups undergoing unilateral adrenalectomy, but these latter groups showed no significant differences among themselves in all parameters analyzed. One patient with nonfunctioning tumor and another with Cushing's adenoma were converted to open surgery, and two patients with Cushing's disease had urinary infection. Isolation of Pheo was associated with significant release of catecholamines but not with hemodynamic changes. LpA may be the most suitable method for removing functioning adrenal tumors.

Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata.

The cholinergic agonist-induced secretion of catecholamines from chromaffin cells in the American eel, Anguilla rostrata, was assessed using a saline-perfused posterior cardinal vein preparation. Direct membrane depolarization with 60 mmol.l-1 K+ caused a significant release of catecholamines (adrenaline+noradrenaline) into the perfusate which was unaffected by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The nicotinic receptor agonist, 1,1-dimethyl-4-phenyl-piperazinium iodide, evoked catecholamine release in response to several doses exceeding 10(-7) mol; at 10(-5) mol the response was abolished by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The muscarinic receptor agonist, pilocarpine, did not elicit catecholamine release in response to any of the doses administered (10(-8)-10(-4) mol). A single injection of the mixed nicotinic/muscarinic cholinoceptor agonist, carbachol (10(-5) mol), caused the release of catecholamines which was abolished by pre-treatment with hexamethonium but which was unaffected by pre-treatment with the muscarinic receptor antagonist atropine (final concentration = 10(-5) mol.l-1). The results of this study indicate that the process of cholinergic agonist-induced catecholamine secretion from the chromaffin cells in the American eel is mediated exclusively by activation of nicotinic receptors with no involvement of the muscarinic receptor.

Storage and Release of Catecholamines from the Chromaffin Tissue of the Atlantic Hagfish Myxine Glutinosa

ABSTRACT A variety of in vivo and in situ experiments were performed on the Atlantic hagfish (Myxine glutinosa) (i) to characterize the levels of circulating catecholamines during acute stresses, including hypoxia, anoxia or physical disturbance (air-exposure), and (ii) to evaluate the potential mechanisms of catecholamine release from the major sites of storage, the systemic heart and posterior cardinal vein (PCV). Adrenaline and noradrenaline were stored at roughly equivalent concentrations (approximately 20 μgg-1) in cardiac tissue, whereas noradrenaline was the predominant catecholamine stored in the PCV (approximately 50 μgg-1). The heart stored larger quantities of total catecholamines than did the PCV (approximately three times greater) owing to its larger mass and higher concentration of adrenaline. Exposure of chronically cannulated hagfish to acute hypoxia [mean water 10.5mmHg) for 30min caused a significant decrease in arterial (from 11.5±1.3kPa to 1.2±0.3kPa) and arterial O2 content (from 3.9±0.3ml100ml-1 to 0.9±0.2ml100ml−1). The hypoxaemia was associated with a significant increase in plasma noradrenaline levels, whereas plasma adrenaline levels were unaffected. Exposure of uncannulated fish to anoxia ( approximately 0kPa) or physical disturbance (15min of air-exposure) also elicited pronounced increases in plasma noradrenaline levels (6–10 times) and, to a lesser extent, adrenaline levels (2–3 times). An in situ saline-perfused heart preparation was utilized in an attempt to elucidate the mechanism(s) underlying the stress-induced release of catecholamines from the chromaffin tissue of the heart and PCV. Non-specific cell membrane depolarization using 40 or 60mmol l−1 K+ in the saline elicited a marked release of catecholamines, confirming the suitability of the preparation to assess specific physiological mechanisms of catecholamine release. Lower concentrations of K+ (15–20mmol l−1) did not evoke catecholamine release, indicating that relatively minor elevation in plasma [K+], as might occur during hypoxia, is not a contributing factor. The cholinergic receptor agonist carbachol (10−5–10−4 molkg−1) caused a significant release of catecholamines, yet the likelihood of a similar mechanism operating in vivo is doubtful because the hagfish heart is not thought to be innervated. Simulation of (i) internal hypoxaemia by perfusing with anoxic saline or (ii) physical disturbance by perfusing with relatively acidic saline (pH approximately 7.0) failed to elicit catecholamine release. Further, the elevation of perfusion (input) pressure to simulate a rise in venous blood pressure, as might occur during hypoxia or physical disturbance, was also without effect on release. The addition of pituitary extract (from Atlantic cod, Gadus morhua) to the inflowing saline caused a marked release of catecholamines from the chromaffin tissue. Thus, the mechanism(s) of release of catecholamines from the heart of hagfish during stress in vivo remains unclear, although preliminary experiments suggest the possible involvement of pituitary hormones.

Catecholamine release from bovine adrenal chromaffin cells during anoxia or metabolic inhibition.

A significant release of catecholamines within the heart has been observed during myocardial ischemia. Because this can be markedly inhibited by amine-uptake-blocking agents, it has been suggested that its mechanism is a carrier-mediated efflux from neurons, which is not operative under normal conditions. The present work examined this release process in chromaffin cells isolated from the bovine adrenal medulla, a model system for studying the sympathetic nervous system. Chromaffin cells in primary culture retained normal secretory responses for up to 7 days. Conditions designed to mimic ischemia, that is, anoxia or metabolic inhibition, resulted in a significant release of catecholamines. This release was shown to be independent of extracellular calcium but, in contrast to the release observed in ischemic hearts, was not inhibited by amine-uptake blockers. Electrophoresis with immunoblotting demonstrated that significant levels of the chromaffin granule protein, chromogranin A, were released during metabolic inhibition, indicative of an exocytotic mechanism. However, there was no release of the cytosolic protein, lactate dehydrogenase, indicating that there was no concomitant breakdown of the cell membrane. These results provide evidence for an exocytotic release of catecholamines mediated by the direct action of conditions of metabolic inhibition.

Adrenal and pancreatic endocrine responses to hypoxia and hypercapnia in the calf.

1. Adrenal and pancreatic endocrine responses to hypoxia and hypercapnia, of differing degrees of intensity, have been examined in conscious, unrestrained calves 3-5 weeks after birth. 2. The outputs of cortisol and corticosterone from the right adrenal gland were found to vary inversely with arterial Po2 between 17 and 55 mmHg. Significant increase in mean adrenal blood flow was not observed at arterial oxygen tensions above about 30 mmHg. 3. Release of physiologically effective amounts of catecholamines from the adrenal medulla occurred only in response to intense hypoxia (arterial Po2 17-1 +/- 2-8 mmHg) and was effectively abolished by section of both splanchnic nerves. Release of pancreatic glucagon in response to such intense hypoxia was unaffected by section of both splanchnic nerves and administration of atropine. In contrast, the rise in plasma pancreatic glucagon concentration during less intense hypoxia was abolished by autonomic blockade. 4. Hypercapnia produced by inhalation of either 5% or 10% CO2 for 30 min stimulated maximal release of adrenal glucocorticoids and caused a substantial rise in plasma glucagon concentration. In contrast, the adrenal medulla was found to be extremely resistant to hypercapnia. Significant release of catecholamines was only observed during intense hypercapnia (inhalation of 10% CO2) and noradrenaline was invariably found to be the predominant amine. 5. The results of these experiments show how endocrine responses to hypoxia and hypercapnia are graded in the conscious calf. Of the mechanisms we have examined the pituitary-adrenal cortical axis is the most sensitive and the adrenal medulla the most resistant, while the pancreatic alpha cell occupies an intermediate position.

The influence of calcium on catecholamine liberation

(1) Experiments on isolated perfused suprarenals of cattle have shown that the acetylcholine-induced release of catechol amines, but not that of phenylethylamine, is dependent on calcium, since a perfusion with calcium-free Tyrode's solution abolishes the action of acetylcholine and not that of phenylethylamine. (2) Inincubation experiments with isolated chromaffin granules, calcium produces a dose-dependent, significant release of catechol amines even in physiological concentrations (2.5 mM). (3) Acetylcholine does not release catechol amines from isolated granules, either in the presence or in the absence of calcium.