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2015
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tom 87
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nr 4
189-193
EN
An exemplary rare case of neurogenic pulmonary edema induced by intracranial hemorrhage was reported including diagnostic and therapeutic implications as well as management recommendations. A 35-year old man who was treated first by a neurosurgical approach because of a subarachnoid hemorrhage (bore hole trepanation) and subsequently on a surgical intensive care unit because of severe postoperative hemodynamic, cardiocirculatory, and pulmonary disruptions. To monitor cardiopulmonary condition and treatment effects, a Swan-Ganz catheter was placed in the pulmonary artery, since after trepanation, a critical cardiopulmonary status developed during postoperative mechanical ventilation and catecholamine administration. This condition was indicated by neurogenic pulmonary edema detected by control chest X-ray film and high oxygen load in the inspiratory air required for sufficient arterial oxygenation. After use of high positive end-exspiratory pressure (PEEP) (initially directed against neurogenic lesion), adaptation of initial dobutamine doses, initiation of norepinephrine administration, and substitution of fluids, the patient's blood pressure finally rose sufficiently to sustain regular cerebral blood perfusion and achieve better arterial oxygenation. Thus, the patient‘s cardiopulmonary condition stabilized and temporary cardiac insufficiency could be overcome. Subsequently, it became possible to decrease PEEP according to requirements to prevent or limit cerebral edema and to diminish catecholamine doses.
EN
Exposure to LBNP results in body fluid shift to lower extremities similarly as under influence of orthostatic stress. In susceptible persons it leads to syncope. For better understanding why certain individuals are more susceptible to orthostatic challenges it seemed necessary to collect more data on hemodynamic and neuroendocrine adjustments occurring before onset of presyncopal symptoms Accordingly, in this study heart rate (HR), blood pressure (BP), stroke volume (SV), cardiac output (CO), hematocrit, plasma catecholamines, adrenomedullin, ACTH and plasma renin activity (PRA) were measured in 24 healthy men during graded LBNP (-15, -30 and -50 mmHg). Thirteen subjects completed the test (HT group) whereas 11 had presyncope signs or symptoms at -30 mmHg or at the beginning of -50 mmHg (LT group). Comparison of these groups showed that LT subjects had lower baseline total peripheral resistance and higher plasma adrenomedullin. During LBNP plasma catecholamine and PRA increases were even greater in LT than in HT group while plasma adrenomedullin elevations were similar in both groups. Plasma ACTH increased only in LT group following presyncope symptoms. Low tolerant group showed more rapid decline of SV and CO than HT subjects from the beginning of LBNP. It is suggested that measurements of SV at the level of LBNP which did not evoke any adverse symptoms may be of predictive value for lower orthostatic tolerance.
EN
According to current teaching biogenic amines are released by exocytos- is, i. e. by evacuation of amine storing vesicles or granules into the extracellular space. The release of transmitter amines is quantal, i. e. occurs in packs of transmitter molecules. These packs are assumed to be identical with vesicle contents, in other words, the smallest releasable quantum equals the amine content of one vesicle. However, there are experimental observations which do not fit in with this version of an exocytotic release theory. Observed quantitative discrepancies could be explained if the release mechanism allowed a fractional release of transmitter amine from several vesicles instead of the total evacuation of a few. The lack of adequate knowledge about the mechanisms of storage of biogenic amines within the vesicles has up til now rendered it difficult to envisage the machinery behind a fractional release of the amine content of a vesicle. In extensive in-vitro studies we have found that the matrices of amine storing granules (i. e. from mast cells, chromaffin cells and nerve terminals) show the properties of weak cation exchanger materials, carboxyl groups serving as amine binding ionic sites. When exposed to cations like sodium and potassium ions, the amines are released from their storage sites according to kinetics characteristic of weak cation exchangers. In vivo, amine release from cat adrenals on splanchnic nerve stimulation also occurs according to ion echange kinetics. Histamine release from mast cells is considered to occur as the result of degranulation, i. e. the expulsion of histamine storing granules to the extracellular space, a typical example of exocytosis. The granules are assumed to loose their histamine by ion exchange, Na⁺ Hi⁺, on exposure to the sodium-rich extracellular medium. However, recent observations on histamine release from superfused mast cells suggest that the release of histamine, although caused by ion exchange, is due to intracellular ion exchange at granule sites between cytoplasmic potassium and activated mast cells as the consequence of intracellular potassium ion flux across the histamine carrying granules, degranulation and extracellular histamine release from expelled granules occurring only as the result of more extensive activation. The possibility of potassium ions being involved also in an ion exchange process behind the release of other biogenic amines e. g. at nerve terminals will be proposed. The amine release will still be quantal but the size of the released quanta will not depend on the total amine content of a vesicle but on the size of the fractions thereof being released, thereby explaining many of the quantitative discrepancies attached to the current exocytotic release theory. A fractional release theory may have interesting consequences for our thinking as to the physiology and pharmacology of processes involving storage and release of biogenic amines.
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tom 59
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nr 3
603-616
EN
Aim of this study was to elucidate the influence of carbohydrate store modification on exercise capacity and catecholamine thresholds. Nine sedentary students and 10 endurance athletes volunteered for the study consisting of four sessions in one-week intervals. During control session (C) subjects performed graded exercise till exhaustion with workload increasing by 50 Watts every 3 min after an overnight fast. Blood lactate and catecholamines were determined at rest, after each workload and at exhaustion. In the evening preceding each of the remaining three sessions subjects performed glycogen reducing exercise lasting 1.5 hrs at 70% HRmax. Till next morning they did not eat any meal but drank water. Two hours before exercise subjects were given either a high-carbohydrate (H-CHO) or a low-carbohydrate (L-CHO) meal of approx. 1000 kcal or remained fasted (F). Depletion of carbohydrate stores enhanced contribution of fat-derived energy substrates at submaximal workloads, but did not influence either maximal oxygen consumption, workload and lactate concentration or lactate threshold. Low carbohydrate availability resulted in elevated concentration of catecholamines only in untrained subjects. Ingestion of a meal either high or low in carbohydrates diminished those changes. Catecholamine thresholds were similar in all sessions and higher in athletes’ group.
EN
The presence of catecholamines in the nervous system of a plagiorchiid cercaria of Opisthioglyphe ranae (Frölich, 1791) is demonstrated using fluorescence methods (SPG method after De la Torre and Surgeon 1976, exciting filter of 400-410 nm max. wave length). Comparison of the distribution of catecholamines and acetylcholinesterases in the cercaria of the same species showed closely similar patterns. However, some differences in distribution were identified and these are discussed.
EN
The ontogeny of the catecholaminergic system of the median eminence (ME) arcuate nucleus (ARC) complex (MEARC) has been studied in various animal species but so far, nothing has been learnt about the development of catecholaminergic structures in the porcine MEARC. To study this problem the hypothalami from animals at different ages (six groups) were collected. Nerve structures immunoreactive (IR) for the substances studied [(tyrosine hydroxylase (TH), dopamine b-hydroxylase (DbH) and phenylethanoloamine-N-metylthransferase (PNMT)] were found in the pigs at different age periods. In MEARC, TH-IR structures appeared before the 70th day of foetal life, DbH-IR before the 10th week of postnatal life and PNMT-IR only in sexually mature sows.
EN
Myosin VI (MVI) is the only known myosin walking towards minus end of actin filaments. Here, MVI, but not myosins IB or IIB, was detected in chromaffin granules isolated from bovine medulla and found to be tightly associated with the granule apical surface. MVI also localized to secretory granules within rat pheochromocytoma PC12 cells as well as to the Golgi apparatus, endoplasmic reticulum and clathrin-coated pits. Notably, it was also found in the nucleus. RT-PCR revealed that MVI splice variants with a large insert (LI), characteristic of polarized cells, were barely detectable in PC12 cells, whereas variants with a small insert (SI) were the major isoforms. The presented data indicate that MVI in adrenal medulla cells is engaged in secretory vesicle trafficking within the cytoplasm and possibly also involved in transport within the nucleus.
EN
Conscious rats were given i. p. polyethylene glycol (PEG) or dextran injections to compare their efficacy in inducing moderate hypovolaemia. Dextran was found unsuitable, producing large variability in the the plasma vasopressin (A VP) concentrations. Putative neurotransmitters involved in the A VP response to hypovolaemia and in basal release were examined using opioid, and ß-adrenoceptor and dopamine receptor-blocking agents. A dose of PEG was chosen to produce a decrease in blood volume of approx 14.5% giving plasma AVP concentrations of 19.0±4.6 pmol/1. Naloxone and phenoxy- benzamine failed to influence AVP release under both hypovolaemic and basal conditions. Prazosin also failed to influence the AVP response. In contrast propranolol elevated the plasma AVP concentrations in both conditions. Haloperidol enhanced basal AVP release but did not influence release during hypovolaemia. Guanethidine pretreatment partially blocked the response to hypovolaemia, but did not affect basal plasma AVP. Thus it appears that aminergic pathways have an inhibitory influence on AVP release under hypovolaemic and basal conditions. However, endogenous opioids do not appear to contribute significantly to the hypovolaemic response.
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