Search results for "Perfusion"
showing 10 items of 714 documents
Computer Modeling for the Prediction of Thoracic Aortic Stent Graft Collapse
2011
OBJECTIVE: To assess the biomechanical implications of excessive stent protrusion into the aortic arch in relation to thoracic aortic stent graft (TASG) collapse by simulating the structural load and quantifying the fluid dynamics on the TASG wall protrusion extended into a model arch. METHODS: One-way coupled fluid-solid interaction analyses were performed to investigate the flow-induced hemodynamic and structural loads exerted on the proximal protrusion of the TASG and aortic wall reconstructed from a patient who underwent traumatic thoracic aortic injury repair. Mechanical properties of a Gore TAG thoracic endoprosthesis (W. L. Gore and Assoc, Flagstaff, Ariz) were assessed via experimen…
Effects of Atropine on Acetylcholine Overflow from Perfused Chicken Hearts
1978
Isolated chicken hearts were perfused (20 ml/min) with Tyrode’s solution. Release of acetylcholine (ACh) was evoked either by electrical stimulation (1 ms; 15 mA) of both preganglionic vagus nerves or by perfusion with dimethylphenylpiperazinium (DMPP). ACh was extracted from the perfusates by ion-pair extraction and determined by gas chromatography.
Non-adrenergic non-cholinergic nerve-mediated inhibitory control of pigeon oesophageal muscle.
1996
Pigeon oesophageal smooth muscle in vitro has spontaneous electromechanical activity. In the presence of atropine and guanethidine, electrical field stimulation evokes a transient TTX-sensitive response comprising inhibition of electric bursting activity and muscular relaxation. This NANC inhibitory response was analysed using the K+ channel blockers TEA and apamin, TEA perfusion (0.1-5 mM) induced a concentration-dependent reduction in amplitude of EFS-evoked relaxation. Responses to higher stimulation frequencies were more sensitive to TEA than those to lower ones. The maximum reduction in amplitude (29% of control) was obtained on 30 Hz EFS evoked responses during 5 mM TEA perfusion. In …
Autoinhibition of nicotinic release of noradrenaline from postganglionic sympathetic nerves
1970
1. The effects of nicotine, DMPP (1,1-dimethylphenylpiperazine) and acetylcholine (plus atropine) on the isolated rabbit heart were investigated. Heart rate, amplitude of contraction, coronary flow and output of noradrenaline into the perfusate were recorded. Noradrenaline was estimated fluorimetrically. 2. All nicotinic drugs evoked a dose-dependent output of noradrenaline and increased the rate and the amplitude of contraction. Increases of heart rate in response to nicotine and DMPP and increases of amplitude of contraction in response to all nicotinic drugs were clearly related to the output of noradrenaline. 3. The dose-response curves of the noradrenaline output evoked by nicotine, DM…
Safety and feasibility of atropine added in patients with sub-maximal heart rate during exercise myocardial perfusion SPECT.
2006
Failure to reach 80% of maximal predicted heart rate (HR) during exercise may render a myocardial perfusion single photon emission computed tomography (SPECT) study non-diagnostic for ischemia detection. We sought to investigate the injection of atropine in patients who fail to achieve 80% of age-predicted HR during exercise performed for myocardial perfusion SPECT (MPS), defining its safety and efficacy to raise HR to adequate levels as well as its effect on MPS interpretation.Between January 2002 and December 2004, we studied 3,150 consecutive patients (2,253 men and 897 women, mean age 55 +/- 6 years) who were referred to a single office-based nuclear cardiology laboratory for MPS using …
Muscarinic inhibition of potassium-induced noradrenaline release and its dependence on the calcium concentration.
1975
1. Noradrenaline release from the isolated rabbit heart was evoked by perfusion with a medium containing 135 mM potassium and 17 mM sodium ions (high K+-low Na+). 2. The noradrenaline output in response to high K+-low Na+ was dose-dependently decreased by methacholine (0.625-320 muM) and this effect was reserved by atropine 1.44 mM. 3. Lowering the calcium concentration of high K+-low Na+ from 1.8-0.1125 mM decreased the noradrenaline output by 85%. The effect of methacholine, expressed as % inhibition of noradrenaline release, was potentiated by lowering of the calcium concentration. 4. Both at normal and lowered calcium concentrations the inhibitory action of methacholine was larger from …
Effects of several muscarinic agonists on cardiac performance and the release of noradrenaline from sympathetic nerves of the perfused rabbit heart
1972
Summary 1 The effects of several muscarinic agonists on atrial tension development, ventricular rate and noradrenaline release from terminal sympathetic fibres evoked by electrical nerve stimulation (SNS) and 1,1-dimethyl-4-phenylpiperazinium (DMPP) were measured in isolated perfused rabbit hearts. 2 Hexamethonium, in a concentration which almost abolished the release of noradrenaline by DMPP, had no effect on the release produced by SNS, confirming that the stimulation was postganglionic. 3 The order of potency for inhibition of atrial tension development was N-methyl-1,2,5,6, tetrahydro-nicotinic acid prop-2-yne ester (MH-1)>oxotremorine > acetylcholine > methacholine > carbachol > furtre…
A muscarinic inhibition of the noradrenaline release evoked by postganglionic sympathetic nerve stimulation
1969
1. The noradrenaline output from isolated rabbit hearts perfused with Tyrode solution was estimated fluorimetrically. The postganglionic sympathetic nerves of the heart were stimulated (10 shocks/sec; 1 msec) for three 1 min periods with intervals of 10 min. 2. The noradrenaline output evoked by 3 consecutive stimulation periods decreased exponentially. 3. Acetylcholine (10−9–10−6 g/ml) administered continuously one min before to one min after the second stimulation caused a dose-dependent reduction of the noradrenaline output evoked by the second stimulation to as low as 19% of the normal value. Acetylcholine in the concentrations applied did not cause a noradrenaline output by itself. 4. …
Inhibition by parasympathetic nerve stimulation of the release of the adrenergic transmitter
1970
Isolated rabbit atria were perfused with Tyrode solution containing (+)-amphetamine. Electrical stimulation of the right postganglionic sympathetic fibres caused an output of noradrenaline which was significantly decreased by simultaneous stimulation of the vagus nerves.
Some aspects of cardiac antioxidant defence: Ebselen (PZ 51) treatment increases glutathione peroxidase activity in the rat heart
1990
Ebselcn (PZ 5 1 : 2-phenyl1.2-benzisoelenazol-3-( 2H)-one 1 is ii synthetic organoselenium compound with anti-inflammatory activity ( I . 21, which exhibits glutathione peroxidase (GSH-Px)-like activity, catalysing the reduction o f hydrogen peroxide as well as other organic peroxides [3-5]. Its antiinflammatory effect may be mediated by either the GSH-Px activity, the inhibition of leukotriene B4 formation [6], the antioxidant capacity, or a combination of all of them. Many attempts have been made to increase the antioxidant capacity of the myocardium, since free radical generation has been demonstrated in ischaemia-reperfusion damage [7, 81; superoxide dismutase (SOD) and catalase have be…