Experimental and structural analysis of the function of saccus vasculosus in rainbow trout, Salmo gairdneri (Richardson).
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Biomedical subjects
Publications and source records attributed to H Emanuelsson.
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Before, during, and after cardiac intervention, there is occasionally a need for circulatory support because of hemodynamic deterioration. For this purpose, a new minimally invasive cardiac assist device has been developed, and an early prototype has been studied in a bench test and in three pigs. The pump is a catheter system with a distal motor driven propeller (0-15,000 rpm) surrounded by a cage. The catheter was first tested in a tube in a water bath, where efficiency with respect to pressure generation and flow properties was measured. In the pig experiments, the pump was placed in the descending part of the aorta via a graft, and hemodynamic effects were recorded with three different propellers. The bench tests showed a velocity dependent pressure generation in the tube to the second power of the rpm, and 30 cm of water (> 22 mm Hg) could easily be achieved with all propellers. A pressure dependent flow in the tube was observed, with maximum flows of 20 L at 12,000 rpm and 27 L at 15,000 rpm. In the animal experiments, there was a velocity dependent mean pressure difference across the propeller, with up to 48 mm of mercury for the biggest propeller. An increase in cardiac output in all of the pigs was observed as well as a drop in pressure in the proximal part of the aorta. This study demonstrates the efficiency of this new device in vitro and in vivo. Hemodynamic changes are pronounced and are related to the speed and size of the propeller.
We studied nine patients with arteriosclerotic coronary heart disease (Group I) and 10 patients with normal coronary arteries (Group II) to elucidate mechanisms by which nifedipine affects catecholamine arterial levels and myocardial extraction at rest and during pacing. Nifedipine induced signs of general and coronary vasodilatation and improved myocardial lactate metabolism during pacing. Noradrenaline arterial concentration increased significantly after nifedipine in both groups (p less than 0.01). In Group I, the values were 40-50% higher compared with Group II. The net myocardial extraction of noradrenaline was not significantly affected by nifedipine, except during pacing in Group II, in which an increase in myocardial release was seen (p less than 0.05). In Group I, there was no correlation between arterial concentration of noradrenaline and myocardial release, while there was a significant negative correlation in Group II (p less than 0.0001). Adrenaline arterial concentration and myocardial extraction were not altered by nifedipine, but there was a positive significant correlation in Group I between arterial concentration and myocardial extraction of adrenaline (p less than 0.001). In conclusion, nifedipine increased noradrenaline levels in both groups of patients, probably reflecting a rise in sympathetic activity. Because myocardial lactate production turned into extraction in patients with coronary artery disease, the increased sympathetic tone evidently did not outweigh the beneficial antianginal effects of nifedipine.
We determined hemodynamics and myocardial lactate extraction in 11 patients with severe coronary disease after 0.010 (D1), 0.015 (D2), and 0.025 nmol/min (D3) of the arteriolar dilator felodipine during pacing-induced angina pectoris. Plasma concentrations of felodipine after the 3 doses were 12 (5), 25 (6) and 43 (8) nmol/ L, respectively. At corresponding pacing rates, mean blood pressure fell from 126 (24) to 90 (15) mm Hg at D3 (p less than 0.01) and pulmonary capillary wedge pressure was reduced from 14 (10) to 9 (8) mm Hg (p less than 0.05). Cardiac output increased at all three doses (p less than 0.01). The reduction of systemic vascular resistance at D3 was 49% (p less than 0.01) and of coronary vascular resistance 35% (p less than 0.05). At D1, there was no change in lactate extraction, while 8/10 lactate producers improved at D2 and D3. ST depression was diminished at all three doses (p less than 0.05) at the control pacing rate. During maximal pacing rate at D3, the myocardial oxygen consumption was 14% above control level (N.S.). Thus, felodipine was beneficial in most patients at higher dosage. Ventricular unloading and improved coronary perfusion might explain some of these positive effects.