[Sex differences in cardiac resistance to acute ischemia in rats exposed to the effect of chronic hypobaria and physical stress].
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Biomedical subjects
Publications and source records attributed to E Barta.
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The ramus interventricularis ventralis (RIV) of the dog heart was perfused with donor blood from the femoral artery. The inflow and outflow pressure, the blood flow and the diameter of the RIV were recorded. An increase in the blood flow from 11.3 +/- 0.3 to 81.4 +/- 6.2 ml/min induced, in 24.4 +/- 1.7 s a gradual increase in RIV diameter which became stabilized in 90-120 s and amounted to 80.87 +/- 11.68 microns, i.e. to 3.37 +/- 0.70% of the resting diameter. Since the mean pressure at the site where the diameter was recorded was maintained constant, relaxation of RIV smooth muscle has been assumed to have occurred. Dilation could not be evoked after RIV had been dilated by papaverine. Any interference by changes in pressure amplitude accompanying the increase in blood flow was precluded by using non-pulsating perfusion of the RIV. An increase in the non-pulsating blood flow from 12.11 +/- 2.20 to 90.33 +/- 11.30 ml/min likewise--in 19.50 +/- 1.83 s--produced an increase in RIV diameter of 1.8%. Blood flow is being suggested as one factor regulating the tone of the smooth muscle of the major coronary artery. This mechanism is supposed to counteract sympathetic constriction of the major coronary artery.
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The circulating blood volume changes, plasma electrolytes, aldosterone as well as plasma-renin-activity (PRA) were studied in 14 patients following open-heart surgery with cardiopulmonary bypass (CPB) and in 14 patients following cardiac surgery without CPB. In both the groups a postoperative decrease of circulating blood volume was observed. This decrease occurred in spite of the positive fluid balance, and so a shift of fluid from vascular to extravascular compartment was likely. In the bypass group the plasma aldoserone level rose immediately after the operation and reached the peak on the first postoperative day. In the non-bypass group the aldosterone level started to fall after the operation, and reached the lowest level on the third postoperative day. The pattern of the postoperative PRA changes was almost identical with the aldosterone level changes in both the groups studied, which suggests that the activation of renin-angiotensin-aldosterone axis might be responsible for the observed plasma aldosterone changes.
The effect of heart surgery with and without cardiopulmonary by-pass on plasma levels of thyroxine (T4) and triiodothyronine (T3) was studied in 19 patients. It was found that even before the operation the plasma levels of T4 and of T3 were significantly lower in the by-pass group of patients in comparison with those without by-pass. This lower level of thyroid hormones could be explained by greater pre-operative stress. This presumption is supported by the finding of the greater pre-operative plasma concentrations of dopamine-beta-hydroxylase and growth hormone in patients of the by-pass group. While in patients not undergoing CPB a tendency to the decrease of plasma thyroid hormones was observed during the early postoperative phase, in patients of the by-pass group a small increase was observed. On the basis of the finding that thyroid hormones exercise powerful and specific effect on myocardial contractility, it is suggested that the low hormone level might have a role in the pathogenesis of postoperative low cardiac output syndrome.
The diameter of a major coronary artery, the ramus interventricularis ventralis (RIV), was measured in dogs with arrested hearts perfused by an extracorporeal circulation. The resting diastolic diameter was 1.78 +/- 0.07 mm (mean +/- SE) at a diastolic pressure of 74.2 +/- 3.4 mm Hg. Bilateral supramaximal stimulation of fibers leaving the cranial pole of the stellate ganglion decreased the diameter by 71.2 +/- 8.9 micrometer, i.e., 4.0 +/- 0.5% of the resting diameter. Stimulation of the left stellate ganglion contributed 59.8 +/- 5.7% of the maximum response; that of the right contributed 40.3 +/- 5.5%. Stimulation of the thoracic ganglia (T2-4) resulted in a 1.2 +/- 0.4% decrease in coronary vessel diameter. RIV failed to respond to bilateral caudal cervical ganglion stimulation. After iv administration of phentolamine, 1-2 mg/kg, no response to sympathetic stimulation could be elicited. Therefore, it appears that alpha-receptors are activated by the release of the sympathetic neurotransmitter to sympathetic stimulation and that beta-receptors are not involved in the response of RIV to sympathetic stimulation.
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Using El Badawi and Schenk's modification of Karnovski's method for the demonstration of acetylcholinesterase, the authors found cholinergic fibres both in the perivascular connective tissue and directly in the wall (in the adventitia) of the major coronary arteries; the fibres were distributed regularly around the circumference of the arteries. In the case of the smaller intramyocardial arteries, the cholinergic fibres were concentrated at two poles of the blood vessel; none were present in the wall of the veins. The shape and topography of the coronary cholinergic arterial plexus resemble the shape and topography of the coronary sympathetic adrenergic system. In apparent contradiction of this finding, stimulation of the cervical vagus did not affect the diameter of the large coronary arteries. Since acetylcholine (6--10 micrograms/kg i.v.) produced a mean 7.4% increase in the diameter of the ramus interventricularis ventralis, we concluded that there are no postgangliar cholinergic fibres of vasomotor significance for the large coronary arteries in the cervical vagus. The specific acetylcholinesterase activity found in the wall of these vessels belongs either to cholinergic terminals whose ganglion cells are not located in the vagal ganglion, or to cholinergic axones terminating outside the wall of the large coronary arteries.
Total hemodynamic values and left ventricular blood flow were studied using Sapirstein's method of 86Rb uptake in female rats 24 h after a last exposure to high altitude. A stimulated altitude of 1350 m was used, initial exposure being for 30 min, gradually increased by 30 min daily up to 330 min daily for 5 days a week; the total number of exposures was 32. In another animal group the hypobaric exposure was combined with swimming in water at 37 degrees C. In both experimental groups the cardiac output and stroke volume increased, and in rats undergoing swimming the total peripheral resistance decreased as well. In the rats exposed to intermittent hypoxia only, left ventricular blood flow increased by about the same proportion as the cardiac output. The ratio of left ventricular work to coronary blood flow was significantly increased. In rats exposed to the combined influence of hypoxia and swimming, the increase in left ventricular blood flow did not match either the increase in cardiac output, or the weight gain of the left ventricle. The ventricular work to coronary blood flow ratio was the same as in controls.
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