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11. |
Renin and Acute Circulatory Renal Failure in the Rabbit |
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Circulation Research,
Volume 30,
Issue 1,
1972,
Page 114-122
WILLIAM BROWN,
JEHOIDA BROWN,
HARALAMBOS GAVRAS,
ALAN JACKSON,
ANTHONY LEVER,
JAMES MCGREGOR,
ROBERT MACADAM,
J. ROBERTSON,
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摘要:
Plasma renin concentration (PRC) was measured in 25 rabbits before and 6, 24, or 72 hours after subcutaneous injection of glycerol. Renal failure and tubular necrosis developed in most animals and PRC rose sixfold to a maximum at 24 hours. Small insignificant changes of PRC were present at 6 and 72 hours. None of these changes was observed in a control group of nine animals killed 24 hours after an injection of saline. The amount of renin extractable from single superficial glomeruli and from renal cortical tissue was reduced after injection of glycerol. In a second study of 11 anesthetized rabbits, renal venous PRC increased on average from 151 to 1810 units/liter following a 4-hour period of renal artery occlusion. Arterial PRC did not change significantly during this time, but the kidneys showed histological changes of acute tubular necrosis. These experiments are compatible with the suggestion that renin is involved in the pathogenesis of acute circulatory renal failure.
ISSN:0009-7330
出版商:OVID
年代:1972
数据来源: OVID
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12. |
Injury and Repair in Arterial Tissue in the RabbitANALYSIS OF DNA, RNA, HYDROXYPROLINE, AND LACTATE DEHYDROGENASE IN EXPERIMENTAL ARTERIOSCLEROSIS |
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Circulation Research,
Volume 30,
Issue 1,
1972,
Page 123-130
SEPPO LINDY,
HEIKKI TURTO,
JOUNI UITTO,
PEKKA HELIN,
IB LORENZEN,
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摘要:
The aortic wall in rabbits was injured by pulling an inflated balloon catheter through the aorta. This was followed by an increase of the RNA-DNA ratio in the aortic wall 3 days after the injury. At the same time, the cathodic lactate dehydrogenase (LDH) isoenzymes composed of M subunits increased. The changes in LDH may reflect tissue hypoxia at the early phase after the injury. At 6 days protocollagen proline hydroxylase activity was increased, suggesting increased capacity for collagen formation in the injured aorta. Two weeks after injury the total content of hydroxyproline and DNA were increased, indicating connective tissue proliferation and hyperplasia in the injured aorta. The biochemical changes were interpreted as a repair response of the arterial connective tissue to injury. Gross arteriosclerosis of the aorta developed simultaneously with the biochemical alterations.
ISSN:0009-7330
出版商:OVID
年代:1972
数据来源: OVID
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13. |
Mechanism of Prolongation of the R‐R Interval with Electrical Stimulation of the Carotid Sinus Nerves in Man |
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Circulation Research,
Volume 30,
Issue 1,
1972,
Page 131-138
DWAIN ECKBERG,
GERALD FLETCHER,
EUGENE BRAUNWALD,
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摘要:
To elucidate the mechanism by which stimulation of the carotid sinus nerves prolongs the R-R interval, the effects of activating an implanted carotid sinus nerve stimulator were studied in eight patients at varying levels of background autonomic activity and with varying types of efferent autonomic blockade. Beta-receptor blockade was induced with intravenous propranolol, 0.20 mg/kg, and parasympathetic blockade with intravenous atropine, 0.04 mg/kg. In the supine position, average prolongation of the R-R interval due to stimulation of the carotid sinus nerves was 269 ± 56 msec prior to autonomic blocking drugs, 442 ± 214 msec after propranolol (NS), and 44 ± 13 msec after propranolol and atropine (P< 0.025). Comparable changes were produced in the standing position. With moderate treadmill exercise, stimulation of the carotid sinus nerves prolonged the R-R interval by only 40 ± 30 msec prior to blocking drugs, 62 ± 19 msec after propranolol, and 40 ± 30 msec after propranolol and atropine. It is concluded that the prolongation of the R-R interval produced by stimulation of the carotid sinus nerves is secondary to augmented parasympathetic activity, and the attenuation of this response during erect exercise appears to be due to a centrally mediated reduction in the responsiveness of the parasympathetic nervous system to baroreceptor stimuli.
ISSN:0009-7330
出版商:OVID
年代:1972
数据来源: OVID
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14. |
Instructions to Authors |
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Circulation Research,
Volume 30,
Issue 1,
1972,
Page 139-142
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ISSN:0009-7330
出版商:OVID
年代:1972
数据来源: OVID
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15. |
News from the American Heart Association |
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Circulation Research,
Volume 30,
Issue 1,
1972,
Page 143-147
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ISSN:0009-7330
出版商:OVID
年代:1972
数据来源: OVID
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