The Experts below are selected from a list of 159 Experts worldwide ranked by ideXlab platform
Stephen C. Textor - One of the best experts on this subject based on the ideXlab platform.
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The role of the kidney in regulating arterial blood Pressure
Nature Reviews Nephrology, 2012Co-Authors: Hani M. Wadei, Stephen C. TextorAbstract:Hypertension is a leading cause of morbidity and mortality and the kidney has a pivotal role in this condition by regulating arterial blood Pressure. In this Review, Wadei and Textor provide examples of the regulatory mechanisms that are involved in controlling blood Pressure and discuss how disorders that affect the kidney contribute to hypertension. The kidney plays a central role in the regulation of arterial blood Pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal Perfusion Pressure are closely involved in maintaining the arterial circulation and blood Pressure. Renal Artery Perfusion Pressure directly regulates sodium excretion—a process known as Pressure natriuresis—and influences the activity of various vasoactive systems such as the renin–angiotensin–aldosterone system. As a result, many researchers argue that identifying any marked rise in blood Pressure requires resetting of the relationship between arterial blood Pressure and urinary sodium excretion, which can occur by an array of systemic or local mechanisms. Almost all of the monogenic forms of hypertension affect sites in the kidney associated with sodium handling and transport. Experimental models of spontaneous hypertension, such as the Dahl salt-sensitive rat, have been used to study the effects of kidney transplantation on blood Pressure. Results from studies of kidney transplantation indicate that Pressure sensitivity to sodium intake 'follows' the kidney, meaning that the recipient of a 'salt-resistant kidney' acquires sodium resistance, and that the recipient of a 'salt-sensitive kidney' acquires Pressure sensitivity. The examples above and discussed in this Review demonstrate that it should come as no surprise that most disorders that affect the kidney or the renal vasculature commonly lead to secondary forms of hypertension. Renal Artery Perfusion Pressure directly regulates sodium excretion, a process known as Pressure natriuresis The renin–angiotensin–aldosterone system has a central role in maintaining the Pressure–natriuresis relationship Maladaptive changes in tubular sodium and chloride handling leads to arterial hypertension despite the presence of a normal glomerular filtration rate Rare inherited forms of hypertension involve gain or loss of function mutations in a single gene and are associated with increased sodium reabsorption in the distal nephron Reduced nephron number contributes to the development of hypertension The kidney is the origin of afferent sympathetic signalling that modulates the sympathetic nervous system, the activity of which increases in patients with renal failure
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The Role of the Kidney in Regulating Arterial Blood Pressure
Nature reviews. Nephrology, 2012Co-Authors: Hani M. Wadei, Stephen C. TextorAbstract:The kidney plays a central role in the regulation of arterial blood Pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal Perfusion Pressure are closely involved in maintaining the arterial circulation and blood Pressure. Renal Artery Perfusion Pressure directly regulates sodium excretion-a process known as Pressure natriuresis-and influences the activity of various vasoactive systems such as the renin-angiotensin-aldosterone system. As a result, many researchers argue that identifying any marked rise in blood Pressure requires resetting of the relationship between arterial blood Pressure and urinary sodium excretion, which can occur by an array of systemic or local mechanisms. Almost all of the monogenic forms of hypertension affect sites in the kidney associated with sodium handling and transport. Experimental models of spontaneous hypertension, such as the Dahl salt-sensitive rat, have been used to study the effects of kidney transplantation on blood Pressure. Results from studies of kidney transplantation indicate that Pressure sensitivity to sodium intake 'follows' the kidney, meaning that the recipient of a 'salt-resistant kidney' acquires sodium resistance, and that the recipient of a 'salt-sensitive kidney' acquires Pressure sensitivity. The examples above and discussed in this Review demonstrate that it should come as no surprise that most disorders that affect the kidney or the renal vasculature commonly lead to secondary forms of hypertension.
Hani M. Wadei - One of the best experts on this subject based on the ideXlab platform.
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The role of the kidney in regulating arterial blood Pressure
Nature Reviews Nephrology, 2012Co-Authors: Hani M. Wadei, Stephen C. TextorAbstract:Hypertension is a leading cause of morbidity and mortality and the kidney has a pivotal role in this condition by regulating arterial blood Pressure. In this Review, Wadei and Textor provide examples of the regulatory mechanisms that are involved in controlling blood Pressure and discuss how disorders that affect the kidney contribute to hypertension. The kidney plays a central role in the regulation of arterial blood Pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal Perfusion Pressure are closely involved in maintaining the arterial circulation and blood Pressure. Renal Artery Perfusion Pressure directly regulates sodium excretion—a process known as Pressure natriuresis—and influences the activity of various vasoactive systems such as the renin–angiotensin–aldosterone system. As a result, many researchers argue that identifying any marked rise in blood Pressure requires resetting of the relationship between arterial blood Pressure and urinary sodium excretion, which can occur by an array of systemic or local mechanisms. Almost all of the monogenic forms of hypertension affect sites in the kidney associated with sodium handling and transport. Experimental models of spontaneous hypertension, such as the Dahl salt-sensitive rat, have been used to study the effects of kidney transplantation on blood Pressure. Results from studies of kidney transplantation indicate that Pressure sensitivity to sodium intake 'follows' the kidney, meaning that the recipient of a 'salt-resistant kidney' acquires sodium resistance, and that the recipient of a 'salt-sensitive kidney' acquires Pressure sensitivity. The examples above and discussed in this Review demonstrate that it should come as no surprise that most disorders that affect the kidney or the renal vasculature commonly lead to secondary forms of hypertension. Renal Artery Perfusion Pressure directly regulates sodium excretion, a process known as Pressure natriuresis The renin–angiotensin–aldosterone system has a central role in maintaining the Pressure–natriuresis relationship Maladaptive changes in tubular sodium and chloride handling leads to arterial hypertension despite the presence of a normal glomerular filtration rate Rare inherited forms of hypertension involve gain or loss of function mutations in a single gene and are associated with increased sodium reabsorption in the distal nephron Reduced nephron number contributes to the development of hypertension The kidney is the origin of afferent sympathetic signalling that modulates the sympathetic nervous system, the activity of which increases in patients with renal failure
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The Role of the Kidney in Regulating Arterial Blood Pressure
Nature reviews. Nephrology, 2012Co-Authors: Hani M. Wadei, Stephen C. TextorAbstract:The kidney plays a central role in the regulation of arterial blood Pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal Perfusion Pressure are closely involved in maintaining the arterial circulation and blood Pressure. Renal Artery Perfusion Pressure directly regulates sodium excretion-a process known as Pressure natriuresis-and influences the activity of various vasoactive systems such as the renin-angiotensin-aldosterone system. As a result, many researchers argue that identifying any marked rise in blood Pressure requires resetting of the relationship between arterial blood Pressure and urinary sodium excretion, which can occur by an array of systemic or local mechanisms. Almost all of the monogenic forms of hypertension affect sites in the kidney associated with sodium handling and transport. Experimental models of spontaneous hypertension, such as the Dahl salt-sensitive rat, have been used to study the effects of kidney transplantation on blood Pressure. Results from studies of kidney transplantation indicate that Pressure sensitivity to sodium intake 'follows' the kidney, meaning that the recipient of a 'salt-resistant kidney' acquires sodium resistance, and that the recipient of a 'salt-sensitive kidney' acquires Pressure sensitivity. The examples above and discussed in this Review demonstrate that it should come as no surprise that most disorders that affect the kidney or the renal vasculature commonly lead to secondary forms of hypertension.
Dennis W T Nilsen - One of the best experts on this subject based on the ideXlab platform.
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coronary blood flow and Perfusion Pressure during coronary angiography in patients with ongoing mechanical chest compression a report on 6 cases
Resuscitation, 2010Co-Authors: Alf Inge Larsen, Ashild S Hjornevik, Vernon Bonarjee, Stale Barvik, Tor Melberg, Dennis W T NilsenAbstract:Patients with pulseless electrical activity or refractory ventricular fibrillation have a very bad prognosis. Coronary angiography and angioplasty may be required to restore an effective circulation, but this must be performed whilst chest compressions are continued. The LUCAS chest compression device is suitable for this purpose. So far there are no reports on the effect of this device on coronary circulation in humans. We monitored the coronary Perfusion Pressure assessed invasively as the difference between the diastolic Pressures at the coronary ostium and right atrium, and compared these Pressures with coronary flow graded using the TIMI scale in 6 patients. In 4 out of 6 we found a satisfactory coronary Artery Perfusion Pressure and TIMI grade 3 flow (normal) on coronary angiography. Two of these patients survived the first 24 h. Two patients did not have a satisfactory Perfusion Pressure and adequate flow rate was not seen.
Qi Zuoliang - One of the best experts on this subject based on the ideXlab platform.
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Ultralong pedicled superficial temporal fascia island flaps for lower nasal defect.
The Journal of craniofacial surgery, 2009Co-Authors: Zhang Ying, Fang Jianlin, Zhu Guoxian, Wei Min, Wang Wei, Qi ZuoliangAbstract:To explore the method of repairing nose defects of the apex, ala, septum, and even opposite ala nasi with ultralong pedicled superficial temporal fascia (STF) island flaps. There were 29 cases of defects of the apex nasi, ala nasi, and nasal columella that were reconstructed, of which 12 cases were repaired with frontal-branched STF island flaps, 14 cases with apical-branched STF postauricular island flaps, and 3 cases with prefabricated apical-branched STF postauricular island flaps. The flap areas were arranged from 1.2 x 2.3 to 2.0 x 2.8 cm2, the length more than 15 cm on average. Liners were reconstructed at the stage of the prefabricating flaps, with free skin graft in the cases of the alae nasi defects. The surfaces of the wound after flap prefabrications were covered by skin graft as well. Twenty-seven cases were successfully taken without blood circulation blocks; the color, texture, and figure were good, and the outcomes were satisfying. Seven nonprefabricated flap cases have epidermis necrosis due to the lack of Artery Perfusion Pressure and venous return handicap, and the epidermis fall off after 1 month; 2 cases of which required secondary surgeries because of partial necrosis. An ultralong pedicled STF island flap is an available way to repair defects of the apex nasi, ala nasi, and nasal columella. The benefits of a prefabricated flap are good blood circulation, primary made liner, and minute injury of the donor site. It is a good method of repairing defects of the apex nasi, ala nasi, nasal septum, and opposite ala nasi simultaneously.
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Ultralong pedicled superficial temporal fascia island flaps for lower nasal defect.
The Journal of craniofacial surgery, 2009Co-Authors: Zhang Ying, Fang Jianlin, Zhu Guoxian, Wei Min, Wang Wei, Qi ZuoliangAbstract:To explore the method of repairing nose defects of apex, ala, septum, and even opposite ala nasi with ultralong pedicled superficial temporal fascia (STF) island flaps. There were 29 cases with defects of apex nasi, ala nasi, and nasal columella, of which 12 cases were repaired with frontal-branched STF island flaps, 14 cases with apical-branched STF postauricular island flaps, and 3 cases with prefabricated apical-branched STF postauricular island flaps. The flap areas were arranged from 1.2 x 2.3 to 2.0 x 2.8 cm2; the length was more than 15 cm on average. Liners were reconstructed at the stage of prefabricating flaps with free skin graft in the cases of ala nasi defects. The surfaces of wound after flap prefabrications were covered by skin graft as well. Twenty-seven cases were successfully taken without blood circulation blocks; the color, texture, and figure were good, and the outcomes were satisfying. Seven nonprefabricated flap cases have epidermis necrosis because of the lack of Artery Perfusion Pressure and venous return handicap, and the epidermis fell off after 1 month, 2 cases of which required secondary surgery because of partial necrosis. Ultralong pedicled STF island flap is an available way to repair defects of apex nasi, ala nasi, and nasal columella. Prefabricated flaps are with benefits of good blood circulation, primary-made liner, and minute injury of the donor site. It is a good method to repair defects of apex nasi, ala nasi, nasal septum, and opposite ala nasi simultaneously.
Robert J. Bache - One of the best experts on this subject based on the ideXlab platform.
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Coronary vasodilator reserve in ischemic myocardium of the exercising dog.
Circulation, 1992Co-Authors: David D. Laxson, Xue-zheng Dai, D. C. Homans, Robert J. BacheAbstract:BACKGROUNDPrevious work has reported that coronary vasodilator reserve may persist in myocardium rendered ischemic by hypoPerfusion. This study investigated the presence and extent of residual coronary vasomotor tone in myocardial regions made acutely ischemic by a flow-limiting coronary stenosis during exercise.METHODS AND RESULTSStudies were done in chronically instrumented dogs undergoing treadmill exercise in the presence of a coronary stenosis that decreased distal left circumflex coronary Artery Perfusion Pressure to approximately 40 mm Hg. Measurements of myocardial blood flow were made with radioactive microspheres during exercise (6.5 km/hr, 6% grade) before and during intracoronary infusion of the potent coronary vasodilator adenosine (40 micrograms/kg/min). Distal coronary Perfusion Pressure was held equal before and during intracoronary adenosine infusion (43 +/- 5 versus 42 +/- 5 mm Hg) by adjusting the hydraulic coronary occluder. During exercise in the presence of a coronary stenosis, myoca...
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Serotonin selectively aggravates subendocardial ischemia distal to a coronary Artery stenosis during exercise.
Circulation, 1992Co-Authors: Robert J. Bache, Randall P. Stark, Dirk J. DunckerAbstract:BACKGROUNDThe coronary circulation has been shown to remain responsive to vasodilator and vasoconstrictor stimuli during myocardial ischemia. Because serotonin possesses both vasodilator and vasoconstrictor properties, we examined its effect in the coronary circulation distal to an arterial stenosis that resulted in myocardial hypoPerfusion during exercise.METHODS AND RESULTSSeven chronically instrumented dogs were studied during treadmill exercise in the presence of a stenosis that reduced distal left circumflex coronary Artery Perfusion Pressure to 42 +/- 1 mm Hg. Myocardial blood flow was assessed with radioactive microspheres during exercise before and during intracoronary infusion of 0.4 and 2.0 micrograms/kg-1.min-1 serotonin. The stenosis was adjusted to maintain distal coronary Pressure constant during control exercise and with the two doses of serotonin. In seven dogs, the effect of serotonin (2.0 micrograms/kg-1.min-1) was also studied during exercise with normal arterial inflow. During control ...
