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Titolo:
HYPERTENSION-INDUCED DYSFUNCTION OF CIRCULATION IN HEMORRHAGIC-SHOCK
Autore:
RADISAVLJEVIC Z;
Indirizzi:
LOYOLA UNIV,SCH MED,INST SHOCK TRAUMA,BLDG 54-260,2160 S 1ST AVE MAYWOOD IL 60153
Titolo Testata:
American journal of hypertension
fascicolo: 7, volume: 8, anno: 1995,
pagine: 761 - 767
SICI:
0895-7061(1995)8:7<761:HDOCIH>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Keywords:
ESSENTIAL HYPERTENSION; OXYGEN; NITRIC OXIDE; HEMORRHAGIC SHOCK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
NO
Recensione:
Indirizzi per estratti:
Citazione:
Z. Radisavljevic, "HYPERTENSION-INDUCED DYSFUNCTION OF CIRCULATION IN HEMORRHAGIC-SHOCK", American journal of hypertension, 8(7), 1995, pp. 761-767

Abstract

Arterial blood pressure and plasma concentration of Na+, K+, glucose,and urea were studied in patients with essential hypertension during hemorrhagic shock. All 15 patients had established essential hypertension, and all had massive hemorrhage and shock. The control group included 37 normotensive patients in hemorrhagic shock. There were no differences in blood volume loss and age between the hypertensive and normotensive groups. A significant reduction (P <.001) of systolic and diastolic blood pressure as well as plasma concentration of Na+ and K+ were observed in hypertensive patients with hemorrhagic shock as comparedwith normotensive patients in hemorrhagic shock. Hypertensive patients in shock were found to have significantly elevated (P <.001) plasma glucose, urea, and heart rate compared with normotensive patients in shock. The hypertensive group mortality was significantly (P < .001) higher (80%) than the normotensive group in shock (24.3%). These data suggest that essential hypertension induces alterations in regulation and modulation of peripheral resistance, Na+/K+ membrane exchange, and the metabolism of glucose and urea during hemorrhagic shock. This heterogeneity of dysfunction induced by essential hypertension during hemorrhagic shock is probably caused by a change in the mechanism (diminish) of oxygen consumption at the cellular level, which results in an increase in nitric oxide production (which is O-2 dependent), and may play an important role in hypertension and hemorrhagic shock.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 12:39:58