Attention has recently focused on the possibility of an interaction between ethanol and the endorphin system. In this study the opiate blocker naltrexone prevents the expected post-shock increase of ethanol consumption. This provides further evidence that endogenous opiates are involved in the voluntary drinking of ethanol in rats.
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http://dx.doi.org/10.1016/0024-3205(86)90601-6 | DOI Listing |
Intensive Care Med Exp
October 2024
Critical Care Research Group, The Prince Charles Hospital, 627 Rode Road, Level 3 Clinical Sciences Building, Chermside, Brisbane, QLD, 4032, Australia.
Neuroscience
September 2024
Department of Molecular and Cellular Physiology, Albany Medical College, United States; Department of Ophthalmology, Albany Medical College, United States. Electronic address:
Sepsis-associated encephalopathy (SAE) is associated with increased risk of long-term cognitive impairment. SAE is driven, at least in part, by brain endothelial dysfunction in response to systemic cytokine signaling. However, the mechanisms driving SAE and its consequences remain largely unknown.
View Article and Find Full Text PDFResuscitation
September 2024
Paris Fire Brigade, 1 place Jules Renard, 75017 Paris, France.
Aims: During out-of-hospital cardiac arrest (OHCA), an automatic external defibrillator (AED) analyzes the cardiac rhythm every two minutes; however, 80% of refibrillations occur within the first minute post-shock. We have implemented an algorithm for Analyzing cardiac rhythm While performing chest Compression (AWC). When AWC detects a shockable rhythm, it shortens the time between analyses to one minute.
View Article and Find Full Text PDFMicrob Cell Fact
March 2024
State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Rd, Shanghai, 200237, China.
Sepsis-associated encephalopathy (SAE) is a common manifestation in septic patients that is associated with increased risk of long-term cognitive impairment. SAE is driven, at least in part, by brain endothelial dysfunction in response to systemic cytokine signaling. However, the mechanisms driving SAE and its consequences remain largely unknown.
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