Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of low flow low pressure pulsatile bypass were studied in 90 consecutive patients undergoing coronary artery surgery. Overall pump flow rate (OFR) was 19-49 (mean 31 +/- 7) ml/kg/min at all temperatures. Moderate (28 degrees C) hypothermia was used. When cross-clamped flow was 17-49 (mean 27 +/- 7) ml/kg/min and mean perfusion pressure 50-60 mmHg. Priming volume (PV) was reduced to 1.45 +/- 0.02 L (range 1.2-2.0 L) PV, cardioplegia and volume additions were considered as total bypass crystalloid (TBC) and this correlated positively with increased post-operative positive water balance (r = 0.58, P less than 0.001). Bypass urine output averaged 135 +/- 24 ml (range 0-1,000 ml) was unrelated to OFR and correlated only with TBC (r=0.47, P less than 0.001). In 86 a single cardioplegia dose of 0.7 L (range 0.4-0.8 L) sufficed for this ischaemic period (mean 46 +/- 16 min). Four required a further 0.2-0.3 L. Their ischemic times were 44-74 min (mean 59 +/- 13 PNS). Inotropes were used in only 3 patients. Post-operatively 7 required diuretics for low hourly urine flow. Of the 76 with normal pre-operative renal function urea rose transiently in 15. Three had raised urea for over 9 days. Creatinine rose transiently in 7 but persisted in only one. Plasma cortisol (n=78) rose in 67 and fell in 11, indicating, overall, an adequate metabolic response. Plasma free haemoglobin before and after bypass varied widely and did not correlate with flow rate or perfusion time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of low flow, low pressure pulsatile bypass. 387 61

To date, the primary treatments for Alzheimer's disease with proven efficacy have been acetylcholinesterase inhibitors that prevent the hydrolysis of acetylcholine (ACh) in the synaptic cleft, thereby prolonging its activity. Although these agents have some benefit in alleviating cognitive impairment, they have limited clinical utility because of insufficient efficacy and marginal tolerability. Within the last decade, there has been much experimental support for the use of therapeutics that directly target nicotinic ACh receptors (nAChRs) to improve cognitive function and slow neurodegenerative disease progression. These findings have spurred considerable research efforts to develop ligands selective for nAChRs, such as ABT-418 (Arneric et al., 1995), SIB-1553 (Bontempi et al., 2001), TC-2403 (Lippiello et al., 1996), and TC-2559 (Bencherif et al., 2000). There is abundant evidence that nAChR modulators have the potential to alleviate cognitive impairment in demented states. In addition to improving cognitive function, a large body of research implicates a role for nAChRs in neuroprotection, suggesting potential for disease modification. An impact of nAChR agonists on disease progression would provide an advantage over currently available treatments for memory loss. The profile of previous nAChR-targeted clinical candidates has not been adequate to warrant further development owing to poor oral bioavailability, side effects, and/or lack of efficacy. Thus, a challenge in nAChR drug design and development has been the reduction of undesirable effects that result from activity at specific nAChRs in the CNS and PNS, including cardiovascular toxicity, emesis, seizures, and hypothermia.
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PMID:Ispronicline: a novel alpha4beta2 nicotinic acetylcholine receptor-selective agonist with cognition-enhancing and neuroprotective properties. 1719 10