Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235108 (tense)
 2,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased intra-abdominal pressure (IAP) may occur in a number of different situations encountered by intensivists, such as tense ascites, abdominal hemorrhage, use of military antishock trousers, abdominal obstruction, during laparoscopy, large abdominal tumors and peritoneal dialysis.1-3 Both clinical and experimental evidence indicate that increased IAP may adversely affect cardiac, renal, respiratory and metabolic functions.1-5 Despite this, increased IAP is rarely recognized and treated in Intensive Care Unit (ICU) settings. There appears to be two reasons for this: the physiologic consequences of increased IAP are not well know, to most physicians and, more importantly, the capability of easily measuring IAP has not been well documented. In this chapter, we will discuss: 1) the different methods proposed to evaluate IAP in ICU; 2) the physiopathological consequences of increased IAP; 3) the existing clinical data about IAP in critically ill patients. Considering overall our data, we can conclude that: 1) different techniques are available at the bedside to estimate the IAP; 2) the IAP ranges between 10 and 20 cmH2O, substantially increased compared to normal subjects. Most of the patients have IAH, while few of them (<5%) present clinical characteristics of ACS; 3) the IAP is different among different categories of patients and its increase is not limited to surgical patients only; 4) the increase in IAP appears to influence respiratory function, homodynamic, kidney, gut and brain physiology; 5) the IAP seems to be correlated with severity scores but its relation to mortality is controversial; 6) the routine measurements of IAP by means of bladder pressure are not associated with an increased rate of urinary tract infections.
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PMID:The abdominal compartment syndrome. Clinical relevance. 1202 71

The abdominal compartment syndrome has received considerable attention only recently. It may be defined as adverse physiologic consequences that occur as a result of an acute increase in the intraabdominal pressure. The most common causes of ACS are haemorrhage, visceral oedema, pancreatitis, bowel distension, venous mesenterial obstruction, abdominal packs, tense ascites, peritonitis, tumor. The mostly affected organ systems include cardiovascular, pulmonary, renal, central nervous and splanchnic. The diagnosis depends on the recognition of the clinical syndrome followed by an objective measurement of intraabdominal pressure, preferably that of the urinary bladder. The treatment consists of adequate fluid resuscitation and surgical decompression when necessary. (Tab. 1, Ref. 29.).
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PMID:The abdominal compartment syndrome. 1283 Sep 94

Dendrimers have successfully proved themselves as functional nanodevices for drug delivery because they can render drug molecules a greater water solubility, bioavailability, and biocompatibility. It has recently been suggested that the structural changes of cell membranes (e.g., local lipid density and actual pore or hole) could affect the permeability across them for dendrimers. However, to understand these effects requires direct measurements in a single cell and is thus very difficult and more challenging. Here we use mesoscopic simulations to investigate the tension-mediated complexes comprising charged dendrimers and lipid bilayer membranes. The structures of membranes are alternated by adjusting their surface tensions. Our simulations demonstrate that the permeability of charged dendrimers can be effectively enhanced in the tense membranes, and the permeability in the actual hole is several times higher than that in the lipid-poor section. The possible mechanism of charged dendrimer-induced pore nucleation in the tense membranes is evaluated. The findings have implications in tuning intracellular delivery rates and amounts in nanoscale complex and chemotherapeutics.
ACS Nano 2009 Aug 25
PMID:Enhanced permeability of charged dendrimers across tense lipid bilayer membranes. 1958 48