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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Red blood cells (RBCs) modulate nitric oxide (NO) bioavailability in the vasculature. Extracellular free hemoglobin (Hb) in the vascular lumen can cause NO bioavailability related complications seen in pathological conditions such as pancreatitis, sickle cell disease and malaria. In addition, the role of extracellular free Hb has been critical to estimate kinetic and transport properties of NO-RBCs interactions in 'competition experiments'. We recently reported a strong dependence of NO transport on RBC membrane permeability and hematocrit. NO donors combined with anti-inflammatory drugs are an emergent treatment for diseases like cancer, cardiovascular complications and wound healing. However, the role of RBCs in transport NO from NO donors is not clearly understood. To understand the significance of extracellular free Hb in pathophysiology on NO availability and estimation of the NO-RBC interactions, we developed a computational model to simulate NO biotransport to the RBC in the presence of extracellular free Hb. Using this model, we studied the effect of hematocrit, RBC membrane permeability and NO donors on NO-RBC interactions in the presence and absence of extracellular free Hb. The plasma NO concentration gradients and average plasma NO concentrations changed minimally with increase in extracellular free Hb concentrations at the higher hematocrit as compared to those at the lower hematocrit irrespective of the NO delivery method, indicating that the presence of extracellular free Hb affects the NO transport only at a low hematocrit. We also observed that NO concentrations increased with NO donor concentrations in the absence as well as in the presence of extracellular free Hb. In addition, NO donor supplementation may increase NO availability in the plasma in the event of loss of endothelium-derived NO activity.
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PMID:Computational analysis of nitric oxide biotransport to red blood cell in the presence of free hemoglobin and NO donor. 2495 Mar 5

BACKGROUND Splenic aneurysms are rare, asymptomatic, and usually derive from previous surgical interventions. Endovascular repair is the best option, but when A-V shunt is present, open repair might be more suitable. CASE REPORT A 43-year-old man presented to the Internal Medicine Department of AHEPA University Hospital with symptoms of fever and ascites. He was an ex-medical student with a history of sickle cell anemia, who had undergone urgent splenectomy and cholecystectomy 26 years ago and had a transit ischemic attack at the age of 21 years. Diagnostic imaging control revealed a giant splenic aneurysm 9.8 cm in diameter and 5 cm in length, with a concomitant A-V shunt (due to common ligation of the vessels after splenectomy and long stump presence with concomitant erosion of arterial wall). The patient underwent open surgery and cross-clamping the orifice of the splenic artery, also including the splenic vein, and the vessels were ligated. Post-operatively, the patient remained in the Intensive Care Unit for 48 h and suffered a portal vein thrombosis treated with appropriate anticoagulants. One month later, he had acute hemorrhagic pancreatitis and paralytic ileus and underwent laparotomy performed by general surgeons. CONCLUSIONS Giant splenic aneurysms are rare and are usually caused by previous splenectomy and preservation of a long-vessel stump. Immediate surgical repair is mandatory because of the high risk of rupture.
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PMID:Giant Splenic Aneurysm with Arteriovenous (A-V) Shunt, Portal Hypertension, and Ascites. 3047 53

Sickle cell disease is a debilitating hematologic process that affects the entire body. Disease manifestations in the abdomen most commonly result from vaso-occlusion, hemolysis, or infection due to functional asplenia. Organ specific manifestations include those involving the liver (eg, hepatopathy, iron deposition), gallbladder (eg, stone formation), spleen (eg, infarction, abscess formation, sequestration), kidneys (eg, papillary necrosis, infarction), pancreas (eg, pancreatitis), gastrointestinal tract (eg, infarction), reproductive organs (eg, priapism, testicular atrophy), bone (eg, marrow changes, avascular necrosis), vasculature (eg, vasculopathy), and lung bases (eg, acute chest syndrome, infarction). Imaging provides an important clinical tool for evaluation of acute and chronic disease manifestations and complications. In summary, there are multifold abdominal manifestations of sickle cell disease. Recognition of these sequela helps guide management and improves outcomes. The purpose of this article is to review abdominal manifestations of sickle cell disease and discuss common and rare complications of the disease within the abdomen.
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PMID:Abdominal Manifestations of Sickle Cell Disease. 3256 96


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