Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac complications comprise as much as 50% of perioperative vascular surgical morbidity and mortality. Using the Goldman multifactorial index for evaluating cardiac risk pre-operatively, 53 consecutive patients who underwent abdominal aortic aneurysm surgery were prospectively studied. Forty patients (75.5%) were also evaluated with echocardiography for assessment of left ventricular function. There were 14 (23.7%) peri-operative events, of which nine (17.0%) were acute myocardial infarctions--two of whom died (3.8%). The minor complications included three with hypovolaemic renal failure, and one each with acute respiratory failure and cerebrovascular accident. Patients with Goldman cardiac risk index (CRI) classes III and IV were associated with significantly higher risks of peri-operative complications (p less than 0.001), i.e. 77.8% and 66.7% respectively, compared with class II (22.7%) and class I (nil). Echocardiographic left ventricular shortening fraction (LVFS) of less than 28% helped identify high risk groups in all classes, although its positive predictive value was low (42.3%). Combining LVFS less than 28% with Goldman CRI categories II to IV improved the sensitivity to 91.7% and the positive predictive value to 61.1%. Careful pre-operative assessment using the simple Goldman index and echocardiography is helpful in identifying higher risk patients who would benefit from pre-operative stabilisation and more rigorous perioperative hemodynamic monitoring preferably including intensive care (ICU) management, so as to reduce cardiac complications.
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PMID:Noninvasive cardiac risk evaluation before elective abdominal aortic aneurysm surgery--clinical value of the Goldman index and echocardiography. 215 82

An early event in the evolution of acute respiratory failure (ARF) is thought to be the activation of platelets, their pulmonary entrapment and subsequent release of the smooth muscle constrictor serotonin (5HT). This study tests the thesis that inhibition of 5HT will improve lung function. The etiology of ARF in the 18 study patients was sepsis (N = 10), aspiration (N = 3), pancreatitis (N = 1), embolism (N = 2), and abdominal aortic aneurysm surgery (N = 2). Patients were divided into two groups determined by whether their period of endotracheal intubation was less than or equal to 4 days (early ARF, N = 12) or greater than 4 days (late ARF, N = 6). Transpulmonary platelet counts in the early group showed entrapment of 26,300 +/- 5900 platelets/mm3 in contrast to the late group where there was no entrapment (p less than 0.05). The platelet 5HT levels in the early group were 55 +/- 5 ng/10(9) platelets, values lower than 95 +/- 15 ng/10(9) platelets in the late ARF group (p less than 0.05), and 290 +/- 70 ng/10(9) platelets in normals. The selective 5HT receptor antagonist, ketanserin was given as an intravenous bolus over 3 minutes in a dose of 0.1 mg/kg, followed by a 30-minute infusion of 0.08 mg/kg. During this period mean arterial pressure (MAP) fell from 87 +/- 5 to 74 +/- 6 mmHg (mean +/- SEM) (p less than 0.05). One and one-half hours following the start of therapy, MAP returned to baseline. At this time, patients with early ARF showed decreases in: physiologic shunt (Qs/QT) from 26 +/- 3 to 19 +/- 3 (p less than 0.05); peak inspiratory pressure from 35 +/- 2 to 32 +/- 2 cmH2O (p less than 0.05) and in mean pulmonary arterial pressure from 32 +/- 2 to 29 +/- 1 mmHg (p less than 0.05). At 4 hours all changes returned to baseline levels. In early ARF ketanserin did not alter pretreatment values of: pulmonary arterial wedge pressure, 17 +/- 3 mmHg; cardiac index, 2.8 +/- 0.3 L/min X m2; platelet count, 219,000 +/- 45,000/mm3; platelet 5HT, 55 +/- 5 ng/10(9) platelets; plasma 5HT, 142 +/- 21 ng/ml; plasma thromboxane B2, 190 +/- 30 pg/ml; or plasma 6-keto-PGF1 alpha, 40 +/- 10 pg/ml. Ketanserin infusion in patients with late ARF yielded no benefit. In both ARF groups the decreases in QS/QT were inversely related to the duration of intubation (r = 0.70; p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of serotonin in patients with acute respiratory failure. 654 16

In patients with renal disease undergoing cardiovascular surgery, perioperative management continues to be a challenge. Traditional answers have turned into new questions with the introduction of new agents and the redesign of old techniques. For ARF prevention, early recognition of pending deleterious compensatory changes is critical. Theoretically, therapeutic intervention designed to prevent ischemic renal failure should be designed to preserve the balance between RBF and oxygen delivery on one hand and oxygen demand on the other. Maintenance of adequate cardiac output distribution to the kidney is determined by the relative ratio of renal artery vascular resistance to systemic vascular resistance. Indeed, it should not be surprising to learn that norepinephrine (despite its vasoconstricting effect) has been reported to have no deleterious renal effects in patients with low systemic vascular resistance. Until recently, strategies for the treatment of ARF have been directed to supportive care with dialysis (to allow tubular regeneration). Various therapeutic maneuvers have been introduced in an attempt to accelerate the recovery of glomerular filtration, including dialysis, nutritional regimens, and new pharmacologic agents. A recent small prospective trial of low-dose dopamine in the prophylaxis of ARF in patients undergoing abdominal aortic aneurysm repair showed no benefit in those patients receiving dopamine. Conversely, the effects of intravenous atrial natriuretic peptide in the treatment of patients with ARF appear to offer benefit in patients with oliguria. Among 121 patients with oliguric renal failure, 63% of those who received a 24-hour infusion of atrial natriuretic peptide required dialysis within 2 weeks compared with 87% who did not. Whether this effect will be borne out in the future remains to be determined. The administration of epidermal growth factor after induction of ischemic ARF in rats has been shown to enhance tubular regeneration and accelerate recovery of kidney function. Human growth factor administration has been shown to increase GFR 130% greater than baseline in patients with chronic renal failure, but no data for clinical ARF have been reported. In addition, there have been significant improvements in dialysis technology in the treatment of ARF. Modern dialysis uses bicarbonate as a buffer as opposed to acetate, which reduces cardiovascular instability, and has more precise regulation of volume removal. Dialysate profiles and temperatures improve hemodynamics and reduce intradialytic hypotension. Techniques of hemodialysis without anticoagulation have reduced bleeding complications. Finally, dialysis membranes activate neutrophils and complement less with the biocompatible membranes used today that reduce recovery time and dialysis treatment. Evidence indicates that activation of complement and neutrophils by older dialysis membranes caused a greater incidence of hypotension, adding to ischemic renal injury. It remains to be determined whether early and frequent dialysis with biocompatible membranes, as well as other therapeutic interventions, will increase the survival of patients with perioperative ARF.
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PMID:Perioperative renal dysfunction and cardiovascular anesthesia: concerns and controversies. 980 83

The endoplasmic reticulum (ER) is the major intracellular membrane system. The ER is essential for protein and lipid biosynthesis, transport of proteins along the secretory pathway, and calcium storage. Here, we describe our investigations into the dynamics and regulation of the ER in the early Caenorhabditis elegans embryo. Using a GFP fusion to the ER-resident signal peptidase SP12, we observed the morphological transitions of the ER through fertilization and the early cell-cycles in living embryos. These transitions were tightly coordinated with the division cycle: upon onset of mitosis, the ER formed structured sheets that redispersed at the initiation of cleavage. Although microtubules were not required for the transition of the ER between these different states, the actin cytoskeleton facilitated the dispersal of the ER at the end of mitosis. The ER had an asymmetric distribution in the early embryo, which was dependent on the establishment of polarity by the PAR proteins. The small GTPase ARF-1 played an essential role in the ER dynamics, although this function appeared to be unrelated to the role of ARF-1 in vesicular traffic. In addition, the ER-resident heat shock protein BiP and a homologue of the AAA ATPase Cdc48/p97 were found to be crucial for the ER transitions. Both proteins have been implicated in homotypic ER membrane fusion. We provide evidence that homotypic membrane fusion is required to form the sheet structure in the early embryo.
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PMID:Involvement of the actin cytoskeleton and homotypic membrane fusion in ER dynamics in Caenorhabditis elegans. 1571 56

TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell proliferation also in the absence of ARF, raising the question of what are the molecular pathways involved. Herein we demonstrate that stable knock-down of TBP-1 in human immortalized fibroblasts increases cell proliferation, migration and resistance to apoptosis induced by serum deprivation. We observe that TBP-1 silencing causes activation of the Akt/PKB kinase and that in turn TBP-1, itself, is a downstream target of Akt/PKB. Moreover, MDM2, a known Akt target, plays a major role in this regulation. Altogether, our data suggest the existence of a negative feedback loop involving Akt/PKB that might act as a sensor to modulate TBP-1 levels in proliferating cells.
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PMID:A regulatory mechanism involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the control of cell proliferation. 3148 38

The small GTPase Arf1 plays critical roles in membrane traffic by initiating the recruitment of coat proteins and by modulating the activity of lipid-modifying enzymes. Here, we report an unexpected but evolutionarily conserved role for Arf1 and the ArfGEF GBF1 at mitochondria. Loss of function of ARF-1 or GBF-1 impaired mitochondrial morphology and activity in Caenorhabditis elegans. Similarly, mitochondrial defects were observed in mammalian and yeast cells. In Saccharomyces cerevisiae, aberrant clusters of the mitofusin Fzo1 accumulated in arf1-11 mutants and were resolved by overexpression of Cdc48, an AAA-ATPase involved in ER and mitochondria-associated degradation processes. Yeast Arf1 co-fractionated with ER and mitochondrial membranes and interacted genetically with the contact site component Gem1. Furthermore, similar mitochondrial abnormalities resulted from knockdown of either GBF-1 or contact site components in worms, suggesting that the role of Arf1 in mitochondrial functioning is linked to ER-mitochondrial contacts. Thus, Arf1 is involved in mitochondrial homeostasis and dynamics, independent of its role in vesicular traffic.
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PMID:The small GTPase Arf1 modulates mitochondrial morphology and function. 2523 Sep 32

Amiodarone is an antiarrhythmic drug that has been commonly used to treat supraventricular and ventricular arrhythmias. This drug is an iodine-containing compound that tends to accumulate in several organs, including the lungs. Especially, its main metabolically active metabolite desethylamiodarone can adversely affect many organs. A very well-known severe complication of amiodarone therapy is the amiodarone-induced pulmonary toxicity. This article presents the case study of an 82-year-old male patient with acute amiodarone-induced pulmonary toxicity. The patient underwent endovascular aneurysm repair for rapidly increasing abdominal aortic aneurysm. During the postoperative period the patient developed rapid atrial fibrillation and amiodarone therapy was initiated. Subsequently, the patient went into acute respiratory failure and was requiring high supplemental oxygen support and a chest X-ray revealed bilateral pulmonary infiltrates. During the hospital course the patient required mechanical ventilator support. With discontinuation of amiodarone, supportive therapy and steroid treatment patient symptoms significantly improved. Amiodarone-induced pulmonary toxicity must be considered in the differential diagnosis of all patients on the medication with progressive or acute respiratory symptoms. Early discontinuation of amiodarone and aggressive corticosteroid therapy should be considered as a viable treatment strategy.
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PMID:Early Amiodarone-Induced Pulmonary Toxicity after Endovascular Aneurysm Repair: A Case Report. 2757 88