PubMed Health⌕ Search

PubMed · 2045190

Bloodless testing for microporous membrane oxygenator failure: a preliminary study.

Abstract

The use of a bloodless solution and high pressure to accelerate microporous membrane oxygenator (MMO) failure was investigated. It was hypothesized that albumin acts as a wetting agent, contributing to plasma leakage through the membrane, and that high MMO outlet pressure accelerates the process. Three MMO, B-Bentley BCM-40 (n = 7), M-Medtronic Maxima (n = 4), and S-Sarns 16310 (n = 7) were tested at 37 +/- 2 degrees C using three identical closed recirculating circuits and four conditions: 1) Lactated Ringer solution (LR) with MMO outlet pressure (Pmo) 750 mmHg; 2) LR + albumin (4 g/100 ml), Pmo 150 mmHg; 3) LR + albumin, Pmo 300 mmHg; and 4) LR + albumin, Pmo 750 mmHg. "Blood" flow and gas flow were maintained at 2 l/min. Failure was indicated when Na+ was detected in the effluent of the MMO exhaust gas. There were no failures without albumin in the solution. B and M showed no signs of failure under any of the test conditions at 78 hours. S failed at (mean +/- SEM) 4.9 +/- 1.0, 12.1 +/- 0.2, and 19 hours for conditions 4, 3, and 2 respectively. Preceding failure, inlet gas pressure increased more than eightfold (27 +/- 1 to 224 +/- 34 mmH2O). These preliminary results are similar to previous findings with blood and suggest that high MMO outlet pressure and the presence of albumin may promote plasma breakthrough for S. The combination may provide a basis for an accelerated bloodless test for MMO compatibility with long-term respiratory support.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Y Tamari, A J Tortolani, K J Lee-Sensiba. 1991. Bloodless testing for microporous membrane oxygenator failure: a preliminary study.. https://pubmed.ncbi.nlm.nih.gov/2045190/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Contrast-enhanced tissue Doppler imaging of the left atrial appendage is a new quantitative measure of spontaneous echocardiographic contrast in atrial fibrillation.

AIMS: Although left atrial appendage spontaneous echo contrast (LAASEC) is a marker of increased thromboembolic risk in atrial fibrillation, it has previously only been evaluated qualitatively. We sought to determine if an intravenous contrast echocardiographic agent combined with tissue Doppler imaging (TDI) of the LAA could accurately quantify LAA-SEC in patients with atrial fibrillation. METHODS AND RESULTS: We prospectively identified 55 patients with persistent atrial arrhythmias (mean age 63+/-13 years) undergoing a transesophageal echocardiography (TEE), with LAA-SEC prior to direct current cardioversion. In addition to off-line calculation of backscatter index and shear rate, quantification of the velocity in a color TDI region of interest was performed in the LAA cavity following a 0.5-mL intravenous bolus of Optison. LAA-SEC was qualitatively graded by a blindedreader as mild (n = 29) or severe (n = 26), and was compared off-line to TEE-derived quantitative variables. Compared to patients with mild LAA-SEC, those with severe LAA-SEC had significantly decreased LAA emptying velocity, LAA TDI mean velocities and shear rate. Over the whole group, the mean maximal velocity of the LAA using TDI correlated with LAA emptying velocity (r = 0.59; P < 0.0001), shear rate (r = 0.55; P < 0.0001) and LAA area (r = 0.34; P = 0.014). Severe LAA-SEC was found with 72% sensitivity and 82% specificity if TDI mean velocity was <6.13 cm/s. On logistic regression analysis, LAA-TDI was the only predictor of qualitative LAA-SEC grade. CONCLUSION: Contrast-enhanced TDI is an original new tool that provides a quantification of the mean velocity of LAA-SEC that might improve our decision making in patients with atrial fibrillation.

Albumins↗

Preparation and preliminary characterization of concentric multi-walled chitosan microspheres.

Chitosan was first converted into micro-droplets by using a high voltage electrostatic field system. The droplets were then dropped into a series of Na(5)P(3)O(10)/NaOH solution mixtures with volume ratio of 17:3, 19:1, 1:0 (pure aqueous Na(5)P(3)O(10)) or 0:1 (pure aqueous NaOH) in order to fabricate chitosan microspheres with different membrane structures. The microspheres exhibit distinct chemical and physical properties, including release behaviors of encapsulated drugs. These chitosan microspheres prepared by this method exhibited good sphericity within the range of (286.6 +/- 15.9) to (356 +/- 9.5) microm in diameters. SEM observations have indicated that the chitosan microspheres exhibited distinct surface structures depending on the post-treatment solutions. The mechanical strength of the chitosan microspheres significantly improved upon treatment with Na(5)P(3)O(10)/NaOH solution at ratio of 17:3 (v/v), as compared with the same but at ratio of 19:1, 1:0 (pure Na(5)P(3)O(10)) and 0:1 (pure NaOH) solutions. In addition, chitosan microspheres with unique multi-walled concentric shell membrane structures were prepared by treating with Na(5)P(3)O(10)/NaOH solution at ratio of 19:1. Release studies were carried out to evaluate the kinetic profiles of two model drugs (5-fluorouracil and cytochrome C) from these prepared chitosan microspheres. When chitosan microspheres treated with Na(5)P(3)O(10)/NaOH ratio at 17:3, the release of cytochrome C was found to be the slowest as compared to those treated by the same Na(5)P(3)O(10)/NaOH solution of other mixing ratios, after a period of 35-day "endurance" test. However, in one case, 5-fluorouracil released quite quickly in a period of 30 min (about 80% completion). The wide range of drug release results might be attributed to the unique and wide range of surface characteristics, porosities, and various structures of chitosan microspheres upon treatment with Na(5)P(3)O(10)/NaOH solutions. These results indicate that, by adjusting the Na(5)P(3)O(10)/NaOH ratios, without extra manipulation on polymer material formulation, one could obtain an additional degree of freedom in drug release profile that permits the simultaneous regulation of morphologies of surface texture and internal structure, mechanical properties, and molecular permeability of the microspheres.

Albumins↗

CD36 is a novel and potential anti-fibrogenic target in albumin-induced renal proximal tubule fibrosis.

Albumin is not only a risk factor for diabetic nephropathy (DN), but also a therapeutic target. Hence, scientists have long sought ways to elucidate the interactions between albumin and diabetic renal tubule fibrosis. CD36, a surface receptor for thrombospondin-1, has been reported to interact with latent transforming growth factor-beta1 (TGF-beta1) and activate its fibrogenic bioactivity. This study elucidates the interactions between CD36 and renal tubule fibrosis. LLC-PK1 cells were applied to represent renal proximal tubule cells. The expression of CD36 was evaluated by flow cytometry. Fibronectin was assayed by Western blot and enzyme-linked immunosorbent assay (ELISA). Bioactive TGF-beta1 was assayed by ELISA. We demonstrated that albumin was shown significantly to inhibit cell growth without affecting hypertrophy status since protein content and cell size remained unaffected under albumin treatment. Moreover, albumin dose-dependently (0, 1, or 10 mg/ml) enhanced the secretion of bioactive TGF-beta1 and fibronectin with the upregulation of CD36. Intriguingly, CD36 siRNA, a potent silencer for CD36 effectively suppressed the albumin-induced increase in CD36, TGF-beta1, and even fibronectin level. Accordingly, albumin is a pro-fibrogenic factor for proximal tubule cells since albumin per se markedly upregulated the expression of TGF-beta1 and fibronectin. Most importantly, CD36 may mediate albumin-induced cellular fibrosis since CD36 siRNA appeared to have anti-fibrosis effects. This work suggests that CD36 is a novel and potential therapeutic target for diabetic renal tubule fibrosis.

Albumins↗