Biomedical subjects

Y M Smulders

Publications and source records attributed to Y M Smulders.

41 records · Page 3Linked to original sources

PubMed1991

Concept of a soft, compressible artificial ventricle under evaluation.

This study was designed to compare the relative merits of soft and rigid artificial ventricles. A cascade mock circulation was used to measure cardiac output under different circumstances. The data show that these soft air driven ventricles show a Starling's-like response over a wider range of filling pressures than identical, but rigid, ventricles. Compression of soft ventricles by high intrathoracic pressures was simulated in vitro. Air pressures up to +20 mm Hg did not seriously affect soft ventricles. Cardiac tamponade was simulated by compressing the ventricle in a closed fluid compartment. Tamponade became severe when volume reduction of the ventricle rose to 60 ml. Hemolysis caused by soft and rigid ventricles was tested in a blood bag set-up and was 48-82% higher in the rigid ventricle, depending on the driving conditions. Possibly, this could be explained by the authors' finding that rigid ventricles showed a 20% higher intraventricular dP/dtmax value than soft ventricles. Soft ventricles were implanted in three calves as a total artificial heart (TAH). Implantation without quick connectors was easy because the surgeon could easily fold and compress the ventricles. No physiological complications of softness were observed. Blood damage in the animals was low (less than 5 mg/dl). The authors conclude that soft ventricles show distinct surgical and functional advantages over rigid ventricles.

Animals↗

PubMed1989

How soon should drainage tubes be removed after cardiac operations?

Pericardial effusion frequently occurs after cardiac operation. Despite its high incidence, the etiological process of postoperative pericardial effusion remains unclear. Residual blood or thrombus has often been suggested as a possible cause, implying that the occurrence of pericardial effusion could be related to the effectiveness of postoperative thoracic drainage. This possible relationship, however, has never been studied. We found that prolonging the duration of thoracic drainage by 24 hours often increases total chest tube output considerably but does not affect the incidence of postoperative pericardial effusion: approximately 55% of 100 patients in this study were shown by two-dimensional echocardiography to have pericardial effusion on the sixth postoperative day, regardless of the duration of postoperative drainage. Because of this, and because a long period of drainage causes discomfort for the patient, mechanical irritation to the heart and the pericardium, and an increased risk of infection, we recommend removing drains as soon as their efficacy has peaked, preferably on the first postoperative day.

Adult↗

PubMedDate not supplied

No effect of folic acid on markers of endothelial dysfunction or inflammation in patients with type 2 diabetes mellitus and mild hyperhomocysteinaemia.

BACKGROUND: Mild hyperhomocysteinaemia is a cardiovascular risk factor in patients with type 2 diabetes mellitus. Homocysteine may exert its detrimental effects through induction of endothelial dysfunction and/or chronic inflammation. In this study, we examined the effects of homocysteine-lowering therapy with folic acid on biochemical markers of endothelial dysfunction and low-grade inflammation in patients with type 2 diabetes mellitus and mild hyperhomocysteinaemia (> or = 14 micromol/l). METHODS: In a randomised, double-blind, controlled trial, patients were treated with folic acid 5 mg or placebo for six months. At 0 and 6 months, albuminuria, von Willebrand factor, soluble cellular adhesion molecules, C-reactive protein, interleukin-6 and tumour necrosis factor-alpha were determined. RESULTS: Forty-one patients completed the study (folic acid 23, placebo 18). Baseline hyperhomocysteinaemia (median 17 micromol/l, range 14 to 30 micromol/l) was reduced by 29% in the folic-acid-treated group, and remained unchanged in patients receiving placebo. On average, folic acid treatment did not significantly affect any of the endothelial (e.g. von Willebrand factor: difference folic acid minus placebo +1%, confidence interval -3 to +16%) or inflammation (e.g. C-reactive protein: difference folic acid minus placebo +13%, confidence interval -42 to +52%) markers studied. Multiple regression analyses without and with adjustment for baseline differences in cardiovascular disease and ethnicity confirmed these results. An apparent beneficial effect of folic acid on albuminuria in crude analysis was attenuated by multiple adjustment (difference folic acid minus placebo -35%, confidence interval -178 to +32%, p=0.08, adjusted 0.26). CONCLUSION: The data indicate that, in this group of patients with type 2 diabetes mellitus and mild hyperhomocysteinaemia, lowering homocysteine with folic acid for six months does not improve biochemical markers of endothelial dysfunction or low-grade inflammation.

Adult↗

PubMedDate not supplied

Sino-nasal bony and cartilaginous destruction associated with cocaine abuse, S. aureus and antineutrophil cytoplasmic antibodies.

Three male patients aged 29, 30 and 34 years and a 36-year-old female are reported with nasal septum perforation and a history of cocaine abuse. Two of the patients also had a perforation of the hard palate. In all four, antineutrophil cytoplasmic antibodies (ANCA) were found. One had a cytoplasmic immunofluorescence-staining pattern (c-ANCA), the other three showed a perinuclear staining pattern (p-ANCA). Furthermore, all patients were found to be nasal carriers of S. aureus. We hypothesise that tissue damage to the nasal and palatal area in patients using cocaine may partly be mediated by the presence of ANCA antibodies. Furthermore, we speculate that S. aureus facilitates the development of these ANCA antibodies.

Adult↗

PubMedDate not supplied

Renal tubular acidosis. Pathophysiology and diagnosis.

The pathophysiology of renal tubular acidosis is slowly being unraveled, which has implications for the traditional classification of the condition. Nonetheless, the diagnosis of renal tubular acidosis is still easy to establish, and identification of the specific pathophysiological subtype is relatively straightforward. The diagnostic information required usually includes only urinary pH and sodium, potassium, and chloride concentrations and serum potassium level. The urinary pH is not a diagnostic test for renal tubular acidosis, but it serves to distinguish between the various subtypes.

Acidosis, Renal Tubular↗