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Biomedical subjects

M Vermeulen

Publications and source records attributed to M Vermeulen.

At least 145 records · Page 8Linked to original sources
PubMed1991

Treatment of acute hydrocephalus after subarachnoid hemorrhage with serial lumbar puncture.

Computed tomography demonstrated acute hydrocephalus less than or equal to 72 hours after subarachnoid hemorrhage in 24 (23%) of 104 patients. Of these 24 patients, six (25%) had no impairment of consciousness. In nine (11%) of the remaining 80 patients, acute hydrocephalus developed within 1 week after subarachnoid hemorrhage. With the exception of three patients, all 104 patients received antifibrinolytic treatment. Delayed clinical deterioration from acute hydrocephalus occurred in seven (29%) of the 24 patients with acute hydrocephalus on admission and in six (8%) of the remaining 80 patients. Serial lumbar puncture was performed in 17 patients. Twelve (71%) of the 17 patients treated with serial lumbar puncture, including 10 (77%) of the 13 patients with delayed deterioration from acute hydrocephalus after admission, achieved improvement in the level of consciousness. Four of these 17 patients (4% of all 104 patients) required an internal shunt. No patient deteriorated from coning following serial lumbar puncture. The rebleeding rate within 12 days after subarachnoid hemorrhage in hydrocephalic patients with serial lumbar puncture was not higher than the rate in those without hydrocephalus (two [12%] of 17 versus nine [13%] of 71). Neither meningitis nor ventriculitis was observed. We conclude that if neither a hematoma with a mass effect nor an obstructive element exists, cerebrospinal fluid drainage with serial lumbar puncture is a good alternative to ventricular drainage in patients with acute hydrocephalus after subarachnoid hemorrhage.

Acute Disease↗
PubMed1990

Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage.

The association between hyponatremia and cerebral ischemia was investigated in a consecutive series of 208 patients with subarachnoid hemorrhage who had a daily fluid intake of at least 3 L and in whom fluid restriction, to correct hyponatremia, was not applied. Hyponatremia occurred in 70 (34%) of the 208 patients. The occurrence of cerebral ischemia in patients with hyponatremia, 17 (24%) of 70 patients, was significantly higher than in patients without hyponatremia, 17 (12%) of 138 patients (chi 2 = 4.028, p = 0.045). Cerebral ischemia was not more often fatal in hyponatremic patients than in patients without hyponatremia. We conclude that patients with hyponatremia are at increased risk of developing cerebral ischemia even if fluid restriction is not applied.

Brain Ischemia↗
PubMed1990

Simulation and experimental studies of the factors influencing the frequency spectrum of cardiac extracellular waveforms.

Spectral analysis of electrocardiographic signals has been proposed as a tool to detect features reflecting cardiac diseases, such as ventricular hypertrophy, myocardial infarction, and a predisposition to sustained ventricular tachycardia. The lack of a theoretical basis to address this question prompted the authors to undertake a simulation study using a bidomain volume conductor model of a strip of cardiac tissue, combined with Fourier analysis, and electrograms recorded from an isolated right atrial canine preparation. In the crista terminalis, the bandwidth of the normal electrogram was 840 +/- 200 Hz (mean +/- SD) during longitudinal propagation and 660 +/- 370 Hz during transverse propagation. During premature stimulation, signal bandwidth and propagation velocity increase with the coupling interval. In the model, a linear combination of Vmax and propagation velocity values allows simulation of the various features of premature excitation. Vmax is the major determinant of the high-frequency content of the signal. An important decrease in the high-frequency content of electrograms occurs when the recording electrode is moved away from the preparation or the simulation model; at distances larger than 1-5 mm, the bandwidth levels off to a value of 50-120 Hz. Partial blockade of axial current flow in the direction of propagation due to microscopic discontinuities and variable activation delays at these discontinuities may be the cause of fragmented activity in necrotic myocardium, which is associated with a reduced bandwidth. Thus, short- and long-term effects of ischemia followed by infarction, such as decreased propagation velocity, decreased action potential upstroke, and fragmentation, tend to decrease the electrocardiographic bandwidth.

Action Potentials↗
PubMed1990

The effects of treating hypertension following aneurysmal subarachnoid hemorrhage.

We investigated in a consecutive series of 134 patients with aneurysmal subarachnoid hemorrhage whether institution of antihypertensive treatment was related to the incidence of cerebral ischemia and rebleeding. The aim of hypertensive treatment was to reduce the diastolic blood pressure to levels below 100 mm Hg. There was no difference in outcome between patients with or without antihypertensive drugs. Rebleeding was less frequent in patients with antihypertensive treatment (12/80 patients (15%) versus 18/54 patients (33%) without anti-hypertensive treatment (p = 0.012)). Nevertheless, patients with anti-hypertensive treatment had, on average, still higher blood pressures than untreated patients. Conversely, infarction occurred more often in patients with anti-hypertensive treatment (34/80 patients (43%) versus 12/54 (22%) without antihypertensives (p = 0.03)). This relationship was partly explained by co-existing hyponatremia. Our results suggest that the need for antihypertensive treatment is questionable, since the prevention of rebleeding is offset by an increased risk of cerebral infarction.

Antihypertensive Agents↗
PubMed1990

Chronic doxorubicin induced cardiomyopathy in rabbits: mechanical, intracellular action potential, and beta adrenergic characteristics of the failing myocardium.

STUDY OBJECTIVE: The aim was to assess myocardial, electrophysiological, and adrenergic changes caused by chronic administration of doxorubicin. DESIGN: Doxorubicin induced cardiotoxicity was produced in three groups of rabbits by injecting doxorubicin 0.75 mg.kg-1 three times a week for 7, 9 and 11 weeks. There were 36 controls. All studies were conducted within 16 to 36 h after the last injection. Histological, mechanical, and action potential changes produced by doxorubicin were examined in vitro. The effects of doxorubicin on beta adrenergic receptors and cyclic adenosine monophosphate (AMP) generation in myocardial membrane preparations were also evaluated. EXPERIMENTAL MATERIAL: 145 New Zealand white rabbits, 2.4-2.7 kg, were used. After excision of the heart, a papillary muscle was used for mechanical studies, a portion of the septum for intracellular action potential studies, and the rest of the heart for histological or biochemical studies. MEASUREMENTS AND RESULTS: Histological studies showed widespread myocardial damage that became more severe as the cumulative doses increased. Right ventricular papillary muscles of doxorubicin treated rabbits had lower total tension (1.5 v 3.3 g.mm-2 for controls, p less than 0.05) and dT/dt, shorter contraction duration, and lower velocity of shortening than the control muscles under all loading conditions. The changes progressed as the cumulative doxorubicin dose increased. Action potential duration was shorter in the doxorubicin treated groups (APD50 = 76 v 62 ms for controls, p less than 0.01), although resting action potential amplitude was normal. Tension-frequency response (6-36 stimuli.min-1) and response to increasing calcium concentrations (2.54-6.32 mM) were attenuated in the doxorubicin group. Percent change in tension and dT/dt in response to noradrenaline (50 microM), isoprenaline (20 microM), or dibutyryl cyclic AMP (40 mM), was increased in the doxorubicin group v controls (300-600% v 100-200% respectively), despite chronic increase in circulating catecholamines, depletion of myocardial catecholamines, and no change in beta adrenergic receptor number or affinity. The apparent increase in beta adrenergic responsiveness in the doxorubicin group may have been partly due to decreased basal cyclic AMP production (13 v 31 pMol.mg-1 protein.min-1, p less than 0.01), although maximum catecholamine stimulated cyclic AMP production was only mildly decreased (251 v 315 pMol.mg-1 protein.min-1, p less than 0.05). CONCLUSIONS - The subacute effects of chronic doxorubicin become progressively more marked as the cumulative dose increases, and there are significant differences in the myocardial characteristics between this chronic model and other models of heart failure. These differences may be related to the cytotoxic effects of doxorubicin on membranes and membrane bound enzymes.

Action Potentials↗
PubMed1990

Grading the amount of blood on computed tomograms after subarachnoid hemorrhage.

According to several studies, the amount of subarachnoid blood on the initial computed tomogram of patients with aneurysmal subarachnoid hemorrhage has predictive value with respect to infarction and outcome. Of several methods for assessing the amount of subarachnoid blood, none has been subjected to a study of interobserver agreement. We describe our own method, applied in previous studies, in which the amounts of blood in 10 basal cisterns and fissures and in four ventricles are graded separately. In grading single computed tomograms of 182 consecutive patients with subarachnoid hemorrhage, the agreement between pairs of three observers, studied with kappa statistics, was relatively good for individual cisterns or fissures (kappa between 0.35 and 0.65) and ventricles (kappa between 0.47 and 0.74). The Spearman rank correlation coefficients for the sum of the scores for subarachnoid and intraventricular blood were very high. Summed scores for extravasated blood are suitable as a baseline variable in follow-up studies of patients with subarachnoid hemorrhage.

Blood↗
PubMed1990

High-dose intravenous immunoglobulin treatment in chronic inflammatory demyelinating polyneuropathy: a double-blind, placebo-controlled, crossover study.

We discontinued high-dose intravenous immunoglobulin treatment (IVIg) in 7 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) who seemed to have responded to IVIg. After discontinuation of treatment, all 7 patients deteriorated. We then randomized the patients to IVIg or placebo (albumin) treatment in a double-blind crossover study. The clinical condition of all patients improved after IVIg and did not improve after placebo treatment. The mean time lapse from the end of the trial treatment to the occurrence of deterioration was 6.4 weeks after treatment with IVIg and 1.3 weeks after treatment with placebo. This selected group of patients with CIDP had a beneficial response to IVIg.

Adult↗
PubMed1990

Outcome in perimesencephalic (nonaneurysmal) subarachnoid hemorrhage: a follow-up study in 37 patients.

We interviewed 37 patients with perimesencephalic hemorrhage, 18 months to 7 years after the bleed. None rebled or had persisting neurologic deficits. These findings are remarkably good compared with recent series of patients with subarachnoid hemorrhage and normal angiogram. When blood is confined to the mesencephalic cisterns in patients with normal angiogram, repeat angiography may not be indicated.

Adult↗
PubMed1989

Xanthochromia.

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Diagnosis, Differential↗
PubMed1989

Chronic inflammatory demyelinating polyneuropathy. Conduction failure before and during immunoglobulin or plasma therapy.

An earlier study has shown that patients with chronic inflammatory demyelinating polyneuropathy may improve after the infusion of fresh frozen plasma or high dose intravenous immunoglobulin. We studied 8 such responding patients with neurophysiological techniques. Before treatment all patients had decreased compound muscle action potentials (CMAP) and slowing of conduction. During several courses of treatment a progressive increase of the CMAPs occurred and in 5 patients a correlation between the CMAPs of the abductor pollicis brevis muscle and grasp force could be demonstrated. In 2 patients, increase in strength was correlated with shortening of the distal motor latency; no significant relationships were found between strength and conduction velocity. Different patterns in the distribution of conduction failure were observed. In 2 patients, lesions were distributed along the length of the motor fibres, whereas the sensory system was spared. In another 2 patients the lesions, most likely demyelinating, were localized distally and included the sensory system. The 4 remaining patients were more difficult to classify, but individually showed greater resemblance to one or other of the two described patterns. Different patterns of conduction failure may reflect different pathogenetic mechanisms.

Action Potentials↗
PubMed1989

Effect of sotalol against reperfusion-induced arrhythmias in Sprague-Dawley and Wistar rats.

The effect of (+/-)-sotalol (a beta-blocker with class III antiarrhythmic activity) against reperfusion-induced arrhythmias was studied in artificially ventilated, open-chest, Sprague-Dawley and Wistar rats. Coronary artery occlusion was produced for 5 min and reperfusion allowed for 10 min. A somewhat different arrhythmic profile was observed between saline-treated rats of the 2 strains studied, with more Sprague-Dawley rats experiencing an irreversible ventricular fibrillation (VF) upon reperfusion, compared to Wistar rats, in whom a combination of reversible ventricular tachycardia (VT) and VF was more frequently observed. No difference in action potential characteristics and ventricular effective refractory period determined in vitro, nor in myocardial noradrenaline content, was found between the 2 strains of rats. (+/-)-Sotalol (5 and 10 mg/kg, IV) showed marked beta-blocking activity and reduced the mean duration of VT-VF in both strains studied. It also produced similar increases in action potential duration and refractory period in vitro in these 2 strains. In a different series of experiments, the antiarrhythmic action of the racemic form was compared to that of (+)-sotalol using Wistar rats. (+)-Sotalol had much less beta-blocking activity, and was found to be similarly effective against reperfusion-induced VT-VF. It is concluded that the antiarrhythmic effect of sotalol against reperfusion-induced arrhythmias may not be related to beta-adrenergic blockade but probably to class III type activity. Despite differences in the profile of reperfusion-induced arrhythmias between Sprague-Dawley and Wistar rats, both strains were sensitive to the antiarrhythmic action of (+/-)-sotalol.

Animals↗
PubMed1989

Regulation of autoantibodies in inflammatory demyelinating polyneuropathy: spontaneous and therapeutic.

We have analyzed the role and regulation of autoantibodies in inflammatory demyelinating polyneuropathy (GBS/CIDP). The clinical significance of pathogenic autoantibodies to peripheral nerve tissue is suggested by the beneficial response of many of these patients to plasmapheresis and treatment with high doses of polyspecific IVIgG. Recovery, whether spontaneous or therapeutically-induced, is associated with anti-idiotypic suppression of the antoantibodies. Preliminary results suggest that these autoantibodies share cross-reactive idiotypes or, alternatively, that the regulatory anti-idiotypic antibodies are multireactive.

Autoantibodies↗
PubMed1989

Xanthochromia after subarachnoid haemorrhage needs no revisitation.

Recently it was contended that it is bloodstained cerebrospinal fluid (CSF) that is important in the diagnosis of subarachnoid haemorrhage (SAH) and not xanthochromia, and also that a normal CT scan and the absence of xanthochromia in the CSF do not exclude a ruptured intracranial aneurysm. The CSF findings were therefore reviewed of 111 patients with a proven SAH. All patients had xanthochromia of the CSF. Lumbar punctures were performed between 12 hours and one week after the ictus. Xanthochromia was still present in all (41) patients after 1 week, in all (32) patients after 2 weeks, in 20 of 22 patients after three weeks and in 10 of 14 patients after four weeks. In six years we identified only 12 patients with sudden headache, normal CT, bloodstained CSF, and no xanthochromia. Angiography was carried out in three and was negative. All 12 patients survived without disability and were not re-admitted with a SAH (mean follow up 4 years). It is concluded that it is still xanthochromia that is important in the diagnosis of SAH and not bloodstained CSF. Furthermore a normal CT scan and the absence of xanthochromia do exclude a ruptured aneurysm, provided xanthochromia is investigated by spectrophotometry and lumbar puncture is carried out between 12 hours and 2 weeks after the ictus.

Humans↗
PubMed1989

Opposite effects of lidocaine and diltiazem on electrophysiologic alterations in acutely ischemic porcine myocardium.

To investigate the actions of lidocaine and diltiazem on the ischemic alterations associated with the onset of acute ischemic arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine (2.4-3.8 micrograms/mL of plasma) or diltiazem (390-510 ng/mL) in open-chest anesthetized pigs. Sixty-one unipolar electrograms were continuously recorded in the ischemic zone. Isochronal maps and isopotential maps were determined by computer analysis. The magnitude of beat-to-beat alternation of unipolar waveforms was described by the difference between the time integrals subtended by electrograms of consecutive beats. Activation times were prolonged by ischemia and the ST segment became elevated. Delay and ST elevation developed at a faster rate in the presence of lidocaine than under control conditions, but were reduced by diltiazem. ST-T alternation was not significantly different between control and lidocaine occlusions, but the incidence of negative T waves and that of ventricular tachycardia degenerating to fibrillation were higher in lidocaine occlusions than in control occlusions. In contrast, unipolar waveform alternation and negative T waves were virtually abolished by diltiazem, even at fast pacing rates (180-210 beats/min) at which diltiazem did not reduce ST elevation. Ventricular arrhythmias also were abolished by diltiazem. Thus, lidocaine and diltiazem produce opposite effects on the ischemic alterations most closely associated with the initiating mechanism of tachycardia. This could be related to differences between these drugs with regard to their actions on transmembrane currents during repolarization.

Animals↗