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Biomedical subjects

W Wieling

Publications and source records attributed to W Wieling.

124 records · Page 7Linked to original sources
PubMed1984

Mechanisms of initial blood pressure response to postural change.

The influence of supine rest on the blood pressure response to standing and 70 degrees head-up tilt was studied in detail for the first 30 s after the change of posture. Following 20 min of supine rest, the active transition to standing was accompanied by an immediate increase in systolic pressure of 29 +/- 6 mmHg (mean +/- SEM). This was followed by large fluctuations in systolic pressure: to -28 +/- 2 mmHg below control after 7 s and to 22 +/- 2 mmHg above control after 22 s (17 mmHg in excess of the systolic pressure level after head-up tilt). Following 1 min of supine rest, there was no difference in the immediate increase in systolic pressure. However, the magnitude of the subsequent changes was significantly diminished. With head-up tilt the immediate increase in blood pressure was absent and afterwards small changes were found that were also significantly influenced by the period of prior rest. Taken in conjunction with earlier studies, the following mechanisms are suggested. The immediate blood pressure increase resulted from compression of arteries by the contracting postural muscles. The subsequent blood pressure fall was caused by at least two mechanisms: (a) the fall was predominantly of reflex origin, because the immediate pressure increase stimulated the systemic baroreceptors; (b) supine rest possibly augmented the translocation of blood from the thorax which contributed, approx. 5 s from standing, to the reflex fall of blood pressure.

Adult↗
PubMed1983

Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus.

We have investigated the relationship between vagal and sympathetic lesions in 62 diabetic patients and compared the results with those from 37 healthy subjects. Vagal function was assessed by heart rate changes with forced breathing. Sympathetic control was measured by the heart rate and blood pressure changes after standing and the concomitant plasma catecholamine response. The integrity of the postganglionic sympathetic neuron was evaluated separately by testing sudomotor function. Impaired sympathetic control was found only in 15 diabetic patients with severely impaired or absent vagal heart rate control. In 12 patients the chief abnormalities consisted of a delayed and diminished heart rate increase, an excessive fall in systolic blood pressure (greater than 20 mmHg) in combination with an abnormally small noradrenaline increment (less than 120 ng/l) and a lesion of the postganglionic sympathetic neuron. Three patients with severely impaired parasympathetic heart rate control in combination with an intact postganglionic sympathetic neuron demonstrated a large noradrenaline increase on standing (greater than 700 ng/l). Measurement of vagal heart rate control and testing of sudomotor function makes it possible to classify a spectrum of abnormal cardiovascular responses to standing in diabetic patients.

Adult↗
PubMed1983

Testing for autonomic neuropathy: heart rate changes after orthostatic manoeuvres and static muscle contractions.

1. The initial heart rate (HR) response evoked by standing, 70 degrees head-up tilt, handgrip and contraction of abdominal and leg muscles was analysed in diabetic patients with autonomic neuropathy and in matched controls. 2. In healthy subjects standing induced an immediate, large, HR increase lasting 20s that far exceeded the small HR rise induced by tilt. The HR response with handgrip and to contraction of abdominal and leg muscles was strikingly similar for the first 5 s to the HR increase after standing. 3. In diabetic patients handgrip and standing induced a small HR increase starting after 2-3 s. Contraction of abdominal and leg muscles evoked little or no HR changes. The HR rise after tilt up was delayed by 10 s compared with healthy controls. 4. It is concluded that the circulatory response to active and passive changes of posture differs fundamentally. Standing and handgrip are superior to head-up tilt as a test for vagal HR control. An abrupt and large HR increase after standing excludes cardiac parasympathetic neuropathy. A modified response, however, may be due to afferent as well as to efferent lesions, e.g. in muscle afferents or in vagal afferents from cardiopulmonary receptors.

Adult↗
PubMed1982

Reflex control of heart rate in normal subjects in relation to age: a data base for cardiac vagal neuropathy.

We examined the heart rate changes induced by forced breathing and by standing up in 133 healthy subjects in the age range 10-65 years in order to establish a data base for studies on parasympathetic heart rate control in autonomic neuropathy. Test results declined with age. Log-transformation was used to define the lower limit of normal (P0.10) and an uncertainty range (values between P0.10 and P0.025). The lower limit of normal decreased from 22 to 11 beats/min for forced breathing and from 26 to 16 beats/min for standing up, with age increasing from 10 to 65 years. No subject scored below and only two subjects scored in or below the uncertainty range for both tests. Lack of correlation between both tests (r = 0.17) documents the different afferent mechanisms of the reflex heart rate changes. In combination these two tests form a simple and reliable bedside method to establish cardiac vagal neuropathy.

Adolescent↗
PubMed1982

Mechanisms of initial heart rate response to postural change.

We explored in 43 healthy subjects the afferent mechanisms of the initial heart rate response to standing by comparing free standing, 70 degrees head-up tilt, handgrip, and contraction of abdominal and leg muscles. The results indicate the following. 1) Standing evokes an immediate, large, bimodal increase of heart rate (HR) of about 20 s duration that far exceeds the gradual HR rise induced by 70 degrees head-up tilt. 2) The immediate HR increase with active standing is due to the exercise reflex and results in a first peak about 3 s after standing briskly. 3) The secondary, more gradual HR increase after 5 s of standing and the subsequent rapid decrease of HR between about 12 and 20 s corresponds through the baroreceptor reflex with a striking fall, recovery, and sometimes overshoot of arterial pressure. 4) The maximum HR increase found after about 12 s of standing is augmented and delayed after rest. 5) The time course of the initial HR response is not modified by physical training. We conclude that active and passive changes of posture result in fundamentally different cardiovascular effects for about 20 s and that "central command," muscle receptors, high-pressure receptors, low-pressure receptors, and the plasma catecholamine level are probably all involved in the initial HR response to standing.

Acclimatization↗
PubMed1981

Is the coronary care unit a coronary scare unit?

In order to evaluate the influence of stress associated with admission to a coronary care unit (CCU), we measured the plasma noradrenaline and adrenaline concentrations during the first CCU hour in 47 patients with suspected acute myocardial infarction (AMI). These values were compared with those in healthy hospital personnel. AMI patients had significantly higher plasma catecholamines than patients with no apparent cardiac disease. The highest values were found in patients with complicated AMI. Although the patients had significantly higher plasma catecholamines than hospital personnel, it is concluded that the circulation rather than the situation determines plasma noradrenaline and adrenaline levels and that stress does not play a major role. This study provides no support for the suggestion that home care is preferable for patients with AMI as a means of avoiding the stress of admission to hospital.

Adult↗
PubMed1981

Myocardial perfusion imaging with thallium-201 to assess left ventricular hypertrophy and regional ischaemia in hypertensive patients.

The increase in mortality from cardiovascular disease in the presence of electrocardiographic signs of left ventricular hypertrophy (LVH) has been ascribed to ischaemic changes in the hypertrophied left ventricle even in the absence of overt coronary artery disease. To test this hypothesis and to investigate the usefulness in the detection of LVH myocardial perfusion scintigraphy with thallium-201 and echocardiography was performed in thirty-three hypertensive patients. Sixteen had had electrocardiographic signs of left ventricular hypertrophy. Twelve patients had symptoms of cardiovascular disease. In twenty-six subjects the scintigraphic procedure consisted of a combined rest--exercise study, in the other seven only resting images were obtained. Measurement of septal wall thickness on the scintiscans correlated fairly well with echographic dimensions and allowed separation of a group of patients with LVH from a group without. In individual patients, however, the perfusion scan was not a reliable tool to affirm the presence of LVH. A total of eight patients, six with LVH on the echocardiogram, had an abnormal rest--exercise perfusion scan, either with a new perfusion defect after exercise and/or with a resting defect alone. In nine other patients with echocardiographic LVH, on the other hand, no abnormal perfusion was found. Thus, perfusion abnormalities did not correlate with the presence of LVH. The presence of such abnormalities in relation to increasing age and symptomatic cardiovascular disease could well be the expression of anatomic coronary artery disease and cannot be differentiated from the possible ischaemia of the hypertrophied left ventricle.

Adult↗
PubMed1981

Echocardiographic dimensions and maximal oxygen uptake in oarsmen during training.

We studied nine freshmen and 14 senior oarsmen undergraduates during seven months of training and compared them with 17 age and sex-matched sedentary control subjects in order to assess the influence of heavy physical exercise on cardiac dimensions and maximal oxygen uptake. Standard M-mode echocardiographic techniques were used. At the start of the season senior oarsmen had a greater left ventricular end-diastolic dimension, and a thicker interventricular septum and posterior left ventricular wall than control subjects and freshmen oarsmen. The two latter groups did not differ from each other. During the training period there was a slight and gradual increase in left ventricular end-diastolic dimension, and interventricular septum and posterior wall thickness in freshmen. In seniors only left ventricular end-diastolic dimension increased significantly. Maximal oxygen uptake showed a distinct increase between the fourth and seventh month during the period of intensive rowing training. There was no relation between echocardiographic variables and maximal oxygen uptake. A combination of heavy dynamic and static exercise can thus lead to significant changes in both left ventricular wall thickness and chamber size within months. Echocardiographic variables measured at rest cannot be used as a suitable index of performance capacity.

Adult↗
PubMedDate not supplied

Initial and delayed circulatory responses to orthostatic stress in normal humans and in subjects with orthostatic intolerance.

Gravitational stresses, which are common daily event for humans, result in a diminution in central blood volume, due to displacement of blood to the lower parts of the body. They demand complex adjustments in the cardiovascular system to offset the decrease in cardiac filling pressure. Such changes are necessary to sustain arterial blood pressure at an appropriate level so that there is adequate perfusion of vital organs, especially the brain. These adjustments must compensate for both the initial and sustained orthostatic stress. The rapid short-term adaptations are mediated primarily by the cardiovascular reflexes with humoral agents reinforcing these reflexes during severe and prolonged orthostatic stress. Understanding these complex reflex adjustments in normal humans is necessary in order to appreciate subjects with orthostatic intolerance.

Atrial Natriuretic Factor↗