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Biomedical subjects

C Borst

Publications and source records attributed to C Borst.

At least 145 records · Page 8Linked to original sources
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

Frequency limitation in the human baroreceptor reflex.

In 10 unsedated normotensive subjects, low-level bilateral electrical stimulation of the carotid sinus nerves (0.35 ms, 1-2 V) was applied with frequencies of 20-200 Hz for therapeutic purposes. Both peak and steady-state reflex effects increased with the stimulus rate up to 80 Hz. After 1 min of stimulation, the largest fall of arterial pressure (21.0 +/- 5.8%, mean +/- S.D.) was produced by stimulus frequencies of 80-120 Hz. Right atrial pacing did not modify the results. After 1 min of stimulation at 200 Hz, the arterial pressure fall was reduced to 13.6 +/- 5.2% (P less than 0.001), whereas peak effects, reached after 15-40 s, were near maximal. The reduction of the depressor response emerged after about 10 s of stimulation and was complete after about 1 min. Peak RR-interval prolongation occurred within 10 s and showed no adaptation. Comparison of continuous stimulation and R-wave-triggered intermittent stimulation in 3 subjects suggested that the reflex effect was determined by the mean stimulus frequency. We conclude that frequency limitation in the baroreceptor reflex begins when the stimulus rate exceeds about 80 Hz. It leads to a frequency-dependent, gradual adaptation of the reflex effects when the stimulus rate exceeds 120 Hz. This conclusion is limited to the part of the reflex that is subserved by myelinated afferent fibers.

Adult↗
PubMed1983

Time delays in the human baroreceptor reflex.

In 11 normotensive subjects with coronary artery disease, low intensity electrical stimulation of the carotid sinus nerves (CSN) was triggered by the R-wave in the electrocardiogram with an adjustable delay. The latent period was estimated between the start of CSN stimulation and the onset of the reflex-PP-interval prolongation and, during right atrial pacing, the onset of the reflex fall of diastolic arterial pressure and prolongation of the AV-interval. The latency to the reverse changes was determined after switching CSN stimulation off. The PP-interval changes started after a latency of 0.5-0.6 s. This latency was independent of the respiratory phase and it was independent of the directional change of the afferent activity. AV-interval changes started after about 1 s. When heart rate was fixed, arterial pressure changes started after 2-3 s. It is estimated that central processing of baroreceptor afferent activity may require 0.25 s in the human.

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↗
PubMed1983

Protective effect of nifedipine in myocardial ischemia assessed by phosphorus-31 nuclear magnetic resonance.

Calcium antagonists may protect the myocardium against the consequences of ischemia. Phosphorus-31 nuclear magnetic resonance (31P NMR) was used to study the effect of nifedipine on intracellular acidosis and high energy phosphate depletion during global ischemia. Isolated rat hearts were paced (300 beats/min), perfused with a modified Tyrode solution for 30 min, made totally ischemic for 30 min (37 degrees C) and then reperfused for 30 min. When required, nifedipine (1 mg/l) was added to the perfusion fluid 10 min before ischemia. During ischemia intracellular pH fell from 7.11 +/- 0.03 (mean +/- S.E.M.) to 5.88 +/- 0.04 in the untreated hearts (n = 6), and from 7.11 +/- 0.03 to 5.95 +/- 0.02 in the treated hearts (n = 6). During the first 20 min of ischemia, intracellular pH was significantly higher in the treated than in the untreated hearts (P less than 0.001). Myocardial creatine phosphate (CP) content was depleted after 15 min of ischemia in the untreated hearts, and after 20 min of ischemia in the hearts treated with nifedipine. Myocardial adenosine triphosphate (ATP) content was depleted after 20 min of ischemia in the untreated hearts; ATP content in hearts that received nifedipine amounted to 23.5 +/- 6.2% of control after 30 min of ischemia. In contrast with the untreated hearts, the nifedipine-treated hearts showed a rapid recovery of CP content during reperfusion. The results indicate that nifedipine protects the myocardium against the metabolic consequences of ischemia and reperfusion.

Adenosine Triphosphate↗
PubMed1983

Bretschneider's histidine-buffered cardioplegic solution and the calcium paradox.

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether rat hearts could be predisposed to the calcium paradox by perfusion with Bretschneider's calcium-free histidine-buffered cardioplegic solution. Creatine kinase (CK) release during the reperfusion phase was used to quantitate cell damage. Perfusion with cardioplegic solution was performed at 37 degrees and 20 degrees C. Reperfusion after 10 minutes of perfusion with this solution at 37 degrees C resulted in a full calcium paradox. After 120 minutes of perfusion with cardioplegic solution at 20 degrees C, CK release during reperfusion amounted to 30% of the release during a full calcium paradox. This CK release could be further reduced by lowering the coronary flow rate or by adding 50 mumol X L-1 CaCl2 to the cardioplegic solution. It is concluded that a combination of hypothermia, a low coronary flow rate, and a limited duration of exposure to Bretschneider's histidine-buffered cardioplegic solution will minimize the risk of evoking the calcium paradox.

Animals↗
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↗
PubMed1982

Prolongation of atrioventricular conduction time by electrical stimulation of the carotid sinus nerves in man.

Electrical stimulation of the carotid sinus nerves was applied during diagnostic catheterization of two patients who had coronary artery disease. The immediate reflex prolongation of the atrioventricular (AV) interval was due to prolongation of the AH interval only and was roughly parallel to the reflex RR interval prolongation evoked without atrial pacing. After cholinergic block, the reduced prolongation of both the RR interval and the AV interval caused by reflex inhibition of sympathetic tone followed a time course similar to the arterial pressure decrease. This is the first demonstration in man of the parallel baroreflex effects on the sinoatrial node and the AV node.

Adrenergic Fibers↗
PubMed1982

Cardiac function, fiber shortening, and dynamic geometry.

Many models for the study of the pump function of the heart emphasize the importance of cardiac geometry and detailed dimensional data. Because of the lack of accurate measuring techniques, approximate geometries such as shells of revolution have been applied. In this study, methods are presented that measure the dynamic geometry of the working, isolated canine heart by means of ultrasound-velocity tomography techniques. In addition, cardiac dimensions, intramural deformations, and fiber shortening have been measured dynamically in the in situ canine heart throughout the cardiac cycle with implanted radiopaque markers and biplane roentgen techniques. Results of regional contraction and relaxation patterns are presented. Epicardial fiber shortening between apex and base were computed and found to be dependent on the duration of the preceding RR interval.

Animals↗
PubMed1981

Intravenous naphazoline intoxication.

Nine pale perspiring drug addicts with drowsiness, nausea, headache, normal blood pressure and marked sinus bradycardia with premature ventricular beats were seen at the Casualty Department soon after alleged i.v. cocaine administration. Eight were treated with atropine, as the bradycardia suggested intoxication with a parasympathomimetic compound. Seven were discharged in good condition after a few hours' observation. One patient developed a blood pressure of 150/120 mmHg after atropine. Subsequently, a hemiparesis was found and an intracerebral haematoma was evaluated at surgery. Another patient was admitted forthwith to the CCU. He did not receive any medication and recovered within two days. Urinalysis of these two patients disclosed contents of naphazoline, a powerful alpha-adrenergic agent. Samples of the alleged cocaine contained 97% naphazoline HCl. A conscious rabbit was injected with naphazoline and thereafter with atropine. I.v. naphazoline doubled mean arterial pressure (MAP) and reduced heart rate (HR) from 167 to 30 beats/min. Atropine doubled HR, but caused a marked rise in MAP, too, stressing the adverse effects of atropine in these cases. When confronted with patients after alleged cocaine abuse, the role of substitute drugs, especially alpha-adrenergic compounds, should be considered as this should influence the therapeutic approach.

Adult↗
PubMed1980

Implantable stimulating electrode for baroreceptor afferent nerves in rabbits.

An implantable stimulating electrode was developed for baroreceptor afferent nerves in the freely moving rabbit (nerve diam 0.1-0.2 mm). It consists of highly flexible electrode leads (coiled Pt-Ir wire) and silicone rubber (Silastic) as insulation. The electrodes were shown to be effective for up to 245 days after implantation in the neck. Electrode failure was due to dislodgment of the electrode (early failures) or (ultimately) cable breakage. Heart rate and blood pressure responses of separate and combined stimulation of depressor and carotid sinus nerves are shown. In vitro studies demonstrated some current leakage from the electrode to surrounding tissues, but the in vivo measurements show the validity of the method.

Afferent Pathways↗
PubMed1979

A model of left ventricular function in the denervated heart.

A model has been formulated for the function of the denervated left ventricle. Using the model it is possible to generate realistic waveforms for aortic flow, aortic pressure, left ventricular volume and left ventricular pressure over a wide range of simulated haemodynamic conditions. The effect of changes in contractile state is introduced through the concept of left ventricular pumping capacity. Model results compare well with similar data obtained from denervated hearts in open-chest dogs anaesthetized with halothane under positive pressure ventilation. Simulation of changes in contractile state shows excellent agreement with data published by previous investigators.

Animals↗