[Maximum values for work load and oxygen consumption in Surinam creoles].
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Biomedical subjects
Publications and source records attributed to J J Schipperheyn.
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Cross-clamping of the descending thoracic aorta for surgical correction of coarctation carries a risk of injury to the spinal cord, which is usually attributed to insufficient blood supply along the spinal arteries. To detect inadvertent interruption of spinal cord perfusion, lumbar pressure was monitored during operation on the aorta in eight patients. One patient incurred ischemic damage of the spinal cord, resulting in paraparesis. In this patient, spinal fluid pressure increased to such high levels that it may have caused tamponade of the cord. The pressure increase resulted from expansion of cerebral vessels caused by an acute rise of arterial pressure after clamping, probably aggravated by the administration of a vasodilating drug. During operations in which the circulation of the spinal cord is compromised long enough to cause ischemic damage, the femoral artery and spinal fluid pressures should be monitored. If the pressure difference between femoral artery and lumbar cavity drops to a dangerously low level, a shunting procedure should be performed.
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The value of electromagnetic flow measurements for the detection of graft stenosis during aortocoronary bypass and subsequent prevention of early closure by reimplantation of the graft was assessed. Postoperative angiograms were studied in 102 grafts in 55 patients in whom flow was measured during operation. Patients with recurrent angina or insufficient improvement after operation were selected to include many early occluded grafts; 30 grafts became occluded within six months. Applying a criterion of acceptable specificity based on flow pattern analysis, only 6 grafts were found to be abnormal immediately after implantation. It appears that in most instances, early closure is caused by a process of scar tissue formation which takes several months to develop completely. As a rule, the graft is patent after implantation and flow pattern analysis has nothing to offer. The value of flow pattern analysis during operation for the prevention of early closure is limited, and its value for the prediction of long-term prognosis of the grafts remains to be evaluated.
The case history, skeletal muscle and heart muscle biopsy findings from an affected member of a family suffering from hypokalaemic periodic paralysis associated with permanent muscular weakness are reported. The patient, a female aged 35 years, while treated with 750 mg and later 1000 mg of acetazolamide daily, developed typical exercise angina pectoris. The ECG during exercise showed ST-segment depression. A coronary angiography was performed because coronary artery disease was suspected. To exclude cardiac muscle disease a biopsy of the left ventricular wall was taken. The angiography was normal. Ultrastructural analysis of the biopsy specimen showed an unusual amount of intermyofibrillary glycogen resembling, although far less abundant, the increase of glycogen found in the skeletal muscle biopsy specimen obtained from the same patient. The possible implications of these findings are discussed with reference to the normal echocardiographic findings in the family.
The occurrence and the cause of arterial hypoxaemia were studied in spontaneously breathing dogs in which myocardial ischaemia was induced during anaesthesia. Changes in several circulatory and ventilatory variables and in parameters of gas exchange were assessed in twelve dogs in the two 1st h after the intervention; these included changes in the distribution of ventilation-perfusion ratios determined with an inert tracer gas method. Eight out of 12 dogs developed haemodynamic signs of an acute myocardial infarction after occlusion of a branch of the left coronary artery; the circulatory changes were moderate in 6 and severe in 2 animals. A drop in Pa,O2 occurred in 5 dogs. In one without significant haemodynamic changes it was largely due to a decrease in alveolar ventilation. The ventilation-perfusion ratio distribution in the other 4 dogs did not change in a consistent way; appreciable shunt circulation (6.6%) developed in one dog. Neither ventilation-perfusion mismatch nor shunt circulation contributed much to the hypoxaemia. The most consistent finding in the 5 dogs in whom Pa,O2 fell, was a drop in Pv,O2 (mean 1.3 kPa); it accounted for 86% of the drop in Pa,O2.
Coronary vasodilation after brief (less than 15 s) occlusions was studied in closed-chest, anesthetized dogs, using constant-flow perfusion of a large coronary artery. We assumed occlusion duration to be a measure of the concentration of endogeneous adenosine and determined adenosine dose-response curves by varying occlusion duration and measuring the resulting drop in vascular resistance. The curves were compared to dose-response curves measured by continuously infusing adenosine. Both dose-response relations were found to follow the Hill equation for ligand receptor interaction; the slopes of the two curves were not significantly different, and the estimated adenosine accumulation rate in the myocardium was found to be in close agreement with data in the literature, measured by direct tissue assay. The time course of recovery of vascular tone after short occlusions was not very sensitive to flow, at least not for normal flow levels or higher. The results confirm that adenosine accumulation plays an important role in causing postocclusion vasodilation. However, autoregulation of coronary flow based on an adenosine washout mechanism additionally requires tissue clearance to be highly flow dependent for flow levels below normal, but approaches a constant value when flow increases above normal.
An adjustable constant-flow coronary artery perfusion system has been developed for use in the anesthetized closed-chest dog. Coronary flow and perfusion pressure measurements are obtained over the entire autoregulatory range. Coronary flow was briefly diverted to a bypass cannula and then returned to its original level. Coronary vasodilatation resulted in a fall of perfusion pressure below its preocclusion value, but recovery of vascular tone was complete in about twice the time required during unrestricted reactive hyperemia. It is concluded that no flow debt repayment is required for the restoration of vascular tone after brief occlusions. In the measurements made with this system, intramyocardial pressure distribution is not influenced by thoracotomy, pericardotomy, or positive-pressure respiration, and surgical trauma is minimal.
The results are reported of cardiological examinations, including echocardiography, in nine members of a family suffering from hypokalaemic periodic paralysis, associated with permanent muscular weakness. The studies were performed in periods between attacks of paralysis. The slowly progressive permanent muscular weakness which is found in most of the patients with hypokalaemic periodic paralysis resembles a limb-girdle type dystrophy. Involvement of cardiac muscle is not uncommon in patients with limb-girdle dystrophy. Using a combination of echocardiography and ECG examination, nowadays the most sensitive screening method for the detection of cardiomyopathy, no evidence was obtained for cardiac involvement in hypokalaemic periodic paralysis patients with permanent muscular weakness.
Multiple dipole models of activation of the heart, in combination with a model of the thorax as an electrical conductor relate the action of individual cells to features of the electrocardiogram. The models can be used to develop diagnostic electrocardiographic criteria for ventricular hypertrophy, myocardial infarction or conduction disorders. Criteria derived with the use of Holt, Barnard and Lynn's model proved to be superior to well-established empirical rules. Their approach restricts position, direction and polarity of the current dipole vectors in the model. In the Selvester model, and later in the Ritsema van Eck model, in addition to these restrictions time-constraints are imposed on the dipole activity. In a validation study of the Ritsema van Eck model activation of a beating dog heart is compared in detail with simulated activation in a computer replica of the same heart. Myocardial spread of activation is found to be stimulated correctly. Simulated spread of activation along the Purkinje fiber network however, differs considerably from reality. In apical regions excitation spreads in reality much faster than in the model, in basal regions much slower. The model can be improved by slowing endocardial excitation from apex to base with the time-course of activation. Further improvement is obtained by the use of a more detailed pattern of endocardial excitation, based on studies of endocardial excitation in opened ventricles. The model can predict the time-course of activation with an accuracy of 5% of total ventricular activation time.
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Haemodynamic side effects of antilymphocyte serum (ALS) have been studied in six dogs treated with equine anti-dog ALS. All animals responded with a severe but transient reduction of cardiac output and, in most cases, a drop in aortic pressure. This effect is best explained by a direct negative inotropic action followed by secondary vasoconstriction. An indirect effect of ALS by release of cardiotoxic substances from damaged blood cells seems to be a more probable explanation than a direct action of ALS on cardiac cell membranes.
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Thermal dilution cardiac output determinations in dogs were compared to simultaneously performed Fick oxygen measurements. The purpose of this study was to validate in dog experiments a method for thermal dilution measurement which employs a double-thermistor catheter combined with an automatic computer as described by Olsson et al. Dilution and injectate temperature are entered directly into the calculation. The method does not employ logarithmic extrapolation, integration of the dilution signal being terminated when a preset cut-off level is reached. Errors due to recirculation, thermal capacitance of the right heart and heat exchange with the catheter's dead space require the use of an empirically derived correction factor, which in dogs was found to be significantly different from the factor used for human thermal dilution curves. With the appropriate cut-off level and correction factor a good agreement was found between the results of the thermal dilution and the Fick method. The regression equation for 47 experiments was found to be COtd = 0.95 COFick + 0.08; the correlation coefficient was 0.94.
Contractility is often depressed in isolated heart muscle. To analyze this phenomenon, we measured the derivative of left ventricular pressure (dP/dt) in intact and in isolated, blood perfused pig hearts, and peak force (F) or stress (F/mm2) in ventricular trabeculae of man and pig. When the heart was in the steady state at a priming frequency of 2 Hz an extrasystolic interval of 0.3 s was interposed, followed by four postextrasystolic intervals of 0.8 s. In the case of isolated trabeculae the priming frequency was 0.2 Hz, the extra interval 0.4 s, and the post-extrasystolic intervals were 5 s. The exponential decay of potentiation is characterized by the constant D: a low value of D indicates a rapid decay of potentiation. DP/dt was about 1000 mm Hg/s in the intact hearts, but within 1 h after isolation dP/dt decreased to about 700 mm Hg/s, and this was associated with a decrease in D from 0.63 to 0.40. Developed stress in the isolated trabeculae was about 2 mN/mm2 and D was about 0.20 under standard, in vitro conditions (a.o. 1.5 mM Ca2+. 0.2 Hz stimulus frequency). This stress is only 10% of the calculated stress in the intact heart. An increase of priming frequency, or of [Ca2+], or addition of 30 nM isoproterenol to the perfusate caused a marked increase in F and D. Properties of human and porcine trabeculae were quantitatively similar. The strong correlation between dP/dt, or F, and D suggests a causal relationship. This is consistent with the current model of e-c coupling in heart muscle, in which the activity of the Ca2+ pump of the sarcoplasmic reticulum determines the decay of potentiation and the amount of releasable Ca2+ in the reticulum determines force of contraction. Since isoproterenol stimulates the Ca2+ pump in the reticulum, the increase in D and F induced by this drug is consistent with the model. We conclude, that the decreased dP/dt, F, and D in isolated preparations was due to impaired sarcoplasmic reticulum function. The role of this phenomenon in the stunned heart syndrome, species differences and possible causes are discussed.