Reduced side effects of low osmolality non-ionic contrast media in coronary arteriography. Comparative experimental study in dogs.
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Angiography↗
Biomedical subjects
A Hoeft
Publications and source records attributed to A Hoeft.
[Measurement of coronary blood flow using a double fiber optic system and computer-assisted development of transcoronary dye dilution tracings].
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Animals↗
Improvement of the metabolic and energetic situation of ischemically stressed myocardium by verapamil after experimental coronary artery occlusion.
On anaesthetized open-chest mongrel dogs (n = 7) short-time (3 min), repeated ischemia of relatively large parts of the myocardium was produced by proximal, intermittent occlusion of the LAD artery in intervals of 45 min. Usually, 2-3 control occlusions and 2-3 occlusions under therapy were performed. From hemodynamic data, coronary blood flow and AVD-O2 myocardial oxygen consumption (MVO2) and energy demand (Et) were continuously recorded by use of a micro-computer. The occurring difference between MVO2 and Et (dO2) allowed to calculate during the occlusion period the O2-debt (DO2) and during the reperfusion period the O2-repayment (RO2). Furthermore, the releases of the metabolic ischemia parameters lactate, inorganic phosphate and potassium were determined in the first minute of postischemic reperfusion. Compared to control occlusions, premedication with verapamil (Isoptin) 0.12--0.2 mg/kg b.w.) led intra- and interindividually to a significantly reduced O2-debt (p less than 0.001) during the occlusion period combined with a significantly reduced amount of oxygen, additionally taken up in the early reperfusion period (p less than 0.001). Under verapamil the amounts of metabolic parameters released in the first minute of reperfusion decreased significantly: lactate: -36% (p less than 0.001), inorganic phosphate: -32% (p less than 0.001), potassium: -30% (p less than 0.001). The improvement of the metabolic and energetic situation of ischemic myocardium indicates that verapamil may be of importance in reducing the extent and severity of acute myocardial ischemic injury.
Animals↗
[Effects of radiographic contrast media on cellular electrophysiology in the beating heart (author's transl)].
Electrophysiological effects of intracoronarily administered contrast media have been documented in 12 thoracotomized dogs at the cellular level by use of a modified microelectrode technique. Injections (n = 63) of 4 different contrast media uniformly led to a temporary cellular hyperpolarisation of the resting potential and prolongation of the action potential. Additional experiments with intracoronary injections of several electrolyte solutions indicate that the observed effects can be explained by contrast-induced changes in the extracellular electrolyte concentrations, mainly by a local deficiency of potassium ions and an excess of sodium ions. The significance of the findings for mechanisms underlying ECG-changes and ventricular arrhythmia by radiographic contrast media will be discussed.
Animals↗
Basic physiological studies on cardiac pacing with special reference to the optimal mode and rate after cardiac surgery.
Temporary cardiac pacing (CP) is frequently applied postoperatively in the management of low cardiac output (CO) and rhythm instability. However, uncertainty exists about the "optimal" pacing rate, range and mode due to incomplete information on myocardial oxygen consumption (MVO2), related to its hemodynamic determinants, and on myocardial pumping efficiency (eta) at CP. In 10 intact dogs atrial pacing (AP) (90 to 210 beats/min) and ventricular pacing (VP) (70 to 330 beats/min) were investigated in normal and failing hearts. AP and VP were compared at identical rates. MVO2 (4 to 20 ml/min . 100 gr) was measured directly according to the Fick principle. Cardiac efficiency was calculated as the ratio of oxygen equivalent of external cardiac work to MVO2. Rates with maximum CO and a maximal eta occurred only in heart failure. However, maximal CO and eta were obtained at different heart rates (HR). MVO2 was significantly higher (p less than 0.001) under VP as compared to AP at identical rates with a mean increase of 26.5% +/- 6% over AP, although hemodynamics were significantly lower under VP (p less than 0.001). Myocardial pumping efficiency was markedly better under AP with a mean increase of 63% +/- 4.5% over VP even in normal heart. Adjustment of HR at maximal response in CO may become dangerous, particularly under VP, in heart failure. AP, if applicable, may be regarded as the optimal pacing technique due to an optimal relation of improved hemodynamics to MVO2. It may be helpful in correcting an imbalance between oxygen supply and demand in cases of low output syndrome. The pathophysiologic mechanisms and further clinical implications are discussed.
Animals↗
[Effects of adaptation to work in heat of rectal temperature evolution during recovery].
Evolution of rectal temperature (Tre) during recovery in different air temperatures was studied following different patterns of heat load before and after adaptation to work in heat (10 consecutive days). Three subjects have been exposed, after a 30 min rest period (Ta=28degrees C, Pwa=14 mb) to 4 heat loads, each producing 1 degreeC increase in Tre in approximatively 30 min (Co:Ta= 50 degrees C, Pwa = 60 mb, W = O watt; C1; 50 degrees C, 42 mb, 50 W on bicycle ergometer; C2;39 degrees C, 38 mb, 100 W and C3: 28 degrees C, 31 mb, 150 W). After of these heat loads, subjects were allowed to recover during 2 h at Ta = 28, 22 or 16 degrees C (Pwa = 14 mb). Results show that: (a) the cooler was the Ta, the faster was the recovery time; (b) before adaptation occurs, the evolution of Tre depended on the preceding heat load pattern; (c) the more intense was the work load, the more the adaptation reduced time for subsequent recovery. The interaction obtained between adaptation and intensity of preceding work load is discussed. The evolutions of leg skin temperatures suggest that a decreased local heat conductance (of inferior limbs) is associated with a local increase in external heat exchange. Adaptation to work in heat would take the form of a local re-adjustment of internal and external heat exchanges.
Acclimatization↗
[Influence of hydrothermal ambient conditions on sweat evaporation efficiency].
Sweat efficiency is defined as the ratio between evaporative and sweat rates. The work was carried out on two resting subjects acclimatised to humid heat. Body sweat rate and rate of sweat loss by dripping were recorded separately by continuous weighing. Evaporation from the skin was obtained by the difference between the two weight loss curves. The subjects were exposed for 75 minutes to increases in humidity levels as constant air temperatures (42, 44, 46, or 48 degrees C). The amplitude of the increases was successively equal to 7.5, 15.0, 22.5 or 50.0 mb of water vapor pressure. During the 75 minutes preceding each increase the water vapor pressure of the air was maintained at 20.0 mb. 1. Sweat efficiency decreases prior to complete wetting of the skin surface. The inter-individual mean value of the wetted skin area threshold over which sweat efficiency is less than 1 is around 60%. 2. Sweat efficiency is linearly related to the reciprocal of the required wetted skin area (see article). These results are compared with those of other authors. The differences observed are explained in terms of physiological or physical variables involved in the sweat rate control or in the evaporative sweat loss. These include wetness of skin, posture, activity of subjects and the velocity of air over the skin surface.
Adult↗
Unfavorable effects of ventricular pacing on myocardial energetics.
The effects of ventricular pacing (90-330 beats/min) and atrial pacing (120-210 beats/min) on myocardial oxygen consumption (MVO2) and its hemodynamic determinants and on myocardial pumping efficiency were studied systematically on intact dogs. In six closed-chest experiments 158 steady states were analyzed. Myocardial blood flow was measured with a differential pressure sinus catheter, oxygen consumption (5-30 ml/min . 100g) was determined simultaneously by the Fick principle and the additive hemodynamic parameter Et. Ventricular and atrial pacing were compared with both methods at identical heart rates. Additionally, the coincidence between both methods of determining MVO2 was examined at sinus rhythm with sympathetic stimulation (norepinephrine, atropine) within each experiment. Ventricular pacing increased MVO2 overproportionally up to 50% in relation to the hemodynamic determinants. Consequently, myocardial pumping efficiency markedly decreased with increasing ventricular rate. The close relation between directly measured MVO2 and Et, found in previous studies, was maintained under sympathetic stimulation. Atrial pacing, as compared to ventricular pacing at identical rates, resulted in a decrease of MVO2 up to 25% although the expected mVO2 according to its hemodynamic determinants rather increased. The hemodynamic and metabolic mechanisms probably responsible for the energetic difference between ventricular and atrial pacing at equal heart rates are discussed.
Animals↗
Increase of myocardial oxygen consumption due to active diastolic wall tension.
A marked increase in left ventricular diastolic pressure ( PLVD ) relative to volume is regularly observed during angina pectoris and may contribute to further deteriorations of myocardial perfusion in the ischemic myocardium and to pulmonary congestion as well. A possible simultaneous increase in myocardial oxygen consumption (MVO2) due to a reversible diastolic tone during transient ischemia has not been taken into consideration in previous studies on alterations in ventricular diastolic properties. 13 closed-chest experiments were carried out in clinical catheterization technique with situations of high PLVD (18-50 mm Hg) relative to volume induced by right ventricular pacing (n = 19; 172 +/- 5 beats/min) and catecholamine-induced reversible diastolic tone (n = 17) in moderate hypothermia (31 degrees C). MVO2 was directly measured and indirectly calculated from its hemodynamic determinants using Bretschneider's equation (Et) that does not consider ventricular diastolic pressure. In addition, an energy demand for maintenance of active diastolic wall tension (E5) was calculated from PLVD , mean ventricular diastolic volume estimated from endsystolic and stroke volume, diastolic time and heart rate in ml O2/min X 100 g. During pacing tachycardia with high PLVD (27.4 +/- 1.8 mm Hg) the MVO2 (12.49 +/- 0.50 ml O2/min X 100 g) exceeds Et (10.11 +/- 0.25 ml O2/min X 100 g) (p less than 0.001), partly due to neglect of E5 (1.39 +/- 0.11 ml O2/min X 100 g). During catecholamine-induced high PLVD (31.1 +/- 2.5 mm Hg) the MVO2 (12.29 +/- 0.83 ml O2/min X 100 g) increases significantly (p less than 0.001) over Et (10.43 +/- 0.81 ml O2/min X 100 g). Addition of E5 (1.76 +/- 0.14 ml O2/min X 100g) to Et abolishes the differences between MVO2 and Et yielding non-significantly different values. Results indicate by means of indirect energetic evidence the occurrence of a diastolic tone of the heart under unphysiologic conditions. Acute increases in PLVD during angina pectoris are supposed to increase MVO2 markedly due to an additional energy demand for maintenance of reversible active diastolic wall tension.
Adrenergic beta-Antagonists↗
Quantification of ischemic stress during repeated coronary artery occlusion in the dog. A method for validation of therapeutic effects. I. Estimation of O2-debt and O2-repayment.
In 9 open-chest mongrel dogs 4-6 intermittent 3-min occlusions of the LAD artery were performed with time intervals of about 45 min. Using a mu-computer, the following variables were calculated online: energy demand according to the Bretschneider equation (Et) from digitized hemodynamic data; myocardial oxygen consumption (MVO2) from fiberoptically measured coronary sinus oxygen saturation and coronary sinus blood flow. Coronary occlusion led to a decrease in MVO2 in comparison to Et. The integral of the difference between MVO2 and Et over the entire occlusion time yielded a total O2-deficiency (DO2) of 76 (+/- 12%) microliter O2/g ischemic tissue and a correlation coefficient with the weights of the intravitally stained ischemic areas of r = 0.96. Additional O2-uptake in relation to Et during the early perfusion period yielded a correlation to the size of the ischemic area of r = 0.95 and an average O2-repayment (RO2) of 32 (+/- 14%) microliter O2/g ischemic tissue. The determination of total myocardial O2-deficiency during ischemic stress as well as determination of O2-repayment during the early reperfusion period could be used to estimate the extent of ischemic stressed myocardium. Subsequently, the evaluation of pharmacological effects on myocardial ischemia should be possible.
Animals↗
Quantification of ischemic stress during repeated coronary artery occlusion in the dog. A method for validation of therapeutic effects. II. Reproducibility of the release and uptake of electrolytes and substrates.
As criterion for the degree of ischemic stress on myocardium during repeated coronary artery occlusion, the reproducibility of the release of potassium, lactate and inorganic phosphate in the early reperfusion period was examined. On 20 anaesthetized open-chest mongrel-dogs, local ischemia was induced by intermittent occlusion of the LAD artery. In each experiment the artery was occluded for 3 min 4 to 6 times with intervals of 45 min. Just before beginning, at the end of occlusion and after 5 min of reperfusion, arterial and coronary venous blood was collected simultaneously. Additionally, 3 ml of blood were withdrawn by syringe-pumps during the first minute of reperfusion. Intra-individually, the following standard-deviations were found in a representative experiment with 5 occlusions: potassium +/- 7% (22.62 +/- 1.6 mumol/min); inorganic phosphate +/- 9% (19.82 +/- 2.06 mumol/min); lactate +/- 11% (55.38 +/- 5.93 mumol/min). Interindividually, the correlation between the release of these markers and the perfusion bed of the ligated artery led to coefficients of about r approximately 0.88. On an average, per gram ischemic tissue/wet weight 0.74 mumol potassium, 0.6 mumol inorganic phosphate and 1.98 mumol lactate were released. The ratios between the releases remained constant independent of the size of ischemic area. An even closer correlation with coefficients of about r approximately 0.97 was found between the O2-debt in the occlusion period. Based on a synoptic assessment of metabolic and energetic parameters, this experimental model may render more detailed information on pharmacological interventions during ischemic stress.
Animals↗
The effect of ion composition on cellular membrane potentials during selective coronary arteriography.
An animal experimental study on seven thoracotomized dogs was designed to investigate the effects of intracoronarily injected sodium meglumine diatrizoate on myocardial electrophysiology and to evaluate the contribution of the corresponding changes of electrolyte levels in coronary blood. For this purpose the effects of alterations in the Na+-, K+- and Ca++-concentrations in coronary blood were studied separately by intracoronarily injected model solutions. Membrane potentials were recorded from the left ventricular myocardium by a modified microelectrode technique which is applicable to the beating and blood perfused heart in situ. Following selective coronary arteriography there was a temporary hyperpolarization of resting potentials and a prolongation of action potentials which may be explained by a contrast-induced local deficiency of potassium and calcium ions and by a relative prevalence of sodium ions in coronary blood. In selective coronary arteriography the synchronicity of cardiac excitation is disturbed by the regional prolongation of action potentials, which may induce ventricular arrhythmias.
Action Potentials↗
Does spinal anesthesia affect cerebral oxygenation during transurethral prostatectomy?
BACKGROUND AND OBJECTIVES: Transurethral resection of the prostate (TURP) is associated with the unique complication of transurethral resection of prostate syndrome (TURS), which is attributed to the absorption of irrigating fluid. This study was initiated to investigate the effects of spinal anesthesia and TURP on cerebral oxygen balance. METHODS: Thirty patients scheduled for TURP were included. Jugular bulb oxygen saturation (SjbO2) was measured via retrograde cannulation of jugular venous bulb. Spinal anesthesia was initiated by 3 mL hyperbaric 0.5% bupivacaine injected at L3-L4 in the sitting position, producing a block to the T10 dermatome. Hemodynamic measurements and arterial and jugular bulb blood gasometry were performed before and after spinal anesthesia, throughout surgery, and during the postoperative period. RESULTS: A significant decrease of cerebral perfusion pressure after spinal anesthesia was accompanied by a significant decrease of SjbO2 below a preoperative value of 61% +/- 1. Eight patients developed yawning, irritability, restlessness, and nausea toward the end of surgery, and these were considered to be early signs of TURS. These patients demonstrated SjbO2 below 55% and 50% in 63% and 42% of respective data set points. CONCLUSION: The neurologic symptoms in patients undergoing TURP during spinal anesthesia might not only be caused by absorption of irrigating fluid but also by impairment of cerebral oxygenation.
Aged↗
Simulation of arterial drug concentration after intravenous application.
The aim of this study was to develop a widely applicable model for circulatory indicator dispersion which could describe the pharmacokinetics of early drug distribution. The model assumes that the substance is injected into the right atrium and measured in the aorta. The dilution curve results from the dispersion and recirculation of the indicator in the body. The concentration time curve in the aorta, r, can be described as r = c0 + g* r, where g is the transport function of the body and c0 is the concentration time course, which is measured for the first time in the aorta. If the body transport function is known, then the aortic dilution curve of a drug can be predicted for different elimination rates and injection times. The site of interest can be chosen arbitrarily, i.e. the concentration of inflow into the kidney or any other organ can be described.
Animals↗
Validity of the lagged normal density function as a model for pulmonary indicator dispersion.
The aim of this study was to investigate whether the lagged normal density function is a useful model for the dispersion of intravascular and diffusible indicators in the lungs. In 18 mongrel dogs anesthetized with N2O-piritramide, 221 sets of thermal-indocyanine green dye kinetics were recorded in the pulmonary artery and in the aorta after central venous indicator injection. A model-free deconvolution technique was used to compute the pulmonary transport functions for dye and heart from the measured indicator kinetics (reference method). The lagged normal density function was used to model pulmonary indicator transport. Its parameters were computed by a nonlinear least-squares procedure by iterative convolution. After baseline measurements in nine dogs, pulmonary edema was induced by central venous application of oleic acid. In nine other dogs, measurements were performed before and after postural changes from the horizontal to the vertical position. The mean transit times derived from the lagged normal density function were in good agreement with those obtained after model-free deconvolution. Although the shape (relative dispersion, skewness) of the transport function is less well described by the model, the authors conclude that the lagged normal density function is useful to determine indicator volumes of distribution that require only the correct mean transit times.
Animals↗