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Biomedical subjects

G Elzinga

Publications and source records attributed to G Elzinga.

At least 109 records · Page 6Linked to original sources
PubMed1978

An analogue device for the measurement of cardiovascular variables.

An analogue device is described which is designed to analyse repetitive signals. It measures peak amplitudes, time to peak values, areas, and values at a preset time. The results can be displayed or recorded on a beat-to-beat basis, or an average can be taken over up to 31 consecutive beats.

Cardiovascular Physiological Phenomena↗
PubMed1978

Enhancement of mechanical performance by stretch during tetanic contractions of vertebrate skeletal muscle fibres.

1. Single fibres from the semitendinosus muscle of Rana temporaria were stretched during fused tetanic contractions and tension and sarcomere length (laser diffraction) responses were recorded. 2. Stretch of the fibres caused proportional increases in length of the sarcomeres. The force increased to a plateau value which was maintained during stretch or increased to a plateau value which was maintained during stretch or increased slightly. 3. The plateau value of force during stretch was dependent upon the velocity of stretch, was independent of the amplitude of stretch and was not proportional to overlap of thick and thin filaments. 4. There was enhancement of force after stretch compared with that produced at the same sarcomere length during isometric tetani. This force enhancement was independent of the velocity at which the stretch had been applied. 5. At sarcomere lengths between 1.9 and 2.3 micrometer, the force enhancement after stretch declayed rapidly, was independent of amplitude of stretch above approximately 25 nm per sarcomere not associated with a shift of the force--velocity curve. At sarcomere lengths above 2.3 micrometer the force enhancement after stretch decayed very slowly and was still present after 4 sec in long tetani. 6. At sarcomere lengths above 2.3 micrometer, force enhancement after stretch increased with amplitude of stretch and increased for any given stretch amplitude with sarcomere length. The force recorded after stretch was thus not proportional to overlap of thick and thin filaments. 7. At sarcomere lengths above 2.3 micrometer, the force enhancement after stretch was associated with a shift towards higher force value of the force--velocity curve. The velocity of shortening and zero load (V max) derived by hyperbolic extrapolation of the force--velocity curve was not affected. 8. Tension enhancement during and after stretch has a stabilizing effect in preventing dispersion of sarcomere length, particularly on the descending limb of the length--tension curve.

Animals↗
PubMed1978

The effect of an increase in inotropic state and end-diastolic volume on the pumping ability of the feline left heart.

In isolated ejecting cat hearts, the pumping ability of the left heart was described quantitatively by the relationship between mean left ventricular pressure and mean left ventricular output. This relationship was determined by making the heart eject against a series of different loads on a beat-to-beat basis. Left ventricular mean pressure-mean output relationships of control and potentiated beats (at the same end-diastolic pressure) have a common intercept on the output axis but diverge toward the pressure axis. When the mean pressure values of the potentiated beats in a given experiment are multiplied by a single factor, superposition of the two relationships is obtained. A change in left ventricular end-diastolic pressure caused a more parallel shift of the left ventricular mean pressure-mean output relationship. Here, superposition could be obtained by using one multiplication factor for the mean pressure data and one for the mean output data of the relationship found after the change in end-diastolic pressure. We concluded that, using the left ventricular mean pressure-mean output relationship, changes in cardiac pumping ability caused by given changes in inotropic state and ventricular end-diastolic volume can be quantified by one or two multiplication factors, respectively.

Animals↗
PubMed1977

The effect of an increase in aortic pressure upon the inotropic state of cat and dog left ventricles.

1. The effect of increased aortic pressure on the inotropic state of the left ventricle was studied in isolated cat hearts, perfused with bovine red cells in Tyrode solution, ejecting into a hydraulic model with the same input impedance as that of the cat aorta.2. Inotropic state was assessed at a controlled left ventricular end-diastolic pressure by interpolating single isovolumic beats by means of an occluder in the aortic cannula.3. When such isovolumic beats during periods of raised aortic pressure were compared with those during control periods, the difference in peak isovolumic pressure ranged from -0.3 to +0.5 kPa indicating differences in inotropic state which were small and inconsistent in direction.4. The maximum rate of rise of left ventricular pressure (dP/dt(max).) of ejecting beats was little affected by a rise of aortic pressure and the direction of changes was inconsistent.5. The effect of increased aortic pressure was studied in intact dogs after cardiac denervation; left ventricular end-diastolic pressure was uncontrolled and therefore rose to a higher steady level.6. No consistent change of dP/dt(max). was found during the period of increased aortic pressure.7. All flow and pressure variables remained steady during the period of increased aortic pressure after the higher level of left ventricular end-diastolic pressure had been established.8. These results demonstrate that neither the positive inotropic effect nor the negative inotropic effect of increased load dominates in these preparations. This may be the result of a balance between the two effects, or they may be of unimportant magnitude under physiological conditions.

Animals↗
PubMed1976

Reflection in the systemic arterial system: effects of aortic and carotid occlusion.

Experiments were performed in seven closed-chest anaesthetized male dogs to determine the role of pulse wave reflection in the pattern of flow and pressure in the ascending aorta. Ten days after implantation of an electromagnetic flow transducer around the ascending aorta a balloon catheter was placed in the descending aorta via the femoral arteries. At the same time a tip manometer was introduced into the ascending aorta. Aortic occlusions at three different sites caused pressure pulses with secondary systolic rises and flow pulses with biphasic deceleration. Secondary rises occurred 45 +/- 9.0 ms after the initial pressure rise for high aortic occlusion; this time was 75 +/- 8.5 ms for occlusion at the level of the diaphragm and 114 +/- 16.5 ms for occlusion near the level of the renal arteries. These times approximate the times in which the pulse travels from the tip manometer to the inflated balloons and back. Forward and reflected pressure and flow waves were calculated from reflection coefficients. Aortic occlusion caused larger reflected waves and the recorded wave forms were caused by the summation of forward and backward waves, the latter contributing the secondary pressure rise and the increased flow deceleration. Occlusion of both carotid arteries showed no specific reflection site but reflected waves were larger. This increased reflection can probably be explained as the result of greater total reflection from distributed sites under increased peripheral resistance.

Animals↗
PubMed1976

The pumping ability of the left heart and the effect of coronary occlusion.

In an isolated preparation of cat heart we studied the pumping capacity of the left heart while left atrial filling pressure was kept constant. We used the source impedance concept to quantify the pumping capacity. In this source impedance concept the relation between left ventricular output and left ventricular pressure is given by the formula (see article) where Zs = source impedance, Plv = left ventricular pressure, Iao = flow in the ascending aorta, and omega = 2pif, f being frequency.. The pressure obtained at zero flow is called the hydromotive pressure (HMP). Only the mean values of pressure and flow were studied. We studied the behavior of 10 hearts in three different experimental situations and in the following sequence: (1) control conditions, (2) after ligating a part of the left coronary arterial system, and (3) after restoring left ventricular output to control level by raising left atrial filling pressure. It was found that source resistance was not significantly different in the three situations but that mean hydromotive pressure (HMP) was significantly lower after ligation of a part of the left coronary arterial system. It was concluded that the decrease in pumping capacity of the left heart after infarction can be compensated for almost completely by an increase in left atrial filling pressure. This compensating mechanism therefore seems to be very efficient.

Animals↗