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Biomedical subjects

E Bassenge

Publications and source records attributed to E Bassenge.

At least 163 records · Page 9Linked to original sources
PubMed1977

Transient effects of norepinephrine on myocardial oxygen balance.

In conscious dogs with experimental atrioventricular block and with ventricles paced at constant rate the effects of norepinephrine (NE) and isoproterenol (ISO) on coronary flow, coronary resistance, and myocardial O2-balance were investigated. Myocardial O2-S balance, as estimated from continuous measurement of coronary venous O2-S saturation, was used for the discrimination of coronary dilation induced either directly by vascular beta-adrenoreceptor stimulation or indirectly by increased myocardial metabolism. Following bolus injection of NE (0.3 microgram/kg) or ISO (0.1 microgram/kg) into the pulmonary artery, coronary venous O2-S saturation increased from a control of 25 +/- 2% O2-S saturation (mean +/- S.D.) transiently to 51 +/- 5 and 62 +/- 5% O2-S saturation respectively. After beta1-adrenoreceptor blockade these increases were reduced to 33 +/- 4 and 41 +/- 3% O2-S saturation, respectively. The remaining increase after NE was abolished when atropine was given in addition to beta1-b blockade. After beta1 + 2-adrenoreceptor blockade neither NE nor ISO injection had an effect on coronary venous O2 saturation. After beta1-b blockade was superimposed on ganglionic blockade NE injection led to a decrease in coronary venous O2-S saturation indicating a latent alpha-a activity of NE. NE seems to act directly via beta1-a adrenoreceptors, since no differences were observed in the time courses of changes in coronary venous O2-S saturation after left atrial injection of NE when compared to adenosine. It is concluded that circulating NE like ISO is able to improve myocardial oxygen balance by a direct vasodilating effect on canine coronary vessels mediated by vascular beta1-adrenoreceptors.

Adenosine↗
PubMed1976

Evaluation of a neurogenic rapid coronary dilatation during an excitatory response in conscious dogs.

The present study was undertaken to evaluate the mechanisms of coronary adaptation to sudden changes in myocardial oxygen demand that occur during excitement. An excitatory response was evoked either by electrical stimulation of the hypothalamic defence area or by noise (discharge of a fire-arm). Continuous measurement of the oxygen saturation in coronary venous blood was used to judge, whether an increase in coronary flow was adequate to match an increased myocardial oxygen demand. During the excitatory response heart rate, cardiac output and coronary flow increased. However, the increase in coronary flow was not adequate to meet the increased metabolic requirement as indicated by a decrease in coronary venous oxygen saturation. In dogs with experimental atrioventricular block, and with heart rate controlled by external pacing, a rapid coronary dilation occurred during the excitatory response and was accompanied by an increase in coronary venous oxygen saturation. This rapid coronary dilation was abolished by beta-adrenergic blockade. The pattern of coronary flow and coronary venous oxygen saturation that occurred during the excitatory response in normal dogs could be mimicked in dogs with atrioventricular block by increasing the ventricular pacing rate. However, when identical increases in heart rate were induced either excitement or by external pacing, the drop in coronary venous oxygen saturation was significantly larger in the paced series. This demonstrates, that an increase in heart rate is responsible for the transient decrease in coronary venous oxygen saturation during the excitatory response. From these experiments it is concluded that a rapid neurogenic dilation of the coronary vessels occurs during the excitatory response. Under normal conditions this rapid neurogenic dilation is masked by the effect of the accompanying increase in heart rate on extravascular coronary resistance.

Adaptation, Physiological↗
PubMed1975

Viscous and inertial fractions of total perfusion energy dissipation in the coronary circulation of the in situ perfused dog heart.

The effects of changes in viscosity on pressure flow relations in the in situ perfused left circumflex coronary artery were studied in open chest dogs. Vascular reactivity was abolished by maximal pharmacological coronary dilatation. Blood and suspensions of red cells (hematocrit 8-14%) in dextran solutions were used as perfusates. Total perfusion energy dissipation, represented by perfusion pressure drop across the perfused vascular bed, can be separated into a viscous and an inertial fraction: P = Pvisc + Pinert. Perfusing the heart with approximately Newtonian fluids of different viscosities enabled us to compute the amount of the inertial fraction of total perfusion pressure dissipation. At constant viscosity, the inertial fraction increased with flow rate. However, the rise of the inertial fraction due to reduced viscosity at a constant perfusion pressure was much more pronounced. Variations of perfusion pressure and viscosity of the perfusates between 70 to 130 mm Hg and 1.2-3.2 cP, respectively, resulted in inertial perfusion pressure dissipation between 16 and 54%. This inertial pressure drop may become a noteworthy factor under conditions of low whole blood viscosity (e.g. anemia or therapeutical hemodilution.

Animals↗
PubMed1975

Effect of increased blood fluidity through hemodilution on coronary circulation at rest and during exercise in dogs.

Coronary flow and myocardial oxygen consumption were measured in conscious dogs at rest and during two levels of submaximal treadmill exercise (3 and 7 km/h at 15% grade, respectively) during adaptation to progressive hemodilution with dextran 60. At rest coronary flow increased to more than seven-fold with diminishing hematocrit to 12.5% in order to cover myocardial oxygen consumption which increased from 6.5 +/- 0.3 ml/min with 100 g at hematocrit 47.5% to 13.5 +/- 0.8 ml/min with 100 g at hematocrit 12.5%. The dilatory capacity of the coronary vessels, estimated from the reactive hyperemia after a 12 sec occlusion of the left circumflex coronary artery, dropped from 602% at control to 45% at lowest hematocrit levels. During the superimposed stress of exercise coronary flow and myocardial oxygen consumption increased further, so that the dilatory capacity of the coronaries was exhausted at hematocrit levels between 16 and 22%. Myocardial oxygen consumption per unit of oxygen delivered to peripheral tissues increased substantially with progressive hemodilution. In the presence of the reduced arterial oxygen content the augmented myocardial oxygen demand limits the overall adaptability to hemodilution by an exhaustion of the coronary dilatory capacity.

Animals↗
PubMed1975

Effect of increased blood fluidity through hemodilution on general circulation at rest and during exercise in dogs.

During progressive normovolemic hemodilution with dextran-60, circulatory functions (cardiac output, oxygen delivery to tissues, arterial pressure and mixed venous oxygen saturation) and total body oxygen consumption were studied in conscious dogs at rest and during two levels of submaximal treadmill exercise. At rest, cardiac output rose continuously with progressive hemodilution. This increase, however, was not sufficient to compensate for the reduced arterial oxygen content. Consequently oxygen delivery fell significantly from 23.3 +/- 1.8 ml/min with kg at hematocrit 47.5% to 15.7 +/- 0.9 ml/min with kg at hematocrit 12.5%. The constant oxygen consumption was maintained by a simultaneous increase in oxygen extraction from blood. During the superimposed stress of exercise, a constant oxygen consumption was maintained between hematocrit ranges of 50 to 15 or 25%, respectively. Again, the increase of cardiac output due to hemodilution did not compensate for the reduced arterial oxygen content and consequently oxygen extraction rate was increased. These data demonstrate that at rest (and even more during submaximal treadmill exercise) the reduced whole blood viscosity or improved fluidity during hemodilution does not initiate an increase in cardiac output that is sufficient to maintain a constant oxygen delivery to the tissues.

Animals↗