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H P Pieper

Publications and source records attributed to H P Pieper.

14 recordsLinked to original sources
PubMed1984

Changes in circulating blood volume influence aortic characteristic impedance in awake dogs.

Experiments on five chronically instrumented dogs were performed to study the effects of changes in circulating blood volume on the aortic smooth muscle activity in awake animals. The external diameter of the proximal descending aorta was measured with a sonomicrometer. Aortic pressure was measured in the same cross-sectional area with a catheter-tip transducer. Acute hemorrhage of 15% of the estimated blood volume was performed 17 times by quickly withdrawing blood through a jugular cannula. At any given arterial pressure within the range of overlap the aortic diameter (D) was always decreased after hemorrhage compared with control, and the pressure-strain elastic modulus (Ep) and the characteristic impedance (Zc) were always increased. For example at 140 kdyn X cm-2 (104.5 mmHg) delta D = -0.61 +/- 0.12 mm or delta D = -3.44 +/- 0.68% of control, delta Ep = 31.0 +/- 8.6%, and delta Zc = 22.6 +/- 4.5%. Each of these changes was significant with P less than 0.01. Volume expansion of 30% was performed eight times by infusing warm saline. At any given arterial pressure D was always increased and Ep and Zc were always decreased. At 140 kdyn X cm-2 delta D = 0.55 +/- 0.15 mm or delta D = 3.12 +/- 0.95% of control, delta Ep = -12.4 +/- 3.2%, and delta Zc = -12.0 +/- 2.1%. Each of these changes was significant with P less than 0.01. Since in these awake animals the changes in circulatory blood volume modified the arterial pressure only slightly, the contribution of viscoelasticity and myogenicity to the observed responses was minimal.

Animals↗
PubMed1982

Effects of blood volume changes on characteristic impedance of the pulmonary artery.

Experiments were performed on eight anesthetized dogs to study the response of the characteristic impedance (Zc) of the main pulmonary artery to changes in circulating blood volume. Pressure and flow were measured in the proximal main pulmonary artery under control conditions, after hemorrhage (-15% of the estimated blood volume), again under control conditions, and finally after volume expansion (+30% of the estimated blood volume). Two different methods were used to determine Zc from these recordings. With the frequency-domain method values for Zc were obtained by averaging the input impedance moduli between 2 and 15 Hz. With the time-domain method Zc was derived as the slope of the early ejection pressure-flow relationship. The values for Zc obtained with the two methods were not statistically different. In the time-domain method the average increase in Zc with hemorrhage was 30.7 +/- 7.4 (SE) %, and the average decrease with volume expansion was -21.1 +/- 5.0 (SE) %. Because the time-domain method allowed the values of Zc during control conditions and after hemorrhage to be obtained in the same pressure range, it was concluded that the observed changes were caused by a change in the activity of the smooth muscle in the pulmonary arterial wall. Similarly, it was concluded that the decrease in Zc after volume expansion was active in nature.

Animals↗
PubMed1980

Effect of acute volume loading on aortic smooth muscle activity in intact dogs.

Experiments were performed to study the aortic smooth muscle responses to acute volume loading with dextran 70. To analyze the aortic smooth muscle activity, diastolic aortic pressure was plotted vs. aortic internal diameter to obtain a pressure-diameter relationship (PDR) curve. Aortic pressure and diameter were measured by means of a catheter-tip instrument. To obtain the relationships over a large range of pressure and diameter, slow oscillations (period, 4-5 s) in aortic pressure were induced by means of an external pump. In 15 anesthetized dogs, the blood volume was expanded by 33.6 +/- 0.6% (SE) of the control volume. After this volume expansion, aortic diameter for a given pressure was increased by 6.0 +/- 1.0% of the control value. The slope of the PDR curve for a given pressure was decreased by 16.1 +/- 3.9%, and the compliance per centimeter was increased by 30.2 +/- 5.9%. All these changes were significant at P less than 0.001. It was also shown that these responses were not related to the changes in mean arterial pressure and were not mediated by reflexes through the carotid sinus and vagus nerves.

Animals↗
PubMed1980

Response of systemic arterial input impedance to volume expansion and hemorrhage.

Experiments on 12 anesthetized dogs were performed to study the effects of changes in blood volume on the pulsatile hemodynamics of the arterial system as seen from its input. Pressure and flow were measured in the ascending aorta under control conditions, after volume expansion with dextran 70 (+30% of estimated blood volume), and after hemorrhage (-15% of estimated blood volume). The input inpedance of the arterial system was calculated for each condition. It was found that after volume expansion the characteristic impedance of the proximal aorta, Zc, was decreased by 26.6 +/- 5.1% (SE) (P less than 0.01). After hemorrhage Zc was increased by 30.4 +/- 3.4% (P less than 0.01). Since it is well known that Zc is a very weak function of the mean arterial pressure, it is concluded that the changes in Zc seen with volume expansion or hemorrhage are caused mainly by changes in aortic smooth muscle activity. This conclusion is also supported by direct measurements of aortic pressure diameter relationships in earlier work from our lab.

Animals↗
PubMed1975

Nature of aortic smooth muscle responses to changes in venous return in intact dogs.

A response of the aortic smooth muscle to reduction in venous return was demonstrated previously. The present experiments were performed to determine whether these responses were of a reflex origin rather than being attributable to viscoelastic mechanisms. Viscoelastic mechanisms could not account for changes seen in the aortic pressure diameter relationship curve. On the other hand, it was demonstrated that the response was abolished by eliminating sympathetic input to the aorta via spinal cord transection. This and other evidence demonstrate beyond doubt that the aortic response to reduction in venous return is of neurogenic origin and constitutes a well-integrated reflex. However, experimental evidence is presented which clearly indicates that the receptors for the aortic smooth muscle response are not located in either the carotid sinus or aortic arch but must be located elsewhere in the system.

Animals↗