Cardiac and peripheral failure in hemorrhagic shock in the dog

1964 ◽  
Vol 207 (1) ◽  
pp. 203-214 ◽  
Author(s):  
Carl F. Rothe ◽  
Ewald E. Selkurt

Cardiac output by the indocyanine-green-dilution technique, systemic arterial, right atrial, pulmonary arterial, and ventricular end-diastolic pressures were measured without thoracotomy to evaluate cardiac function in seven dogs. In other series of seven, mercury-in-rubber displacement transducers were placed around the left ventricles about 5 days before the experiments. In a third group of five, hemorrhagic hypotension was continued until 40% uptake of the maximum shed volume. Transfusions of blood, plasma, and dextran were given, as needed, to maintain arterial blood pressure above 100 mm Hg. Such therapy prolonged life. In a fourth group of 33, increases in hematocrit and plasma protein concentration, and decreases in central venous pressure suggested a progressive loss of intravascular fluid late in the hypotensive period and following transfusion. It appears that only with extreme degrees of oligemic hypotension, or with moderate hypotension plus prior cardiac damage does the cardiac weakness engendered by the prolonged hypotension become the most significant factor leading to death.

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.


Perfusion ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 261-266
Author(s):  
V. Vainionpää ◽  
A. Hollme'n ◽  
J. Timisjärvi

The occurrence of vasomotor waves during cardiopulmonary bypass (CPB) is a recognized phenomenon. The lesser known oscillation of arterial pressure after cessation of CPB was observed in 18 open-heart patients. The duration of an oscillatory wave was 13.5±5.0 seconds, the amplitude 6.1 ±2.6mmNg and the mean arterial pressure 76.5± 10.7mmHg. Inter-and also intraindividual variations in frequency and amplitude of the oscillation, however, did occur. In 13 patients, this oscillation occurred during ventricular epicardial pacing. The oscillation continued until the end of the operation in eight patients; in others, the oscillation was of shorter duration. An oscillation of pulmonary arterial pressure (PAP) was simultaneously observed in nine patients (eight with pacemaker) and central venous pressure (CVP) oscillation in eight patients (all with pacemaker). The duration of a wave was the same as in systemic arterial pressure and the amplitudes were 1.5-3.0mmHg in PAP and 1.0-2.0mmHg in CVP. These arterial vasomotor waves, seen here after CPB, largely resemble those observed during perfusion in man and also the Mayerwaves explored in experimental animals. The pacing rhythm seems to favourthe appearance of those blood pressure oscillations.


1987 ◽  
Vol 62 (6) ◽  
pp. 2252-2257 ◽  
Author(s):  
M. B. Maron ◽  
C. F. Pilati ◽  
K. C. Maender

The osmotic reflection coefficient (sigma) can be estimated from the increases in hematocrit and plasma protein concentration that result from fluid filtration occurring in an isolated perfused organ. We determined what effect perfusion pump-induced hemolysis has on the value of sigma determined by this technique in both the isolated canine left lower lung lobe (LLL) and forelimb by comparing estimates of sigma obtained before and after correction for hemolysis. Hemolysis was corrected by using the slopes of the relationships between hematocrit and plasma hemoglobin concentration and between the plasma protein and hemoglobin concentrations to correct hematocrit and protein concentration to a state of zero hemolysis. Uncorrected estimates of sigma in the LLL were 1.19 +/- 0.14 (SE) at a venous pressure (Pv) of 12 Torr (n = 7) and 0.90 +/- 0.02 at a Pv of 19 Torr (n = 6). Both sets of LLL's yielded sigma values of 0.77 +/- 0.03 after hemolysis correction. In the forelimb (n = 5), uncorrected and corrected estimates of sigma of 0.99 +/- 0.03 and 0.85 +/- 0.01, respectively, were obtained. The latter values were similar to sigma's (0.88 +/- 0.01) determined by lymph analysis in five additional forelimbs. We conclude that hemolysis results in overestimates of sigma. After hemolysis correction, this technique yields similar results to those obtained from lymph analysis for the forelimb and from published values for the LLL.


2020 ◽  
Vol 10 (4) ◽  
pp. 204589402096294
Author(s):  
Wei-Ting Chang ◽  
Jhih-Yuan Shih ◽  
Yu-Wen Lin ◽  
Zhih-Cherng Chen ◽  
Jun-Neng Roan ◽  
...  

Despite no significant differences of growth differentiation factor-15 expressions in peripheral, right atrial, and right ventricular blood, in the pulmonary arterial blood, there was a significantly high level of growth differentiation factor-15 in Group I pulmonary arterial hypertension patients subsequently developing heart failure. During right heart catheterization, collecting pulmonary blood samples is suggested to measure growth differentiation factor-15.


1981 ◽  
Author(s):  
S Chierchia ◽  
R De Caterina ◽  
F Crea ◽  
W Bernini ◽  
A Distante ◽  
...  

It has been proposed that vasospastic angina, eventually due to local defects of PGI2 production, might benefit from PGI2 administration. We therefore investigated the effects of PGI2 in healthy volunteers and, then, in patients with frequent ischemic episodes (IE) of Prinzmetal angina, to detennine 1. hemodynamic, antiplatelet and possible side effects of the drug and 2. its possible therapeutic usefulness in the management of IE. In 6 healthy volunteers PGI2 was infused i.v. at doses of 2.5,5,10 and 20 ng/kg/min during consecutive periods of 30 min each. Heart rate (HR) and right atrial pressure were monitored continuously; cardiac output (thermodilution in 2 subjects, indirectly by a Doppler technique in all), arterial blood pressure (BP) and in-vitro platelet aggre- gability (PA) by ADP (Born), intermittently. In 2 subjects we also measured pulmonary arterial pressure and, in one, left ventricular pressure, during the infusion and in control conditions. PGI2 was then infused in 6 pts with frequent IE at maximal well tolerable rate (6-26 ng/kg/min) for periods of 3 hours alternated with equal periods of placebo (P), continuosly recording 2 ECG leads to detect ST-T changes, and sampling blood for PA as before. In all healthy volunteers PGI2, at the highest rates of infusion, decreased significantly (p < .001) both systolic BP (-10 ± 3%, mean ± SD) and diastolic BP (-19 ± 5%) increasing HR (+ 21 ± 5%); no significant changes were observed in the other hemodynamic parameters. The maximal decrease in PA was 58 ± 30%(p <. 001). Skin flushing, restlessness and headache, sometimes observed at the highest doses, rapidly disappeared decreasing the infusion rate. In the 6 pts the same trend in BP, HR and PA was evident. 106 IE were observed. PGI2 did not affect severity, duration and number of IE (44 during P, 62 during PGI2 infusion). One of the pts, however,not clinically different from the others, showed a reduction at 10 ng/ kg/min (6 IE during P, 2 during PGI2) and a complete abolition in the 3 following periods at 20 ng/kg/min (4,3,5 IE during P vs. none duringPGI2). We conclude that 1. PGI2 can be safely administered to humans and 2. it may prevent IE is some vasospastic pts, but not in others. Different pathogenetic mechanisms are perhaps involved in apparently similar Prinzmetal anginas.


1990 ◽  
Vol 258 (4) ◽  
pp. H1159-H1163
Author(s):  
A. L. Gest ◽  
T. N. Hansen ◽  
A. A. Moise ◽  
C. J. Hartley

The purpose of this project was to study mechanisms responsible for edema formation in fetuses with hydrops. We produced hydrops fetalis in 28 fetal sheep [gestational age of 125 +/- 5 days (mean +/- SD)] by pacing their atria at 300-320 beats/min for 68 +/- 40 (SD) h. All fetuses developed peripheral edema and ascites [volume of ascitic fluid was 134 +/- 75 (SD) ml; total protein concentration was 3.10 +/- 0.6 (SD) g/dl, and total albumin concentration was 1.68 +/- 0.3 (SD) g/dl]. Pacing did not affect aortic pressure but increased venous pressure from 4 +/- 1 to 8 +/- 1 (SE) Torr. Pacing did not affect pH, arterial partial pressure of O2 (PaO2), or Na+ but increased PaCO2 from 53 +/- 1 to 55 +/- 1 (SE) Torr and K+ from 3.9 +/- 0.1 to 4.3 +/- 0.1 (SE) meq/l. Hematocrit increased from 29 +/- 1 to 32 +/- 1 (SE)% acutely with pacing but returned to base line by the last day of the experiment. Plasma protein concentration decreased slightly from 3.7 +/- 0.1 to 3.5 +/- 0.1 (SE) g/dl by the last day of the experiment; plasma albumin concentration did not change. Plasma volume decreased acutely from 271 +/- 19 to 238 +/- 16 (SE) ml and then remained decreased throughout the experiment. Red blood cell mass and the turnover time for albumin were not affected by pacing. We found no consistent relationship between edema formation and changes in arterial blood gas tensions, plasma protein concentrations, or the turnover time for albumin.2


1980 ◽  
Vol 239 (6) ◽  
pp. G516-G523
Author(s):  
D. N. Granger ◽  
P. R. Kvietys ◽  
N. A. Mortillaro ◽  
A. E. Taylor

The direct effects of luminal distension pressure on intestinal transcapillary fluid exchange were studied in isolated autoperfused cat ileum preparations. Intestinal lymph flow, lymphatic pressure, lymph-to-plasma protein concentration ratio (L/P), blood flow, and perfusion pressures were allowed to reach a steady state at different luminal distension pressures (0–40 mmHg). Luminal distension was induced using a nonabsorbable silicone solution, thereby eliminating an influence of net water absorption. At a venous outflow pressure of 0 mmHg, lymph flow and lymphatic pressure increased, whereas blood flow and L/P decreased as luminal pressure was increased. The relationship between lymph flow, blood flow, and venous pressure was acquired at luminal pressures of 0 and 20 mmHg. When luminal pressure was 0, lymph flow increased and blood flow decreased progressively with venous pressure elevation; however, when luminal pressure was 20 mmHg, lymph flow and blood flow were unaffected until pressure exceeded 20 mmHg. The results of this study indicate that luminal pressure elevation enhances transcapillary fluid exchange and imposes a “waterfall” effect on the intestinal vasculature.


1989 ◽  
Vol 257 (6) ◽  
pp. H2025-H2032 ◽  
Author(s):  
M. B. Wolf ◽  
L. P. Porter ◽  
P. D. Watson

We investigated the effects of elevated venous pressure, Pv, (up to 140 mmHg) on the solvent drag reflection coefficient, sigma f, for protein and on the capillary filtration coefficient, CFC, in the isolated cat hindlimb perfused at constant flow. The perfusate contained 30% cat plasma and the remainder was a dialyzed albumin-electrolyte mixture. Cat red cells were added to a hematocrit of approximately 2%. sigma f was measured from the changes in hematocrit and plasma protein concentration (Integral-Mass Balance method) resulting from the fluid filtration caused by the Pv elevation. CFC was measured from the slope of the limb weight recording 2-4 min after the Pv elevation. sigma f decreased linearly from 0.807 (Pv less than 50 mmHg) to approximately 0.2 at 140 mmHg. CFC increased linearly from 0.0086 ml.min-1.mmHg-1.100 g-1 to about 0.04 over the same pressure range. A weight-independent filtration coefficient calculated from the change in hematocrit and a measurement of the initial perfusate volume gave comparable results, except at the very highest of pressures, where this coefficient was sometimes 20-40% less than CFC. Successive sigma f determinations at Pv at about 40 mmHg did not return to control after an initial measurement in which Pv was approximately 110 mmHg. Pore-theory analysis of the data suggests that the elevated Pv causes large pores to open as opposed to the stretching of small pores. Also, these large pores may remain open for a period of hours.


1981 ◽  
Author(s):  
A B Malik ◽  
F L Minnear ◽  
M V Tahamont ◽  
D G Moon ◽  
J E Kaplan

We determined the effects of ADP-induced platelet aggregation on lung fluid and protein exchange to examine whether platelet aggregation mediates lung vascular injury. The studies were made in intact sheep in which pulmonary lymph was obtained, and the protein concentration of lymph was compared to that of plasma. Two groups were studied: Control sheep receiving i.v. infusion of 10 mg/kg of ADP and experimental sheep in which platelets were depleted with anti-platelet serum prior to ADP infusion. In the control group, ADP decreased the platelet count from 178,554 ± 62,750 to 103,500 ± 47,828 cells/mm3, suggesting the entrapment of platelet in the pulmonary circulation. The pulmonary arterial pressure (Ppa) increased from 13.1 ± 1.8 to 15.9 ± 1.2 mmHg. Lung lymph flow (Qlym) increased from 8.4 ± 1.8 to 11.4 ± 2.3ml/hr (p < 0.05) and transvascular protein clearance (Qlym x lymph/plasma protein concentration), a measure of protein exchange, increased from 6.7 ± 1.3 to 9.4 ± 3.0 ml/hr (p < 0.05). These increases could be explained by an increase in microvascular pressure (Pmv) and ultrafiltration since mechanically elevation of Pmv produced the same changes in Qlym and clearance. Platelet depletion prevented the ADP-induced increases in platelet aggregation does not mediate lung vascular injury, but increases fluid filtration by increasing the microvascular pressure. This effect may be mediated by release of pulmonary vasoconstrictor substances such as thromboxane A2 and serotonin after platelet aggregation.


Sign in / Sign up

Export Citation Format

Share Document