Myocardial and systemic responses to arterial hypoxemia during cardiac tamponade

1989 ◽  
Vol 257 (3) ◽  
pp. H726-H733
Author(s):  
G. J. Crystal ◽  
M. R. Salem

Experiments were performed on 14 anesthetized, open-chest dogs to assess myocardial and systemic responses to cardiac tamponade alone (TAMP) and combined with arterial hypoxemia (HYP). Regional blood flow (RBF) was measured with radioactive microspheres and used to compute regional O2 supply. Myocardial oxygen and lactate extraction were determined. Myocardial oxygen consumption (MVO2) was calculated with Fick equation. An increase in pericardial pressure, sufficient to reduce mean aortic pressure (MAP) by 20%, caused proportional decreases in myocardial RBF and MVO2 but had no effect on endo-to-epi flow ratio or on myocardial lactate extraction. TAMP alone decreased RBF and O2 supply in kidney, splanchnic organs, skeletal muscle, and skin, but it had no effect in brain. HYP (arterial PO2, 35 +/- 2 mmHg) during TAMP restored MAP and caused transmurally uniform increases in myocardial RBF that were adequate to maintain MVO2 and lactate extraction. RBF increased sufficiently in brain to maintain regional O2 supply, whereas unchanged or inadequate increases in RBF in other tissues accentuated reductions in O2 supply. During combined TAMP and HYP, local vasodilator mechanisms were capable of maintaining adequate oxygen supply in myocardium and brain but not apparently in the nonvital tissues where these mechanisms were antagonized by reflex vasoconstriction.

1988 ◽  
Vol 65 (6) ◽  
pp. 2624-2631 ◽  
Author(s):  
C. N. Sessler ◽  
F. L. Glauser ◽  
D. Davis ◽  
A. A. Fowler

We investigated whether platelet-activating factor (PAF) mediates endotoxin-induced systemic and pulmonary vascular derangements by studying the effects of a selective PAF receptor antagonist, SRI 63-441, during endotoxemia in sheep. Endotoxin infusion (1.3 micrograms/kg over 0.5 h) caused a rapid, transient rise in pulmonary arterial pressure (Ppa) from 16 +/- 3 to 36 +/- 10 mmHg (P less than 0.001) and pulmonary vascular resistance (PVR) from 187 +/- 84 to 682 +/- 340 dyn.s.cm-5 (P less than 0.05) at 0.5 h, followed by a persistent elevation in Ppa to 22 +/- 3 mmHg and in PVR to 522 +/- 285 dyn.s.cm-5 at 5 h in anesthetized sheep. Arterial PO2 (PaO2) decreased from 341 +/- 79 to 198 +/- 97 (P less than 0.01) and 202 +/- 161 Torr at 0.5 and 5 h, respectively (inspired O2 fraction = 1.0). SRI 63-441, 20 mg.kg-1.h-1 infused for 5 h, blocked the early rise in Ppa and PVR and fall in PaO2, but had no effect on the late phase pulmonary hypertension or hypoxemia. Endotoxin caused a gradual decrease in mean aortic pressure, which was unaffected by SRI 63-441. Infusion of SRI 63-441 alone caused no hemodynamic alterations. In follow-up studies, endotoxin caused an increase in lung lymph flow (QL) from 3.8 +/- 1.1 to 14.1 +/- 8.0 (P less than 0.05) and 12.7 +/- 8.6 ml/h at 1 and 4 h, respectively. SRI 63-441 abolished the early and attenuated the late increase in QL.(ABSTRACT TRUNCATED AT 250 WORDS)


2003 ◽  
Vol 10 (3) ◽  
pp. 424-432 ◽  
Author(s):  
Chuh K. Chong ◽  
Thien V. How ◽  
Geoffrey L. Gilling-Smith ◽  
Peter L. Harris

Purpose: To investigate the effect on intrasac pressure of stent-graft deployment within a life-size silicone rubber model of an abdominal aortic aneurysm (AAA) maintained under physiological conditions of pressure and flow. Methods: A commercial bifurcated device with the polyester fabric preclotted with gelatin was deployed in the AAA model. A pump system generated physiological flow. Mean and pulse aortic and intrasac pressures were measured simultaneously using pressure transducers. To simulate a type I endoleak, plastic tubing was placed between the aortic wall and the stent-graft at the proximal anchoring site. Type II endoleak was simulated by means of side branches with set inflow and outflow pressures and perfusion rates. Type IV endoleak was replicated by removal of gelatin from the graft fabric. Results: With no endoleak, the coated graft reduced the mean and pulse sac pressures to negligible values. When a type I endoleak was present, mean sac pressure reached a value similar to mean aortic pressure. When net flow through the sac due to a type II endoleak was present, mean sac pressure was a function of the inlet pressure, while pulse pressure in the sac was dependent on both inlet and outlet pressures. As perfusion rates increased, both mean and pulse sac pressures decreased. When there was no outflow, mean sac pressure was similar to mean aortic pressure. In the presence of both type I and type II endoleaks, mean sac pressure reached mean aortic pressure when the net perfusion rate was low. Conclusions: In vitro studies are useful in gaining an understanding of the impact of different types of endoleaks, in isolation and in combination, on intrasac pressure after aortic stent-graft deployment.


1979 ◽  
Vol 237 (6) ◽  
pp. H705-H712 ◽  
Author(s):  
J. R. Hales ◽  
L. B. Rowell ◽  
R. B. King

Radioactive microspheres (containing six different nuclide labels) were used to measure blood flow (BF) to most major organs of eight conscious baboons during heat stress. Cardiac output (CO), arterial mean pressure, and arterial PO2, PCO2, and pH did not change, but heart rate increased and stroke volume fell as body temperature increased by as much as 2.56 degrees C. Skin BF increased in all regions sampled so that the fraction of CO distributed to skin (not including feet and hands) increased from 3% (control) to 14%. Increased skin BF was compensated for by decreases in splanchnic (intestines, stomach, pancreas, and spleen) (35%), renal (27%), and possibly muscle BF. There was no change in BF to the brain, spinal cord, coronary, or subcutaneous adipose tissue during heating. Therefore, baboons show a generalized redistribution of BF during heat stress, so that increments in skin BF are provided without increases in CO, whereas man depends on changes in both; despite this latter difference between the baboon and man, the similarity in magnitude of the splanchnic and renal vasoconstriction between the two primates may indicate that the baboon would be a suitable animal model for investigations into mechanisms of changes in regional blood flow in man during heat stress.


1981 ◽  
Vol 240 (4) ◽  
pp. H505-H510
Author(s):  
N. M. Buckley ◽  
P. Brazeau ◽  
I. D. Frasier ◽  
P. M. Gootman

The maturation of femoral circulatory responses to efferent lumbar nerve stimulation was tested in 51 developing swine (1 day-3 mo old) under pentobarbital sodium anesthesia (10-30 mg/kg). Aortic pressure, heart rate, and femoral and carotid arterial flows (measured by electromagnetic flow transducers) were recorded simultaneously. Femoral vascular resistance was calculated as mean aortic pressure/mean flow. Transection of the lumbar nerve fibers below the last ganglion in the sympathetic chain did not after femoral resistance in day-old animals but decreased femoral resistance in swine 1 wk of age and older. Efferent lumbar nerve stimulation at various combinations of frequencies and intensities revealed an atropine-blockable vasodilator component in the femoral circulatory response in swine 1 mo of age and older. After alpha-adrenergic receptor blockade with phentolamine (0.25 or 0.5 mg/kg), femoral vasodilation occurred during low-frequency and -intensity stimulation of the lumbar nerve only in animals 1 mo of age and older. Acetylcholine (2 micrograms ia) caused a decrease in femoral resistance at all ages. Vasoconstrictor effects of high-frequency stimulation (5-10 Hz) were present at all ages and were age dependent. The results of these experiments suggest that the femoral circulation in swine at birth in innervated by functionally active vasoconstrictor fibers, which do not provide a tonic influence on femoral resistance until late in the first postnatal week. Furthermore, although femoral vascular cholinergic receptors are demonstrable at birth, there appears to be a delay in the maturation of functionally active vasodilator fibers.


1980 ◽  
Vol 239 (2) ◽  
pp. H163-H171 ◽  
Author(s):  
S. R. Jolly ◽  
G. J. Gross

The effect of FR 7534, a new dihydropyridine CA2+ antagonist, nitroglycerin, and dipyridamole have been compared on coronary collateral function in pentobarbital-anesthetized open-chest dogs following acute ligation of the left anterior descending coronary artery. Measurements of tissue blood flow using radioactive microspheres were made 60 min postligation after low and high doses of each drug and at the higher dose with methoxamine added to to return mean aortic pressure. FR 7534 treatment increased subepicardial, subendocardial, and transmural tissue flow by 100% in the central ischemic zone when perfusion pressure was controlled by methoxamine. Nitroglycerin also increased ischemic tissue flow, but to a lesser degree, 18% transmurally. Dipyridamole produced no significant change. Tissue flow in normal myocardium was similarly increased by FR 7534 and dipyridamole but slightly reduced by nitroglycerin. FR 7534 and nitroglycerin also increased retrograde coronary pressure when aortic presure was maintained constant. FR 7534, but not nitroglycerin, increased ischemic contractile force. In this model, FR 7534 may produce greater effects than nitroglycerin in increasing blood supply to ischemic myocardium delivered by endogenous collaterals especially when aortic perfusion pressure was controlled.


1975 ◽  
Vol 39 (6) ◽  
pp. 879-884 ◽  
Author(s):  
N. O. Fowler ◽  
J. C. Holmes ◽  
H. Spitz

The effect of acutely induced hypertension on aortic valve competence was studied in anesthetized dogs. Aortic pressure was increased by infusion of methoxamine or mechanically; aortic valve competence was evaluated by aortogrphy and by indicator dye. The aortic valve was normally competent; aortic insufficiency appeared with increase of mean pressure by as little as 20–50 mmHg; 6 of 9 animals showed aortic incompetence when mean aortic pressure was elevated 45–70 mmHg, but the valve remained competent in 2 of 9 animals with mean pressure increments of 60–90 mmHg. The aortic root was appreciably less distensible than was the proximal descending aorta; this factor may limit the degree of aortic insufficiency in response to acute hypertension in the dog.


1990 ◽  
Vol 258 (5) ◽  
pp. R1201-R1206 ◽  
Author(s):  
S. Benyajati ◽  
S. D. Yokota

The effects of atrial natriuretic peptide on the renal function of the spiny dogfish (Squalus acanthias) in seawater were evaluated. A synthetic mammalian peptide, atriopeptin II (2 micrograms/kg), was injected intravascularly into unanesthetized, unrestrained fish prepared for renal clearance studies. The aortic pressure, glomerular filtration rate (GFR), urine flow rate (V), and urinary excretion of sodium, potassium, and total osmolytes were continuously monitored. Atriopeptin II significantly decreased mean aortic pressure (-12%), GFR (-40%), V (-66%), and the absolute excretion rates of sodium (-47%), potassium (-43%), and total osmolytes (-44%). However, the renal effects of atriopeptin II were temporally dissociated from the vasodepressor effect. Mean aortic pressure decreased quickly and returned to control values approximately 2 h after injection, whereas GFR did not decrease significantly until the third hour after injection. The decreases in renal water and solute excretion in response to atriopeptin could be accounted for by the decrease in GFR, since there were no significant changes in fractional water or solute excretion. Similar decreases in GFR were observed during constant infusions of a lower physiological dose of the peptide (80 pg.kg-1.min-1). The observed antidiuretic and antinatriuretic effect of synthetic atriopeptin in the dogfish contrasts with its putative role as a hormone mediating hypervolemic regulation.


1982 ◽  
Vol 52 (5) ◽  
pp. 1338-1342 ◽  
Author(s):  
R. Gunther ◽  
C. Zaiss ◽  
R. H. Demling

We studied the effect of prostacyclin (PGI2) infusion and cessation of infusion on the pulmonary microcirculation. We used lung lymph flow (QL) and the lymph to plasma protein ratio as sensitive indices of net fluid (QF) and protein flux (CP). After a 4-h base line period, we infused PGI2 (0.2 micrograms . kg(-1).min(-1) into eight unanesthetized sheep for 2 h. We monitored vascular pressures and lymph during infusion and for another 18 h after PGI2. During infusion, QL and cardiac output increased by 75 and 50%, respectively, over base line, whereas the lymph-to-plasma ratio (L/P) remained constant for both albumin and globulin. This resulted in a significant increase in both fluid and protein flux. Pulmonary vascular pressures remained unchanged, whereas mean aortic pressure decreased. The increase in QF and CP was felt to be due to an increase in the surface area of fluid exchange vessels rather than increased permeability. After infusion, cardiac output rapidly returned to base line, whereas mean QL remained increased by 70% over base line for 2–8 h. Mean L/P decreased from 0.65 to 0.53. Pulmonary arterial pressure and pulmonary vascular resistance increased. The increase in QL and decrease in L/P indicate a rebound increase in pulmonary microvascular pressure in the postperfusion period.


1986 ◽  
Vol 60 (5) ◽  
pp. 1571-1577 ◽  
Author(s):  
M. Manohar

Eight healthy adult grade ponies were studied at rest as well as during maximal exertion carried out with and without adenosine infusion (3 microM X kg-1 X min-1 into the pulmonary artery) on a treadmill to compare levels of blood flow in respiratory muscles with those in other vigorously working muscles and to ascertain whether there remained any unutilized vasodilator reserve in respiratory muscles of maximally exercising ponies. Radionuclide-labeled 15-micron-diam microspheres, injected into the left ventricle, were used to study tissue blood flows. During maximal exertion, there were increases above base-line values in heart rate (336%), mean aortic pressure (41%), cardiac output (722%), and arterial O2 content (56%). The whole-body O2 consumption was 123 +/- 11 ml X min-1 X kg-1, and the stride/respiratory frequency of the galloping ponies was 138 +/- 4/min. With adenosine infusion during maximal exertion, mean aortic pressure decreased (P less than 0.05), but none of the above variables was different from maximal exercise alone. During maximal exertion, blood flow in the adrenal glands, myocardium, respiratory, and limb muscles increased, whereas that in the kidneys decreased and the cerebral perfusion remained unaltered. With adenosine infusion during maximal exercise, renal vasoconstriction intensified, whereas adrenal and coronary beds exhibited further vasodilatation. During maximal exertion, blood flow in the equine diaphragm (265 +/- 36 ml X min-1 X 100 g-1) was not different from that in the gluteus medius (253 +/- 36) and biceps femoris (233 +/- 29); both are principal muscles of propulsion in the equine subjects) or the triceps brachii (227 +/- 26) muscles.(ABSTRACT TRUNCATED AT 250 WORDS)


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