Embolus size affects gas exchange in canine autologous blood clot pulmonary embolism

1993 ◽  
Vol 74 (3) ◽  
pp. 1140-1148 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
P. Vanderhoeft ◽  
R. Naeije
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Blood Clot ◽  
Autologous Blood ◽  
Inert Gas ◽  
Experimental Conditions ◽  
Arterial Ph ◽  
Pulmonary Arterial ◽  
Vascular Obstruction ◽  
Autologous Blood Clot

Embolic pulmonary hypertension is associated with alterations in gas exchange of variable severity, which we hypothesized to be related to embolus size. We therefore examined the effects of different-size autologous blood clot embolization on pulmonary arterial pressure-cardiac output relationships (Ppa/Q) and on the distribution of ventilation-perfusion ratios (VA/Q) in 18 intact anesthetized and ventilated (inspired fraction of O2 0.4) dogs. Multipoint Ppa/Q plots were generated by a manipulation of venous return before and 60 min after sufficient amounts of small (1 mm, n = 6 dogs), medium (5 mm, n = 6 dogs), or large (10 mm, n = 6 dogs) clots to increase Ppa to 50 mmHg. The distribution of VA/Q was determined by the multiple inert gas elimination technique at the same intermediate Q in each of these experimental conditions. All three sizes of emboli resulted in an 82–92% mean angiographic pulmonary vascular obstruction and increased both the extrapolated pressure intercepts and the slopes of the linear Ppa/Q plots. Gas exchange was altered the most after large clots, which were associated with lower arterial pH, higher physiological and inert gas dead spaces, higher dispersion of ventilation, and also lower mean VA/Q of perfusion distributions. In contrast, inert gas dead space was decreased after small clots. We conclude that, in autologous blood clot embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size but that gas exchange is affected differently, mainly in high-VA/Q regions and most often after the largest clots.

Effects of embolus size on hemodynamics and gas exchange in canine embolic pulmonary hypertension

1990 ◽  
Vol 69 (6) ◽  
pp. 2254-2261 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
J. L. Vachiery ◽  
P. Lejeune ◽  
M. Leeman ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Inert Gas ◽  
Experimental Conditions ◽  
Pulmonary Hemodynamics ◽  
Arterial Pco2 ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Vascular Obstruction ◽  
Arterial Po2

We examined the effects of different-sized glass-bead embolization on pulmonary hemodynamics and gas exchange in 12 intact anesthetized dogs. Pulmonary hemodynamics were evaluated by multipoint pulmonary arterial pressure (Ppa)/cardiac output (Q) plots before and 60 min after sufficient amounts of 100-microns (n = 6 dogs) or 1,000-microns (n = 6 dogs) glass beads to triple baseline Ppa were given and again 20 min after 5 mg/kg hydralazine in all the animals. Gas exchange was assessed using the multiple inert gas elimination technique in each of these experimental conditions. Embolization increased both the extrapolated pressure intercepts (by 6 mmHg) and the slopes (by 5 mmHg.l-1.min.m2) of the linear Ppa/Q plots, together with an 80% angiographic pulmonary vascular obstruction. These changes were not significantly different in the two subgroups of dogs. However, arterial PO2 was most decreased after the 100-microns beads, and arterial PCO2 was most increased after the 1,000-microns beads. Both bead sizes deteriorated the distribution of ventilation (VA)/perfusion (Q) ratios, with development of lung units with higher as well as with lower than normal VA/Q. Only 100-microns beads generated a shunt. Only 1,000-microns beads generated a high VA/Q mode and increased inert gas dead space. Hydralazine increased the shunt and decreased the slope of the Ppa/Q plots after 100-microns beads and had no effect after 1,000-microns beads. We conclude that in embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size up to 1,000 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Mechanisms for elevated fibrin/fibrinogen degradation products in acute experimental pulmonary embolism

Blood ◽  
1975 ◽  
Vol 45 (4) ◽  
pp. 563-568 ◽  
Author(s):  
J Cade ◽  
J Hirsh ◽  
E Regoeczi
Keyword(s):  
Pulmonary Embolism ◽  
Degradation Products ◽  
Blood Clot ◽  
Autologous Blood ◽  
Peak Level ◽  
Fibrin Deposition ◽  
Experimental Conditions ◽  
Fibrin Degradation Products ◽  
Serial Measurements ◽  
Autologous Blood Clot

Abstract The mechanism and significance of elevated levels of serum fibrin degradation products (FDP) in pulmonary embolism were investigated experimentally. Dogs were embolized with autologous blood clot-incorporating canine 125I-fibrin and were infused with either saline, heparin, or streptokinase. Serial measurements were made of total FDP by hemagglutination inhibition assay and of radioactive FDP. After saline, the peak level of total FDP was 323 mug/ml, but radioactive FDP was only 8 mug/ml. After heparin, these values were 44 and 11 mug/ml, respectively, and after streptokinase, 415 and 20 mug/ml. The results suggest that under these experimental conditions the elevated levels of FDP in pulmonary embolism are derived mainly from lysis of fibrin deposited after embolization rather than from lysis of the original embolus. Heparin inhibits both fibrin deposition and elevation of FDP levels after embolism.

Hypoxic pulmonary vasoconstriction and gas exchange in acute canine pulmonary embolism

1996 ◽  
Vol 80 (4) ◽  
pp. 1240-1248 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
F. Vermeulen ◽  
R. Naeije
Keyword(s):  
Pulmonary Embolism ◽  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Blood Clot ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Autologous Blood ◽  
Response Curves ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

Hypoxic pulmonary vasoconstriction (HPV) is inhibited in several models of acute lung injury. Whether HPV is preserved in pulmonary embolism is unknown. We investigated the effects of a reduction in the fraction of inspired O2 (FIO2) on pulmonary hemodynamics and gas exchange in anesthetized dogs before and after autologous blood clot pulmonary embolism. In a first group of 14 dogs, stimulus-response curves for HPV were constructed as pulmonary arterial pressure (Ppa) vs. FIO2 varied between 1.0 and 0.06 at a cardiac output (Q) kept constant at 3.5 l.min-1.m-2. Gas exchange was evaluated by using the multiple inert-gas elimination technique at FIO2 of 1.0, 0.4, and 0.1. Embolism decreased the relative magnitude of HPV, expressed as the gradient between Ppa and pulmonary arterial occluded pressure in hypoxia divided by (Ppa-pulmonary arterial occluded pressure) at FIO2 of 1.0, from 1.8 to 1.2 (P < 0.05). Retention minus excretion gradients for sulfur hexafluoride and ethane were increased by decreased FIO2 (P < 0.005 and P < 0.05, respectively) before but not after embolism. Hypoxia-induced deterioration in gas exchange before embolism was related to the amount of baseline very low ventilation-perfusion (VA/Q) ratios. Similar results were obtained in a second group of seven dogs with Q decreased to maintain Ppa at the same average value as before embolism. However, gas exchange was not affected by inspiratory hypoxia before as well as after embolism in this group, which presented with a lesser amount of baseline very low VA/Q. In both groups of dogs, increase in the FIO2 from 0.4 to 1.0 did not affect gas exchange. We conclude that 1) pulmonary embolism is associated with a partial inhibition of HPV, 2) HPV does not contribute to preserve gas exchange in pulmonary embolism, and 3) a strong HPV may deteriorate gas exchange in severe hypoxia in the presence of minor very low VA/Q inequality.

scholarly journals Mechanisms for elevated fibrin/fibrinogen degradation products in acute experimental pulmonary embolism

Blood ◽  
1975 ◽  
Vol 45 (4) ◽  
pp. 563-568
Author(s):  
J Cade ◽  
J Hirsh ◽  
E Regoeczi
Keyword(s):  
Pulmonary Embolism ◽  
Degradation Products ◽  
Blood Clot ◽  
Autologous Blood ◽  
Peak Level ◽  
Fibrin Deposition ◽  
Experimental Conditions ◽  
Fibrin Degradation Products ◽  
Serial Measurements ◽  
Autologous Blood Clot

The mechanism and significance of elevated levels of serum fibrin degradation products (FDP) in pulmonary embolism were investigated experimentally. Dogs were embolized with autologous blood clot-incorporating canine 125I-fibrin and were infused with either saline, heparin, or streptokinase. Serial measurements were made of total FDP by hemagglutination inhibition assay and of radioactive FDP. After saline, the peak level of total FDP was 323 mug/ml, but radioactive FDP was only 8 mug/ml. After heparin, these values were 44 and 11 mug/ml, respectively, and after streptokinase, 415 and 20 mug/ml. The results suggest that under these experimental conditions the elevated levels of FDP in pulmonary embolism are derived mainly from lysis of fibrin deposited after embolization rather than from lysis of the original embolus. Heparin inhibits both fibrin deposition and elevation of FDP levels after embolism.

Appearance of Nuclear-sorted Caspase-12 Fragments in Cerebral Cortical and Hippocampal Neurons in Rats Damaged by Autologous Blood Clot Embolic Brain Infarctions

2011 ◽  
Vol 31 (5) ◽  
pp. 795-802 ◽  
Author(s):  
Koji Shimoke ◽  
Yoshinori Matsuki ◽  
Kenji Fukunaga ◽  
Yoshinobu Matsumura ◽  
Eriko Fujita ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Blood Clot ◽  
Autologous Blood ◽  
Caspase 12 ◽  
Autologous Blood Clot

scholarly journals Intranasal salvinorin A improves neurological outcome in rhesus monkey ischemic stroke model using autologous blood clot

2020 ◽  
pp. 0271678X2093813
Author(s):  
Longfei Wu ◽  
Di Wu ◽  
Jian Chen ◽  
Chunhua Chen ◽  
Tianqi Yao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Rhesus Monkeys ◽  
Infarct Volume ◽  
Blood Clot ◽  
Autologous Blood ◽  
Control Group ◽  
Stroke Model ◽  
Neurological Outcomes ◽  
Observation Period ◽  
Autologous Blood Clot

Salvinorin A (SA) exerts neuroprotection and improves neurological outcomes in ischemic stroke models in rodents. In this study, we investigated whether intranasal SA administration could improve neurological outcomes in a monkey ischemic stroke model. The stroke model was induced in adult male rhesus monkeys by occluding the middle cerebral artery M2 segment with an autologous blood clot. Eight adult rhesus monkeys were randomly administered SA or 10% dimethyl sulfoxide as control 20 min after ischemia. Magnetic resonance imaging was used to confirm the ischemia and extent of injury. Neurological function was evaluated using the Non-Human Primate Stroke Scale (NHPSS) over a 28-day observation period. SA significantly reduced infarct volume (3.9 ± 0.7 cm3 vs. 7.2 ± 1.0 cm3; P =  0.002), occupying effect (0.3 ± 0.2% vs. 1.4 ± 0.3%; P =  0.002), and diffusion limitation in the lesion (−28.2 ± 11.0% vs. −51.5 ± 7.1%; P =  0.012) when compared to the control group. SA significantly reduced the NHPSS scores to almost normal in a 28-day observation period as compared to the control group ( P =  0.005). Intranasal SA reduces infarct volume and improves neurological outcomes in a rhesus monkey ischemic stroke model using autologous blood clot.

scholarly journals Residence at 3,800-m altitude for 5 mo in growing dogs enhances lung diffusing capacity for oxygen that persists at least 2.5 years

2007 ◽  
Vol 102 (4) ◽  
pp. 1448-1455 ◽  
Author(s):  
Connie C. W. Hsia ◽  
Robert L. Johnson ◽  
Paul McDonough ◽  
D. Merrill Dane ◽  
Myresa D. Hurst ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Base Excess ◽  
Lactate Concentration ◽  
Diffusing Capacity ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Peak Lactate ◽  
Pulmonary Arterial ◽  
Hypoxic Exercise

Mammals native to high altitude (HA) exhibit larger lung volumes than their lowland counterparts. To test the hypothesis that adaptation induced by HA residence during somatic maturation improves pulmonary gas exchange in adulthood, male foxhounds born at sea level (SL) were raised at HA (3,800 m) from 2.5 to 7.5 mo of age and then returned to SL prior to somatic maturity while their littermates were simultaneously raised at SL. Following return to SL, all animals were trained to run on a treadmill; gas exchange and hemodynamics were measured 2.5 years later at rest and during exercise while breathing 21% and 13% O2. The multiple inert gas elimination technique was employed to estimate ventilation-perfusion (V̇a/Q̇) distributions and lung diffusing capacity for O2 (DlO2). There were no significant intergroup differences during exercise breathing 21% O2. During exercise breathing 13% O2, peak O2 uptake and V̇a/Q̇ distributions were similar between groups but arterial pH, base excess, and O2 saturation were higher while peak lactate concentration was lower in animals raised at HA than at SL. At a given exercise intensity, alveolar-arterial O2 tension gradient (A-aDo2) attributable to diffusion limitation was lower while Dlo2 was 12–25% higher in HA-raised animals. Mean systemic arterial blood pressure was also lower in HA-raised animals; mean pulmonary arterial pressures were similar. We conclude that 5 mo of HA residence during maturation enhances long-term gas exchange efficiency and DlO2 without impacting V̇a/Q̇ inequality during hypoxic exercise at SL.

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