Intraluminal Pulsed Doppler Evaluation of the Pulmonary Artery Velocity Time Curve in a Canine Model of Acute Pulmonary Hypertension

CHEST Journal ◽  
1991 ◽  
Vol 100 (2) ◽  
pp. 474-479 ◽  
Author(s):  
G. William Henry ◽  
Hiroshi Katayama ◽  
Manuel E. Lores ◽  
Carol L. Lucas ◽  
Jose I. Ferreiro
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Canine Model ◽  
Pulsed Doppler ◽  
Time Curve ◽  
Acute Pulmonary Hypertension ◽  
Doppler Evaluation

Efficacy of vasodilator therapy in canine model of acute pulmonary hypertension

1988 ◽  
Vol 255 (5) ◽  
pp. H1232-H1239 ◽  
Author(s):  
H. J. Priebe
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Pulmonary Artery ◽  
Prostaglandin E1 ◽  
Canine Model ◽  
Lung Compliance ◽  
Myocardial Segment ◽  
Vasodilator Therapy ◽  
Artery Flow ◽  
Subsequent Administration

This study was performed to determine 1) the effects of acute pulmonary embolization (induced by injection of autologous muscle) on right ventricular (RV) performance, coronary hemodynamics, and gas exchange; and 2) the efficacy of subsequent administration of nitroglycerin, prostaglandin E1, and hydralazine with regard to improvement in RV function and gas exchange in eight open-chest dogs. After embolization, pulmonary artery (PA) pressure and vascular resistance (PVR) increased three- to fivefold without changes in RV end-diastolic dimensions (ultrasonic dimension technique) or pressure. However, systolic dimensions increased, and stroke volume (SV) fell. Gas exchange, lung compliance, and pH worsened. Subsequent administration of nitroglycerin (5 micrograms.kg-1.min-1) and prostaglandin E1 (0.2 micrograms.kg-1.min-1) caused further decreases in SV and pH. In contrast, hydralazine (mean 0.15 mg/kg) improved myocardial segment shortening, SV, PVR, pulmonary artery flow, and gas exchange. Coronary blood flow increased by 110%. Thus in this canine model of combined pulmonary hypertension and respiratory insufficiency, nitroglycerin and prostaglandin E1 exerted no beneficial cardiopulmonary effects. In contrast, hydralazine improved regional and global RV performance and gas exchange.

Thromboxane mediates acute pulmonary hypertension in sheep extracorporeal perfusion

1982 ◽  
Vol 243 (3) ◽  
pp. H471-H479 ◽  
Author(s):  
M. B. Peterson ◽  
P. C. Huttemeier ◽  
W. M. Zapol ◽  
E. G. Martin ◽  
W. D. Watkins
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Acid Metabolism ◽  
Plasma Concentrations ◽  
Arachidonic Acid Metabolism ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Vasodilator ◽  
Systemic Hypoxia ◽  
General Activation ◽  
Acute Pulmonary Hypertension

We measured serial plasma concentrations of thromboxane B2 (TXB2), the stable metabolite of the putative pulmonary vasoconstrictor thromboxane A2 (TXA2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of the pulmonary vasodilator prostacyclin (PGI2) by double-antibody radioimmunoassay during partial venovenous bypass in 25 awake sheep. The onset of bypass caused mean pulmonary artery pressure (PAP) to increase from 16 +/- 1 to 28 +/- 2 mmHg at 12 +/- 2 min, due to an increase of pulmonary vascular resistance, followed by a return to control within 45 min. There was no systemic hypoxia. TXB2 increased simultaneously with the onset of pulmonary hypertension (PH) (236 +/- 36 to 700 +/- 120 pg/ml at 0 and 5 min) and peaked at 1,724 +/- 172 pg/ml 10 min after maximum PAP was achieved. Positive pulmonary artery-to-aortic differences of TXB2 were measured. 6-Keto-PGF1 alpha increased from 51 +/- 3 to 842 +/- 367 pg/ml at 35 min. PGF2 alpha was unchanged (130 +/- 45 pg/ml). PH, TXB2, and 6-keto-PGF1 alpha increases were blocked by pretreatment with indomethacin or ibuprofen. PH and TXB2 increases were prevented with an imidazole derivative. PH caused by a continuous infusion of an endoperoxide analog did not induce lung release of TXB2 or PGF2 alpha. We conclude that 1) transient pulmonary vasoconstriction is caused by thromboxane; 2) the lung is the primary site of thromboxane synthesis; and 3) bypass causes selective alterations in arachidonic acid metabolism rather than general activation of the cascade.

Redistribution in left ventricular regional flow following acute right ventricular pressure overload

1978 ◽  
Vol 56 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Francois Sestier ◽  
Richard R. Mildenberger ◽  
Gerald A. Klassen
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Coronary Flow ◽  
Fold Increase ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Left Ventricular Myocardium ◽  
Regional Flow ◽  
Acute Pulmonary Hypertension

The left ventricular dysfunction following acute pulmonary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10–30 min of banding of the pulmonary artery. The left ventricular subendocardial: epicardial ratio fell by 12 and 31% (p < 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 ± 2.4 to 3.6 ± 1.9 and 6.0 ± 2.1 (p < 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.

Acute pulmonary hypertension after wedging of a pulmonary artery catheter as clues to pulmonary artery perforation

1993 ◽  
Vol 7 (4) ◽  
pp. 508-509 ◽  
Author(s):  
Thieu T. Duong ◽  
Gabriel S. Aldea ◽  
Gilbert P. Connelly ◽  
Benjamin S. Suaco ◽  
Lawrence C. Weinfeld ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Catheter ◽  
Acute Pulmonary Hypertension ◽  
Pulmonary Artery Perforation

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension

2005 ◽  
Vol 98 (2) ◽  
pp. 605-613 ◽  
Author(s):  
Daniel Bia Santana ◽  
Juan Gabriel Barra ◽  
Juan Carlos Grignola ◽  
Fernando Florencio Ginés ◽  
Ricardo Luis Armentano
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Muscle Activation ◽  
Arterial Compliance ◽  
Characteristic Impedance ◽  
Main Pulmonary Artery ◽  
Pressure Rise ◽  
Cross Sectional ◽  
Acute Pulmonary Hypertension

Acute pulmonary hypertension (PH) may arise with or without an increase in vascular smooth muscle (VSM) tone. Our objective was to determine how VSM activation affects both the conduit (CF) and wall buffering (BF) functions of the pulmonary artery (PA) during acute PH states. PA instantaneous flow, pressure, and diameter of six sheep were recorded during normal pressure (CTL) and different states of acute PH: 1) passively induced by PA mechanical occlusion (PPH); 2) actively induced by intravenous administration of phenylephrine (APH); and 3) a combination of both (APPH). To evaluate the direct effect of VSM activation, isobaric (PPH vs. APH) and isometric (CTL vs. APPH) analyses were performed. We calculated the local BF from the elastic (EPD) and viscous (ηPD) indexes as ηPD/EPD and the characteristic impedance (ZC) from pressure and flow to evaluate CF as 1/ZC. We also calculated the absolute and normalized cross-sectional pulsatility (PCS and NPCS, respectively), the dynamic compliance (CDYN), the cross-sectional distensibility (DCS), and the pressure-strain elastic modulus (EP). The isobaric analysis showed increase of CF, BF, and ηPD ( P < 0.01) and decrease of EPD ( P < 0.05) during APH in respect to PPH (concomitant with isobaric VSM activation-induced vasoconstriction, P < 0.01). The isometric analysis showed increase of EPD and ηPD ( P < 0.01), nonsignificant difference in BF (even in the presence of a significant mean PA pressure rise, from 14 (SD 6) to 25 (SD 8) mmHg, P < 0.01), and decrease in CF ( P < 0.01) during APPH respect to CTL. Mechanical occlusions (PPH and APPH) reduced BF ( P < 0.01) and increased EPD ( P < 0.05) with regard to their previous steady states (CTL and APH). Nonsignificant differences were found in EPD between PPH and APPH. VSM activation (APH and APPH) increased ηPD ( P < 0.01) respect to their previous passive states (CTL and PPH), but no significant differences were found within similar levels of VSM activation. In conclusion, VSM plays a relevant role in main pulmonary artery function during acute pulmonary hypertension, because isobaric vasoconstriction induced by VSM activation improves both BF and CF, mainly due to the increase in ηPD concomitant with the arterial compliance. CDYN and DCS were the more pertinent clinical indexes of arterial elasticity. Additionally, the ηPD-mediated preservation of the BF could be evaluated by the geometric related indexes (PCS and NPCS), which appear to be qualitative markers of arterial wall viscosity status.

Pulmonary impedance and right ventricular-vascular coupling during coronary angioplasty

1993 ◽  
Vol 74 (1) ◽  
pp. 161-169 ◽  
Author(s):  
W. G. Kussmaul ◽  
J. Wieland ◽  
J. Altschuler ◽  
W. K. Laskey
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Coronary Angioplasty ◽  
Characteristic Impedance ◽  
Low Frequency ◽  
Resistance Vessels ◽  
Additional Resistance ◽  
Acute Pulmonary Hypertension ◽  
Artery Disease

Right ventricular ejection may be modified by alterations in pulmonary vascular properties during acute pulmonary hypertension. Pulmonary artery impedance and reflection properties were analyzed during coronary angioplasty in nine patients with single-vessel disease involving the left anterior descending artery by use of high-fidelity catheter recordings of pulmonary pressure and flow made before angioplasty balloon inflation and at peak ischemia. Acute pulmonary hypertension in this resting model resulted in a significant decrease in pulmonary vascular resistance (142 +/- 54 to 92 +/- 64 dyn.s.cm-5, P < 0.05), increase in low-frequency impedance (67 +/- 36 to 101 +/- 43 dyn.s.cm-5, P < 0.05), and no change in high-frequency (characteristic) impedance (38 +/- 14 to 41 +/- 13 dyn.s.cm-5). Pulmonary wave reflection amplitudes were increased, and the amount of hydraulic power expended per unit of net forward flow significantly increased (3.1 +/- 0.7 to 4.3 +/- 0.7 mW.ml-1.s-1, P < 0.001). These findings indicate that, during acute pulmonary hypertension in humans, 1) recruitment of additional resistance vessels can occur, 2) pulsatile pulmonary artery properties are significantly altered, and 3) right ventricular power output requirements are increased. Because episodic pulmonary hypertension occurs frequently in coronary artery disease, these changes may help explain eventual right ventricular hypertrophy or failure.

Sign in / Sign up

Export Citation Format

Share Document