Effect of endotoxemia on hypoxic pulmonary vasoconstriction in unanesthetized sheep

This study examined the effect of acute endotoxemia on hypoxic pulmonary vasoconstriction (HPV) in awake sheep. Thirteen sheep were chronically instrumented with Silastic catheters in the pulmonary artery, left atrium, jugular vein, and carotid artery; with a Swan-Ganz catheter in the main pulmonary artery; with a chronic lung lymph fistula; and with a tracheostomy. Base-line HPV was determined by measuring the change in pulmonary vascular resistance (PVR) while sheep breathed 12% O2 for 7 min. Concentrations of immunoreactive 6-keto-PGF1 alpha and thromboxane B2 (TXB2) were measured in lung lymph during the hypoxic challenge. Escherichia coli endotoxin (0.2–0.5 micrograms/kg) was infused intravenously. Four hours after endotoxemia, HPV was measured. In five sheep, meclofenamate was infused at 4.5 h after endotoxemia and HPV measured again. During the base-line hypoxic challenge, PVR increased by 36 +/- 9% (mean +/- SE). There was no significant change in lung lymph 6-keto-PGF1 alpha or TXB2 levels with hypoxia. Twelve of the 13 sheep showed a decrease in HPV 4 h after endotoxemia; the mean change in PVR with hypoxia was -8 +/- 5%, which was significantly (P less than 0.05) reduced compared with base-line HPV. The infusion of meclofenamate at 4.5 h after endotoxin did not restore HPV.

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Breaking the Rules: Left Common Carotid Artery from the Main Pulmonary Artery in an Infant with a Vascular Ring

CASE ◽

10.1016/j.case.2021.07.011 ◽

2021 ◽

Author(s):

Stephan Juergensen ◽

Emilio Quezada ◽

Norman H. Silverman ◽

Jeffrey G. Gossett ◽

Peter Kouretas ◽

...

Keyword(s):

Carotid Artery ◽

Pulmonary Artery ◽

Common Carotid Artery ◽

Vascular Ring ◽

Main Pulmonary Artery ◽

Left Common Carotid Artery

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DECISION MAKING FOR DEVICE CLOSURE IN ADULTS WITH ‘HYPERTENSIVE PDA’–NON-INVASIVE CRITERIA: IMMEDIATE RESULTS

Pakistan Armed Forces Medical Journal ◽

10.51253/pafmj.v70isuppl-4.6020 ◽

2021 ◽

Vol 70 (Suppl-4) ◽

pp. S762-67

Author(s):

Ahsan Beg ◽

Abdul Malik ◽

Amjad Mahmood ◽

M Younas ◽

Fakher -e- Fayaz

Keyword(s):

Pulmonary Hypertension ◽

Retrospective Study ◽

Pulmonary Artery ◽

Main Pulmonary Artery ◽

Tertiary Care ◽

Referral Hospital ◽

Device Closure ◽

X Ray ◽

Non Invasive ◽

The Mean

Objective: To find the mean pulmonary artery pressures (PAP) in adults (>12 years) Patent Ductus Arteriosus (PDA) with ‘reversible pulmonary hypertension’ after the device closure. Residual PDA and immediate complications (embolization, pulse loss, obstruction in the aorta or pulmonary artery) are to be reported. Study Design: Retrospective study. Place and Duration of Study: Tertiary Care Referral Hospital, from Aug 2007 to Jun 2020. Methodology: This retrospective study is descriptive. Data collected by convenience sampling from 3 tertiary care referral hospital. 981 patients were undergone PDA device closure during the period from Aug 2007 to June 2020. After informed consent, an initial assessment was done by history, clinical examination, x-ray chest PA view, electrocardiography (ECG), and transthoracic echocardiography (TTE). Reversible pulmonary hypertension was labeled based on non-invasive criteria including room air saturation >93% and cardiomegaly on x-ray chest. Patients who had <93% and normal heart size on x-ray chest were excluded. The lower limit for age was 12 years. Results: Nine Hundred Eighty One patients had undergone PDA device closure. 32 (n=32/981 3.3%) had fulfilled our inclusion criteria. The mean age was 22 ± 9 (13–45) years. Mean weight was 41 ± 11 (25-66) kg. Successful device closure was done in 30 patients (93.7%). Mean diameter of PDA was 7 ± 0.1 (4.5-13 mm. Mean PAP decreased from 59 ± 13 mmHg to 38 ± 19 mmHg (p<0.05). Commonest device used was Shasma duct occluder (n=16/32 50%) followed by Occlutech Duct Occluder (n=7/32 21.9%), while 2 had muscular VSD device (n=5/32 15.6%). In 2 patients, there was an underestimation of the size of PDA so the device was retrieved and replaced with another larger one successfully. Two patients had the device fully dropped into the main pulmonary artery before it was released. Larger size device was not available at that time so the patients were referred for surgery. None of our patients had device embolization or residual shunt on echo performed next day to the procedure. Neither any patient had residual pulmonary hypertension on echocardiography. There was no significant obstruction in the aorta in any patients. Two patients had mild left pulmonary artery obstruction. There was no significant obstruction in the aorta in any of our patients. There was pulse loss in 3 patients which were treated successfully with heparin infusion with no residual damage. Conclusion: Device closure is a feasible option in adults with hypertensive PDA while the decision of reversibility is based on non-invasive criteria.

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Effect of hypoxia on responses of respiratory smooth muscle to histamine and LTD4

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.1.435 ◽

1988 ◽

Vol 64 (1) ◽

pp. 435-440 ◽

Cited By ~ 8

Author(s):

N. A. Paterson ◽

J. T. Hamilton ◽

A. Yaghi ◽

D. S. Miller

Keyword(s):

Smooth Muscle ◽

Hypoxic Pulmonary Vasoconstriction ◽

Smooth Muscle Contraction ◽

Base Line ◽

Leukotriene D4 ◽

Pulmonary Vasoconstriction ◽

Voltage Dependent ◽

Vascular Responsiveness ◽

Porcine Pulmonary Artery ◽

Parenchymal Lung

The aim of the present study was to compare the effect of reduced oxygenation on the contractions of pulmonary vascular and airway smooth muscle induced by leukotriene D4 (LTD4) with those induced by histamine (an agonist with similar mechanisms of smooth muscle contraction) and KCl (a voltage-dependent stimulus). During hypoxia (PO2: 40 +/- 4 Torr) the responses of isolated porcine pulmonary artery and vein spiral strips to LTD4 increased approximately three- and two-fold, respectively, and the vein also exhibited an augmented response to histamine. The augmentation was blunted (LTD4) or reversed (histamine) during anoxia (PO2: 0 +/- 2 Torr). Responses to KCl were not systematically altered by reduced oxygenation. In contrast, the contractions of the guinea pig parenchymal lung strip by all three agonists were generally suppressed by reduced oxygenation. After reoxygenation, the contractile responses of each of the three smooth muscle preparations were generally increased compared with previous and concurrent base-line observations, particularly the LTD4-induced pulmonary vein contraction that increased approximately sevenfold after reoxygenation after anoxia. The contribution (if any) of leukotrienes to hypoxic pulmonary vasoconstriction may reflect increased vascular responsiveness to leukotrienes during hypoxia as well as (or instead of) increased leukotriene release.

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Image quality and attenuation values of multidetector CT coronary angiography using high iodine-concentration contrast material: A comparison of the use of iopromide 300 and iopromide 370

QJM ◽

10.1093/qjmed/hcaa041.018 ◽

2020 ◽

Vol 113 (Supplement_1) ◽

Author(s):

A K M Darwish ◽

M M Farouk ◽

H Hafez ◽

A Adel

Keyword(s):

Image Quality ◽

Pulmonary Artery ◽

Coronary Arteries ◽

Main Pulmonary Artery ◽

Iodine Concentration ◽

Ascending Aorta ◽

P Value ◽

Group A ◽

The Mean ◽

Attenuation Values

Abstract Background Iodine concentration is one of the main determinants of arterial enhancement in CTA, and current low-osmolar and iso-osmolar nonionic CM for intravascular administration still come in a handful of molecules, but a relatively wide range of different iodine concentrations. This gives the opportunity to optimize CTA protocols as a function of several factors such as patient characteristics, CT technology, and CM features in an attempt to maximize the diagnostic yield of CTA examinations while considering patient safety and avoiding unnecessary extra costs. Objective To compare image quality and attenuation values of multidetector CT coronary angiography (MDCT) between iopromide 300 and iopromide 370 and to evaluate whether the higher iodine contrast material has better image quality or not. Material and Methods Patients were prospectively enrolled and were randomized into two groups (group A, 30 patients received iopromide 300, iodine flux 1.2g I/s; group B, 30 patients received iomeprol 370, iodine flux 1.48g I/s). CT attenuation values were measured in the proximal end coronary arteries,ascending aorta and main pulmonary artery. The image quality of 15 coronary artery segments was graded by cardiologist in consensus with the use of a four-point scale (1 excellent enhancement to 4 poor enhancement). Non-parametric statistical approaches were used to compare the two groups. Results No statistically significant differences were found between the mean attenuation values (302 HU for iopromide 300 and 326 HU for iopromide 370, P = 0.175) in the coronary arteries in the two groups. The mean attenuation value of the proximal ascending aorta (AA)and main pulmonary artery (MPA) was found to be 345+/-63 HU and 241+/- 89 in group A respectively, whereas the mean attenuation value in proximal ascending aorta and main pulmonary artery in group B was found to be 348+/-74 and 238+/- 50 respectively. No significant difference was found between iopromide 300 and iopromide 370 in terms of contrast enhancement at the level of great arteries, P value AA = 0.826 and P value for MPA = 0.884. 92.9% of coronary arterial segments got score (range 1–2) in group A whereas 93.6 of coronary arterial segments got score (range 1-2) in group with no statistically significant difference P value = 0.755. Conclusion With the current CT technology iopromide 300 is not inferior to iopromide 370 in terms of coronary artery attenuation values and image quality. Iopromide 300 provides similar enhancement of coronary arteries and excellent image quality as compared with iopromide 370 using identical amount of total iodine with fewer cost and less estimated adverse effects owing to low iodine concentration of iopromide 300.

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Effects of thromboxane synthase inhibition on air emboli lung injury in sheep

Journal of Applied Physiology ◽

10.1152/jappl.1986.60.6.1828 ◽

1986 ◽

Vol 60 (6) ◽

pp. 1828-1833 ◽

Cited By ~ 14

Author(s):

M. Fukushima ◽

T. Kobayashi

Keyword(s):

Pulmonary Hypertension ◽

Lung Injury ◽

Pulmonary Artery ◽

Air Embolism ◽

Base Line ◽

Pulmonary Vascular Permeability ◽

Thromboxane Synthase ◽

Pulmonary Hemodynamic ◽

Synthase Inhibitor ◽

Lung Lymph

We tested the effects of OKY-046, a thromboxane synthase inhibitor, on lung injury induced by 2 h of pulmonary air infusion (1.23 ml/min) in the pulmonary artery of unanesthetized sheep with chronic lung lymph fistula so as to assess the role of thromboxane A2 (TxA2) in the lung injury. We measured pulmonary hemodynamic parameters and the lung fluid balance. The concentrations of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) in plasma and lung lymph were determined by radioimmunoassay. Air infusion caused sustained pulmonary hypertension and an increase in pulmonary vascular permeability. The levels of TxB2 and 6-keto-PGF1 alpha in both plasma and lung lymph were significantly elevated during the air infusion. TxB2 concentration in plasma obtained from the left atrium was higher than that from the pulmonary artery at 15 min of air infusion. When sheep were pretreated with OKY-046 (10 mg/kg iv) prior to the air infusion, increases in TxB2 were prevented. The pulmonary arterial pressure, however, increased similarly to that of untreated sheep (1.8 X base line). The increase in lung lymph flow was significantly suppressed during the air infusion. Our data suggest that the pulmonary hypertension observed during air embolism is not caused by TxA2.

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Pulmonary artery NADPH-oxidase is activated in hypoxic pulmonary vasoconstriction.

American Journal of Respiratory Cell and Molecular Biology ◽

10.1165/ajrcmb.15.5.8918370 ◽

1996 ◽

Vol 15 (5) ◽

pp. 633-644 ◽

Cited By ~ 207

Author(s):

C Marshall ◽

A J Mamary ◽

A J Verhoeven ◽

B E Marshall

Keyword(s):

Pulmonary Artery ◽

Nadph Oxidase ◽

Hypoxic Pulmonary Vasoconstriction ◽

Pulmonary Vasoconstriction

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SELECTIVE PROTEIN KINASE C INHIBITION ATTENUATES PULMONARY ARTERY CYTOKINE EXPRESSION WITHOUT AFFECTING HYPOXIC PULMONARY VASOCONSTRICTION

Shock ◽

10.1097/01.shk.0000235128.97610.b2 ◽

2007 ◽

Vol 27 (1) ◽

pp. 36-39 ◽

Cited By ~ 4

Author(s):

Ben M. Tsai ◽

Ketan Patel ◽

Meijing Wang ◽

Eric D. Morrell ◽

Paul R. Crisostomo ◽

...

Keyword(s):

Protein Kinase C ◽

Protein Kinase ◽

Pulmonary Artery ◽

Hypoxic Pulmonary Vasoconstriction ◽

Cytokine Expression ◽

Pulmonary Vasoconstriction ◽

Kinase C

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Mechanical properties and dimensions of the major pulmonary arteries

Journal of Applied Physiology ◽

10.1152/jappl.1960.15.1.92 ◽

1960 ◽

Vol 15 (1) ◽

pp. 92-96 ◽

Cited By ~ 69

Author(s):

Dali J. Patel ◽

Donald P. Schilder ◽

Alexander J. Mallos

Keyword(s):

Pulmonary Artery ◽

Pulse Pressure ◽

Technical Assistance ◽

Main Pulmonary Artery ◽

Pulmonary Arteries ◽

Cross Sectional ◽

Measurement Control ◽

The Mean ◽

The Right ◽

The Relationship

The relationship between instantaneous distending pressure and diameter of the pulmonary artery was studied in 18 living thoracotomized dogs. An electrical caliper with adequate recording characteristics was developed for instantaneous diameter measurement. Control observations were made over a range of pressures induced by rapid, right heart dextran-infusion and were compared with those obtained during norepinephrine administration. Results indicate: a) the pulse contours of the pulmonary artery pressure and diameter are essentially identical, indicating negligible inertance and viscous resistance of the vessel wall, b) the mean change in average radius during a cardiac cycle was ±7.8% ± 2.86 S.D. ± .32 S.E.M. (0.48%/cm H2O pulse pressure) under control conditions, c) the ratio of change in radius to pulse pressure, R/P, showed a significant decrease during norepinephrine administration when compared to control values within the same pressure range (P < .01) and d) the cross-sectional area of the main pulmonary artery exceeded that of the right and left combined. Note: (With the Technical Assistance of Alfred G. T. Casper) Submitted on August 25, 1959

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Preservation of Hypoxic Pulmonary Vasoconstriction during Sevoflurane and Desflurane Anesthesia Compared to the Conscious State in Chronically Instrumented Dogs

Anesthesiology ◽

10.1097/00000542-199812000-00029 ◽

1998 ◽

Vol 89 (6) ◽

pp. 1501-1508 ◽

Cited By ~ 22

Author(s):

Marc A. Lesitsky ◽

Steve Davis ◽

Paul A. Murray

Keyword(s):

Hypoxic Pulmonary Vasoconstriction ◽

Main Pulmonary Artery ◽

General Characteristic ◽

Face Mask ◽

Conscious State ◽

Pressure Flow ◽

Pulmonary Vasoconstriction ◽

End Tidal ◽

The Right ◽

Chronically Instrumented Dogs

Background The authors' objective was to assess the extent to which sevoflurane and desflurane anesthesia alter the magnitude of hypoxic pulmonary vasoconstriction compared with the response measured in the same animal in the conscious state. Methods Left pulmonary vascular pressure-flow plots were generated in seven chronically instrumented dogs by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder implanted around the right main pulmonary artery. Pressure-flow plots were generated during normoxia and hypoxia on separate days in the conscious state, during sevoflurane (approximately 3.5% end-tidal), and during desflurane (approximately 10.5% end-tidal) anesthesia. Values are mean+/-SEM. Results In the conscious state, administration of the hypoxic gas mixture by conical face mask decreased (P < 0.01) systemic arterial PO2 from 94+/-2 mmHg to 50+/-1 mmHg and caused a leftward shift (P < 0.01) in the pressure-flow relationship, indicating pulmonary vasoconstriction. The magnitude of hypoxic pulmonary vasoconstriction in the conscious state was flow-dependent (P < 0.01). Neither anesthetic had an effect on the baseline pressure-flow relationship during normoxia. The magnitude of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane was also flow-dependent (P < 0.01). Moreover, at any given value of flow the magnitude of hypoxic pulmonary vasoconstriction was similar during sevoflurane and desflurane compared with the conscious state. Conclusion These results indicate that hypoxic pulmonary vasoconstriction is preserved during sevoflurane and desflurane anesthesia compared with the conscious state. Thus, inhibition of hypoxic pulmonary vasoconstriction is not a general characteristic of inhalational anesthetics. The flow-dependent nature of the response should be considered when assessing the effects of physiologic or pharmacologic interventions on the magnitude of hypoxic pulmonary vasoconstriction.

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