Ragweed sensitization alters pulmonary vascular responses to bronchoprovocation in beagle dogs

1997 ◽  
Vol 83 (3) ◽  
pp. 912-917 ◽  
Author(s):  
Andreas Theodorou ◽  
Natalie Weger ◽  
Kathleen Kunke ◽  
Kyoo Rhee ◽  
David Bice ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Resistance Index ◽  
Lung Compliance ◽  
Pulmonary Vasculature ◽  
Beagle Dogs ◽  
Mechanically Ventilated ◽  
Vascular Responses ◽  
Before And After ◽  
Pulmonary Artery Catheters ◽  
Pulmonary Vascular Resistance Index

Theodorou, Andreas, Natalie Weger, Kathleen Kunke, Kyoo Rhee, David Bice, Bruce Muggenberg, and Richard Lemen. Ragweed sensitization alters pulmonary vascular responses to bronchoprovocation in beagle dogs. J. Appl. Physiol.83(3): 912–917, 1997.—In ragweed (RW)-sensitized beagle dogs, we tested the hypothesis that reactivity of the pulmonary vasculature was enhanced with aerosolized histamine (Hist) and RW. Seven dogs were neonatally sensitized with repeated intraperitoneal RW injections, and 12 dogs were controls (Con). The dogs were anesthetized with intravenous chloralose, mechanically ventilated, and instrumented with femoral arterial and pulmonary artery catheters. Specific lung compliance (Cl sp), specific lung conductance (Gsp), systemic vascular resistance index, and pulmonary vascular resistance index (PVRI) were measured before and after bronchoprovocation with Hist and RW. After Hist inhalation (5 breaths of 30 mg/ml), both Con and RW dogs had significant ( P < 0.05) decreases in Cl sp(−51 ± 4 and −53 ± 5%, respectively) and Gsp (−65 ± 5 and −69 ± 3%, respectively), but only RW-sensitized dogs had a significant increase in PVRI (38 ± 10%). After RW inhalation (60 breaths of 0.8 mg/ml), only RW-sensitized dogs had significant increases (62 ± 20%) in PVRI and decreases in Gsp (−77 ± 4%) and Cl sp(−65 ± 7%). We conclude that, compared with Con, RW-sensitized beagle dogs have increased pulmonary vasoconstrictive responses with Hist or RW inhalation.

Differential vasoactive response to endothelin receptor antagonists and prostacyclin in patients with severe pulmonary hypertension

2002 ◽  
Vol 103 (s2002) ◽  
pp. 298S-301S ◽  
Author(s):  
Sotiria C. APOSTOLOPOULOU ◽  
Georgios KOURGIANNIDIS ◽  
Athanassios MANGINAS ◽  
Zenon S. KYRIAKIDES ◽  
David WEBB ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Resistance Index ◽  
Pulmonary Vasculature ◽  
Endothelin Receptor ◽  
Vasoactive Substances ◽  
Endothelin A Receptor ◽  
Before And After ◽  
Eta Receptor ◽  
Pulmonary Vascular Resistance Index ◽  
Eta Receptor Antagonist

Pulmonary hypertension (PH) is a rare disease of the pulmonary vasculature with diverse pathogenetic mechanisms. Vasoactive substances such as endothelin A receptor (ETA) antagonists and prostanoids have been used to improve haemodynamics and clinical outcome. We compared the hemodynamic response to BQ-123 (an ETA receptor antagonist) and prostacyclin or its analogue iloprost in ten patients (four men) with a mean age of 35.9±15.6 years. Seven patients had primary PH and three had PH owing to connective tissue disease. Patients underwent haemodynamic evaluation before and after administration of intra-atrial BQ-123 (200mmol/min for 60min), intravenous prostacyclin (3ng·kg-1·min-1 for 4h) or iloprost as an aerosol (100µg over 24h). Response to vasodilator administration was defined as >15% decrease in pulmonary vascular resistance index (PVRI). Of the ten patients, five showed a response to BQ-123 and eight responded to prostanoids. Four patients were responders and one patient was a non-responder to both agents. PVRI decreased by 16.6±13.4% with BQ-123, and 24.4±15.7% with prostanoids (not statistically significant). The aetiology of PH did not affect the response to either drug. In conclusion, response to ETA antagonist or prostanoid administration can be achieved in a large group of patients with severe PH, however few patients respond identically to both agents. These findings are consistent with a multifactorial mechanism involved in this disease.

Nitric oxide and endothelial permeability

1997 ◽  
Vol 83 (6) ◽  
pp. 1941-1946 ◽  
Author(s):  
Frank Hinder ◽  
Michael Booke ◽  
Lillian D. Traber ◽  
Daniel L. Traber
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Endothelial Permeability ◽  
Resistance Index ◽  
Venous Occlusion ◽  
Pulmonary Vasculature ◽  
Plasma Protein Concentration ◽  
Pulmonary Vascular Resistance Index ◽  
Lung Lymph

Hinder, Frank, Michael Booke, Lillian D. Traber, and Daniel L. Traber. Nitric oxide and endothelial permeability. J. Appl. Physiol. 83(6): 1941–1946, 1997.—Nitric oxide synthase inhibition reverses systemic vasodilation during sepsis but may increase endothelial permeability. To assess adverse effects on the pulmonary vasculature, 12 sheep were chronically instrumented with lung lymph fistulas and hydraulic pulmonary venous occluders. Escherichia coli endotoxin (lipopolysaccharide; 10 ng ⋅ kg−1 ⋅ min−1) was continuously infused for 32 h. After 24 h, six animals received 25 mg/kg of N ω-nitro-l-arginine methyl ester (l-NAME), and six received saline. All sheep developed a hyperdynamic circulatory response and elevated lymph flows by 24 h of lipopolysaccharide infusion. l-NAME reversed systemic vasodilation, increased pre- and postcapillary pulmonary vascular resistance index, pulmonary arterial pressure, and, transiently, effective pulmonary capillary pressure. Lung lymph flows were not different between groups at 24 h or thereafter. Calculated as changes from baseline, however, lung lymph flow was higher in thel-NAME group than in the control animals, with a trend toward lower lymph-to-plasma protein concentration ratio at 25 h. Permeability analysis at 32 h by the venous occlusion technique showed normal reflection coefficients and elevated filtration coefficients without differences between groups. Reversal by l-NAME of the systemic vasodilation during endotoxemia was associated with high pulmonary vascular resistance without evidence of impaired pulmonary endothelial barrier function.

Pulmonary hemodynamics and tissue damage after one lung infusion of Pseudomonas aeruginosa in sheep

1992 ◽  
Vol 72 (4) ◽  
pp. 1386-1392 ◽  
Author(s):  
H. M. Loick ◽  
D. J. Dehring ◽  
R. Tokyay ◽  
H. A. Linares ◽  
M. J. Evans ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Tissue Damage ◽  
Left Lung ◽  
Resistance Index ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vascular Resistance Index ◽  
Bacterial Toxicity ◽  
Bacterial Infusion

The relative roles of hematogenous mediators and direct bacterial toxicity due to phagocytosis by pulmonary intravascular macrophages were determined by selective bacterial infusion into the left pulmonary artery and comparison of right and left lungs at 24 h. Chronically instrumented sheep received 15-min pulmonary arterial infusions of live Pseudomonas aeruginosa (0.35–2.9 x 10(9), n = 6) or saline (n = 5). The saline group demonstrated stable cardiopulmonary function over time. Left lung blood flow, measured by Doppler flow probe, decreased 15 min into the bacterial infusion, with a concomitant sevenfold increase in left lung pulmonary vascular resistance index. The right lung pulmonary vascular resistance index doubled at 1 h, in association with increased plasma thromboxane B2 levels. An increase in cardiac index and decrease in systemic vascular resistance occurred at 12 h. The wet-to-dry weight ratio of the Pseudomonas-infused left lung was increased compared with that of the sham-infused lung. The tissue count of neutrophils in the lungs was doubled in both sides, but neutrophils on the left were more degranulated. The left lung tissue damage was caused by direct bacterial toxicity, including activation of phagocytic cells. Hematogenous mediators induced pulmonary and systemic hemodynamic changes and right lung neutrophil sequestration, but they did not damage the noninfused lung.

Decline in arterial partial pressure of oxygen after exercise: a surrogate marker of pulmonary vascular obstructive disease in patients with atrial septal defect and severe pulmonary hypertension

2011 ◽  
Vol 21 (3) ◽  
pp. 292-298 ◽  
Author(s):  
Srinivas Laksmivenkateshiah ◽  
Anil K. Singhi ◽  
Balu Vaidyanathan ◽  
Edwin Francis ◽  
Sundaram R. Karimassery ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Partial Pressure ◽  
Atrial Septal Defect ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Septal Defect ◽  
Resistance Index ◽  
Partial Pressure Of Oxygen ◽  
Arterial Partial Pressure ◽  
Pulmonary Vascular Resistance Index

AbstractObjectivesTo examine the utility of decline in arterial partial pressure of oxygen after exercise as a marker of pulmonary vascular obstructive disease in patients with atrial septal defect and pulmonary hypertension.MethodsTreadmill exercise was performed in 18 patients with atrial septal defect and pulmonary hypertension. Arterial blood gas samples were obtained before and after peak exercise. A decline in the arterial pressure of oxygen of more than 10 millimetres of mercury after exercise was considered significant based on preliminary tests conducted on the controls. Cardiac catheterisation was performed in all patients and haemodynamic data sets were obtained on room air, oxygen, and a mixture of oxygen and nitric oxide (30–40 parts per million).ResultsThere were 10 patients who had more than a 10 millimetres of mercury drop in arterial partial pressure of oxygen after exercise and who had a basal pulmonary vascular resistance index of more than 7 Wood units per square metre. Out of eight patients who had less than a 10 millimetres of mercury drop in arterial partial pressure of oxygen after exercise, seven had a basal pulmonary vascular resistance index of less than 7 Wood units per square metre, p equals 0.0001. A decline in arterial partial pressure of oxygen of more than 10 millimetres of mercury predicted a basal pulmonary vascular resistance index of more than 7 Wood units per square metre with a specificity of 100% and a sensitivity of 90%.ConclusionsA decline in arterial partial pressure of oxygen following exercise appears to predict a high pulmonary vascular resistance index in patients with atrial septal defect and pulmonary hypertension. This test is a useful non-invasive marker of pulmonary vascular obstructive disease in this subset.

scholarly journals Effects of Pulmonary Vascular Resistance Index on Oxygen Saturation in Patients with Atrial Septal Defect

2020 ◽  
Vol 31 (1) ◽  
pp. 66
Author(s):  
Supomo Supomo
Keyword(s):  
Oxygen Saturation ◽  
Atrial Septal Defect ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Medical Records ◽  
Septal Defect ◽  
Resistance Index ◽  
Heart Catheterization ◽  
Pulmonary Vascular Resistance Index ◽  
The Right

<p>Atrial septal defect (ASD) is a congenital lesion in atrium septum. The lesion may cause pulmonary hypertension due to the high pressure in the right ventricle. This condition leads to cyanosis in ASD patient, but the pathophysiology of cyanosis in ASD patient is still unknown. This study aimed to identify the pathophysiology of cyanosis in ASD patients using the Pulmonary Vascular Resistance index (PVRi). The design of this study was retrospective cohort study. The data used in this study were the results of right heart catheterization procedure taken from forty ASD patient medical records at Dr. Sardjito general hospital. The exclusions criteria were the history of previous vasodilator administration and incomplete medical records. The median age of the patients was 30 (18-55) years old. The mean of the Qp/Qs ratio was 1.210 (0.57-6.33). Optimum oxygen saturation was found in vessel leaving the heart. The PVRi median is 61.98 (-15.58-676.64). The PVRi has a significant correlation with oxygen saturation, except in the right atrium. There is a significant correlation between PVRi and oxygen saturation in various heart chambers. Pathophysiology of cyanosis in ASD patients is central cyanosis.</p>

Abstract 13551: Invasive Hemodynamic Assessment of Cardiac Output State After MitraClip Therapy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Frantisek Bednar ◽  
Viktor Kocka ◽  
Tomas Budesinsky ◽  
Hana Linkova ◽  
Petr Tousek
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Output State ◽  
Regurgitant Flow ◽  
Hemodynamic Assessment ◽  
Risk Patients ◽  
Pulmonary Vascular Resistance Index ◽  
The Impact ◽  
Mitraclip Therapy

Introduction: MitraClip therapy has become a therapeutic alternative for high surgical risk patients with symptomatic mitral regurgitation (MR). There are limited data about early and no data about later hemodynamic consequences after MR correction and about the impact of elimination of regurgitant flow on cardiac output state . Methods: We studied invasive hemodynamic parameters before operation (conscious non-sedated patients, T1), immediately after MitraClip implantation (still under general anaesthesia, T2) and on day 1 (late) after procedure (conscious, extubated patients, T3) using right heart cathetrization. Results: Of 25 MitraClip patients (72% male; mean age 70y) with functional MR, in 20 were performed invasive measurements in all time points. MitraClip implantation resulted in an increase in cardiac index (CI) from 1.8±0.5 (T1) to 2.4±0.5(T2) and to 3.2±0.5 L/min/m2 (T3), in a decrease in systemic vascular resistance index (SVRI) from 3759±847 (T1) to 2508±551 (T2) and to 1679±360 dyn.s.cm-5/m2 (T3), in a decreese in pulmonary capillary wedge pressure (PCWP) from 17±5 (T1) to 13±5(T2) and to 10±4mmHg(T3), in a decrease in pulmonary vascular resistance index (PVRI) from 598±362 (T1) to 532±260 (T2) and to 363±184 dyn.s.cm-5/m2 (T3), (all p<0.05). Conclusion: MR reduction after successful MitraClip implantation significantly increases CI immediately (27%) and late (75%) and leads to concomitant decrease in SVRI, PVRI and PCWP immediately (33%, 11% and 25%) and late (55%, 39% and 41%) after procedure. No patients showed worsening of cardiac output state immediately (T2) and late (T3) after MR correction.

Endotracheal Administration of Tolazoline in Hypoxia-Induced Pulmonary Hypertension

PEDIATRICS ◽  
1993 ◽  
Vol 92 (3) ◽  
pp. 403-408
Author(s):  
Jerri Curtis ◽  
J. Timothy O'Neill ◽  
Gary Pettett
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Controlled Study ◽  
Control Group ◽  
Study Objective ◽  
Artery Pressure ◽  
Pulmonary Vascular Resistance Index ◽  
To Receive ◽  
Stabilization Period

Study objective. To compare the pulmonary and systemic vascular responses to intravenously (IV) and endotracheally (ET) administered tolazoline (Tz) in newborn lambs with hypoxia-induced pulmonary hypertension. Design. Randomized, controlled study design. Methods. Twenty lambs, 2 to 7 days of age, were anesthetized, intubated, and surgically catheterized for continuous physiologic monitoring and cardiac output meassurements using radiolabeled microspheres. After a postoperative stabilization period, the lambs were ventilated with a hypoxic gas mixture which was titrated to increase mean pulmonary artery pressure (MPAP) 30% to 50% above baseline. Each animal was randomly assigned to receive either IV-Tz (2 mg/kg), ET-Tz (4 mg/kg), or ET-saline (Sal, control group). Results. ET-Tz significantly (P &lt; .05) reduced MPAP, PVRI (pulmonary vascular resistance index), MPAP/mean artery pressure (MAP) and PVRI/systemic vascular resistance index (SVRI), but not SVRI. IV-Tz lowered (P &lt; .05) MPAP, PVRI, and PVRI/SVRI but also produced significant reductions in MAP and SVRI while only transiently decreasing MPAP/MAP. MPAP/MAP and PVRI/SVRI ratios were consistently lower in the ET-Tz animals than either the IV-Tz or ET-Sal animals. Conclusions. Our results suggest that ET-Tz produced a more selective pulmonary vascular response than IV-Tz and may warrant further investigation for potential clinical applications.

Pulmonary vascular resistance index and mortality after paediatric heart transplant

2014 ◽  
Vol 25 (6) ◽  
pp. 1141-1147 ◽  
Author(s):  
Bryan G. Maxwell ◽  
Ahmad Y. Sheikh ◽  
Chinwe C. Ajuba-Iwuji ◽  
Eugenie S. Heitmiller ◽  
Luca A. Vricella
Keyword(s):  
Confidence Interval ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Heart Transplant ◽  
Odds Ratio ◽  
Resistance Index ◽  
Continuous Variable ◽  
Receiver Operating Curve ◽  
Pulmonary Vascular Resistance Index ◽  
The Relationship

AbstractBackground: Although some prior studies have provided evidence to question the historical belief that pulmonary vascular resistance index ⩾6 Wood Units×m2 should be a contraindication to heart transplantation in children, no national analyses specific to the modern area have addressed this question. Methods: Data were analysed for paediatric heart transplant recipients from 1 January, 2002 to 1 September, 2012 (n=699). The relationship between pulmonary vascular resistance and all-cause 30-day mortality was evaluated using univariate and multivariate analyses. Results: The 30-day mortality included 10 patients (1.43%), which is lower than in the previous analyses. Receiver operating curve analysis of pulmonary vascular resistance index as a predictor of mortality yielded a cut-off value of 3.37 Wood Units×m2, but the area under the curve and specificity of this threshold was weaker than in previous analyses. Whereas pulmonary vascular resistance index treated as a dichotomised variable was a significant predictor of mortality in univariate (odds ratio 4.92, 95% confidence interval 1.04–23.33, p=0.045) and multivariate (odds ratio 5.26, 95% confidence interval 1.07–25.80, p=0.041) analyses, pulmonary vascular resistance index treated as a continuous variable was not a significant predictor of mortality in univariate (p=0.12) or multivariate (p=0.11) analyses. Conclusions: The relationship between pulmonary vascular resistance and post-heart transplant mortality in children is less convincing in this analysis of a comprehensive, contemporary database than in previous series. This suggests the possibility that modern improvements in the management of post-transplant right ventricular dysfunction have mitigated the contribution of pulmonary hypertension to early mortality.

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