Direct pulmonary vascular responses in the conscious newborn lamb

1980 ◽  
Vol 48 (1) ◽  
pp. 188-196 ◽  
Author(s):  
J. E. Lock ◽  
F. Hamilton ◽  
H. Luide ◽  
F. Coceani ◽  
P. M. Olley
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Vascular Effects ◽  
Flow Probe ◽  
Pulmonary Artery Flow ◽  
Artery Flow

Electromagnetic flow probes were placed around the right and left pulmonary arteries (RPA and LPA) of nine newborn lambs. Preliminary in vitro and in vivo experiments delineated the accuracy and limitations of this method of flow measurement and the value in vivo of a balloon occlusive zero. Six to nine days after surgery, catheters were placed in the aorta and a branch pulmonary artery permitting simultaneous measurements of RPA and LPA flow, pulmonary arterial pressure, and aortic pressure. Vasoactive agents were injected into one lung, and a shift in blood flow distribution reflected direct active vasoconstruction or vasodilation in that lung. With a normal arterial oxygen tension, acetylcholine had no direct effect on the pulmonary vessels, but indirectly lowered pulmonary resistance via its systemic effects. Histamine was a potent direct pulmonary vasoconstrictor, bradykinin was a weak direct dilator, norepinephrine was a direct constrictor, prostaglandin E1 was a direct dilator, and prostaglandin F2a was a direct constrictor. These results demonstrate the feasibility of isolating the direct pulmonary vascular effects of certain pharmacologic agents using a double pulmonary artery flow probe preparation, agents using a double pulmonary artery flow probe preparation, without the use of anesthetics or extracorporeal perfusion circuits.

Transcutaneous Oxygen Monitors Are Reliable Indicators of Arterial Oxygen Tension (If Used Correctly)

PEDIATRICS ◽  
1987 ◽  
Vol 79 (2) ◽  
pp. 283-286 ◽  
Author(s):  
G. ROOTH ◽  
A. HUCH ◽  
R. HUCH
Keyword(s):  
Premature Infants ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Term Infants ◽  
Transcutaneous Oxygen ◽  
Basic Understanding ◽  
Arterial Po2 ◽  
Transcutaneous Po2

The following recommendations should always be kept in mind: 1. Each new transcutaneous equipment, or modification of equipment, must be adequately tested in vivo as well as in vitro. 2. The users must have basic understanding of the principles and the major requirements for applying the tcPo2 technique. 3. Calibration procedures must be carefully adhered to according to the manufacturer's instruction. 4. The temperature of the electrode must be kept at 44°C for premature infants and at 44° or 45°C for term infants if the clinical aim is to estimate arterial Po2 levels. Resetting of the electrode must then be done every two hours. For sick infants, this may be needed more frequently. 5. Whenever there is cause to compare tcPo2 values with arterial ones, the latter must be obtained from an appropriate vessel. Great care must be taken when drawing and analyzing blood for Po2. The infant should not be crying. 6. Significantly lower transcutaneous Po2 values than arterial Po2 values are due to either one or several of the errors indicated above or to an insufficient circulation under the electrode. In recent years, technical or clinical errors seem to have become more and more common. Thereby the technique has unjustly fallen into disrepute. 7. Insufficient circulation under the electrode rarely occurs in the newborn infant and then only in those who are in overt shock.

scholarly journals Successful Transtracheal Lung Ventilation Using a Manual Respiration Valve

2008 ◽  
Vol 109 (2) ◽  
pp. 251-259 ◽  
Author(s):  
Konrad Meissner ◽  
Thomas Iber ◽  
Jan-Patrick Roesner ◽  
Christian Mutz ◽  
Hans-Erich Wagner ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Arterial Oxygen Tension ◽  
Upper Airway ◽  
Lung Ventilation ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Gas Flows ◽  
Partial Pressures

Background Lung ventilation through a thin transtracheal cannula may be attempted in patients with laryngeal stenosis or "cannot intubate, cannot ventilate" situations. It may be impossible to achieve sufficient ventilation if the lungs are spontaneously emptying only through the thin transtracheal cannula, which imposes high resistance to airflow, resulting in dangerous hyperinflation. Therefore, the authors describe the use of a manual respiration valve that serves as a bidirectional pump providing not only inflation but also active deflation of the lungs in case of emergency transtracheal lung ventilation. Methods The effectiveness of such a valve was tested in vitro using mechanical lungs in combination with two different cannula sizes and various gas flows. The valve was then tested in five pigs using a transtracheal 16-gauge cannula with three different combinations of inspiratory/expiratory times and gas flows and an occluded upper airway. Results In the mechanical lungs, the valve permitted higher minute volumes compared with spontaneous lung emptying. In vivo, the arterial oxygen and carbon dioxide partial pressures increased initially and then remained stable over 1 h (arterial oxygen tension, 470.8 +/- 86.8; arterial carbon dioxide tension, 63.0 +/- 7.2 mmHg). The inspiratory pressures measured in the trachea remained below 10 cm H2O and did not substantially influence central venous and pulmonary artery pressures. Mean arterial pressure and cardiac output were unaffected by the ventilation maneuvers. Conclusions This study demonstrated in vitro and in vivo in adult pigs that satisfactory lung ventilation can be assured with transtracheal ventilation through a 16-gauge cannula for a prolonged period of time if combined with a bidirectional manual respiration valve.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

In Vivo Retrieval of a Trapped Merci Embolectomy Device: Technical Case Report

2010 ◽  
Vol 67 (3) ◽  
pp. onsE304-onsE304 ◽  
Author(s):  
Ajeet Gordhan ◽  
John Soliman
Keyword(s):  
Vertebral Artery ◽  
Conformational Changes ◽  
Basilar Artery ◽  
Technical Note ◽  
Vessel Injury ◽  
Artery Segment ◽  
In Vitro Assessment ◽  
Artery Flow

Abstract BACKGROUND AND IMPORTANCE: This technical note describes a complication related to the use of the Merci embolectomy device not previously reported. The device can induce critical flow limitation within an accessed vessel because of a combination of vasospasm and anatomic conformational changes. Furthermore, this can limit the safe removal of the device from intracranial vasculature. We present a novel rescue technique that can be used to safely retrieve the entrapped Merci device without inciting localized vessel injury. CLINICAL PRESENTATION: A 51-year-old male with embolic occlusion of the distal basilar artery and dissection-related occlusion of the left cervical vertebral underwent mechanical thrombolysis. Flow-limiting vasospasm and/or anatomic conformational changes/ telescoping of the intracranial right vertebral artery segment was induced during deployment with subsequent entrapment of the device. Reclamation of the entrapped device was performed by initially removing the Merci microcatheter. The entrapped and fixated device was then resheathed into a 4F slip catheter within the intracranial vertebral artery. The Merci device and the slip catheter were then removed. Right vertebral and proximal basilar artery flow was reestablished after removal of the Merci device. Successful clot extraction was thereafter performed using a microsnare. CONCLUSION: In vitro assessment of the device has demonstrated its propensity to induce vasospasm. In vivo entrapment of the device has not been previously reported. Successful retrieval can be achieved if the Merci device becomes entrapped and fixated. This may be an important consideration as increased utilization of the device occurs.

Abstract 3570: A Critical and Novel Role of Nogo (Neurite Outgrowth Inhibitor) in Pulmonary Arterial Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Gopinath Sutendra ◽  
Sebastien Bonnet ◽  
Paulette Wright ◽  
Peter Dromparis ◽  
Alois Haromy ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Nuclear Translocation ◽  
Pulmonary Arteries ◽  
Over Expression ◽  
Nfat Activation ◽  
Pulmonary Arterial ◽  
Systemic Arteries

Nogo was first identified as an inhibitor of neuronal axonal regeneration. Recently, Nogo-B was implicated in the proliferative and anti-apoptotic remodeling in systemic arteries; reduced Nogo-B expression was seen in remodeled mouse femoral arteries following injury. Pulmonary arterial hypertension (PAH) is also characterized by proliferative/anti-apoptotic remodeling in pulmonary arteries (PA), sparing systemic vessels. PAH PA smooth muscle cells (PASMC) are characterized by mitochondrial hyperpolarization (increased ΔΨm), decreased production of reactive oxygen species (ROS) (suppressing mitochondria-dependent apoptosis), down-regulation of Kv1.5 and activation of the transcription factor NFAT (promoting contraction and proliferation). We found that in contrast to systemic vessels, Nogo-B expression is significantly increased in vivo and in vitro in PAs and PASMCs from patients (n=6) and mice (n=42) with PAH, compared to normals. We hypothesized that Nogo is involved in the pathogenesis of PAH . Nogo −/− mice (n=7) had a normal phenotype and, in contrast to Nogo +/+ , did not develop chronic hypoxia (CH)-induced PAH assessed invasively (catheterization, RV/LV+Septum) and non-invasively (pulmonary artery acceleration time and treadmill performance) (n=7, Table ). CH- Nogo +/+ PASMC had the expected increase in ΔΨm (measured by TMRM), decreased ROS (MitoSOX), increased [Ca ++ ] i (FLUO3), decreased Kv1.5 (immunohistochemistry) and NFAT activation (nuclear translocation). None of these changes occurred in CH- Nogo −/− PASMC while all were induced in normoxic Nogo +/+ PASMC by adenoviral over-expression of Nogo-B . Heterozygote CH- Nogo +/− (n=7) values were between Nogo −/− and Nogo +/+ suggesting a gene dose-dependent effect. Nogo is over-expressed in human and rodent PAH and induces critical features of the PAH phenotype. Nogo targeting might represent a novel and selective therapeutic strategy for PAH. Table

Utility of the Medtronic microvascular plug™ as a transcatheter implantable and explantable pulmonary artery flow restrictor in a swine model

2019 ◽  
Vol 93 (7) ◽  
pp. 1320-1328 ◽  
Author(s):  
Abdul H. Khan ◽  
Deepthi Hoskoppal ◽  
T. K. Susheel Kumar ◽  
Lindsey Bird ◽  
Kimberly Allen ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Swine Model ◽  
Pulmonary Artery Flow ◽  
Artery Flow
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