Long-term Continuous Intravenous Infusion of Prostacyclin for Severe Primary Pulmonary Hypertension.

Okano, Yoshiaki; Senju, Shoji; Tsutsui, Yasuhiro; Kyotani, Shingo; Ishibashi, Masayoshi; Yoshida, Minoru; Kunieda, Takeyoshi

doi:10.2169/internalmedicine.36.794

Intern. Med.

1997

DOI: 10.2169/internalmedicine.36.794

|View full text |Cite

Long-term Continuous Intravenous Infusion of Prostacyclin for Severe Primary Pulmonary Hypertension.

Yoshiaki Okano¹,

Shoji Senju

Yasuhiro Tsutsui

et al.

Abstract: patient suffering from severe symptomatic primary pulmonary hypertension (PPH) underwent long-term intravenous prostacyclin therapy; the first time for such treatment in Japan. A 26-year-old male had experienced gradually progressive dyspnea for about one year. Despite conventional therapy he suffered repeated syncopal attacks. However, after receiving a permanent central venous access device and a portable infusion pump, he recovered fully and was discharged. This remedy seems to be promising for PPHas has al… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

1999

2013

Publication Types

Select...

Article5

Relationship

Self Cite0

Independent5

Authors

Journals

Cited by 5 publications

(2 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…If no desirable effect is obtained with these medications, we have to consider continuous intravenous infusion of the PGI 2 derivative sodium epoprostenol. 7,8) Meanwhile, a dual endothelin receptor antagonist, bosentan, has been available in Japan since 2005. 9) We report a case of IPAH in which repetitive syncope was successfully treated by bosentan.…”

mentioning

confidence: 99%

Bosentan Improved Syncope in a Hemodialysis Patient With Pulmonary Hypertension and Mild Aortic Stenosis

et al. 2006

View full text Add to dashboard Cite

SUMMARYPulmonary arterial hypertension (PAH), caused by collagen diseases, Eisenmenger syndrome or of idiopathic etiology, generally has a poor prognosis. Recently, bosentan, a dual endothelin receptor antagonist, has become available for treating PAH. This report describes a bosentan-effective case of combined PAH, hemodialysis and mild aortic stenosis. A 71-year-old woman on hemodialysis was referred to our hospital because of repetitive syncope. Although neurological examinations revealed no etiological diseases, echocardiography and cardiac catheterization showed PAH and mild aortic valve stenosis. Bosentan abolished syncope with improvement of hemodynamic parameters. This report suggests bosentan was clinically useful in a hemodialysis patient with pulmonary hypertension and mild aortic valve stenosis. (Int Heart J 2006; 47: 911-917)

show abstract

mentioning

confidence: 99%

Bosentan Improved Syncope in a Hemodialysis Patient With Pulmonary Hypertension and Mild Aortic Stenosis

et al. 2006

View full text Add to dashboard Cite

show abstract

“…This condition predominantly affects females in the third decade of life, and has a mean survival of less than three years from the time of diagnosis (15,16). At present, few satisfactory long-term treatment options other than lung transplantation (17,18) are available; and the principal therapy, continuous intravenous infusion of prostacyclin derivatives (19)(20)(21)(22), is associated with significant morbidity (22)(23)(24). The underlying etiology of PPH remains unclear, however several groups have suggested that endothelial dysfunction associated with a decrease in expression or biologic activity of the vasodilator nitric oxide synthase (NOS), either alone or in combination with the overexpression of the potent vasoconstrictor endothelin (25)(26)(27)(28)(29)(30)(31)(32)(33), plays a critical role.…”

mentioning

confidence: 99%

Cell-Based Gene Transfer to the Pulmonary Vasculature

Campbell

Kuliszewski²,

Stewart³

1999

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

To circumvent the problems of in vivo transfection and avoid the use of viral vectors or proteins, we sought to establish whether smooth-muscle cells (SMCs) transfected ex vivo could be delivered via the systemic venous circulation into the pulmonary bed to achieve local transgene expression in the lung. Primary cultures of pulmonary artery SMCs from Fisher 344 rats were labeled with a fluorescent, membrane-impermeable dye chloromethyl trimethyl rhodamine or transfected with the beta-galactosidase (betaGal) reporter gene under the control of the cytomegalovirus (CMV) enhancer/promoter (pCMV-beta). Transfected or labeled SMCs (5 x 10(5) cells/animal) were delivered to syngeneic recipient rats by injection into the jugular vein; the animals were killed at intervals between 15 min and 2 wk; and the lungs, spleens, kidneys, and skeletal muscle were excised and examined. At 15 min after transplantation, injected cells were detected mainly in the lumen of small pulmonary arteries and arterioles, often in groups of three or more cells. After 24 h, labeled SMCs were found incorporated into the vascular wall of pulmonary arterioles, and transgene expression persisted in situ for 14 d with no evidence of immune response. Using simple geometric assumptions, it was calculated that approximately 57 +/- 5% of the labeled cells reintroduced into the venous circulation could be identified in the lungs after 15 min, 34 +/- 7% at 48 h, 16 +/- 3% at 1 wk, and 15 +/- 5% at 2 wk. Similar results were observed using cells transfected with the reporter gene betaGal. To determine whether this method of gene transfer could prove effective in inhibiting the development of pulmonary vascular disease, pulmonary artery SMCs were transfected with either the full-length coding sequence of endothelial nitric oxide synthase (NOS) under the control of the CMV enhancer/promoter or with the control vector (pcDNA3.1) and injected simultaneously with the pulmonary endothelial toxin monocrotaline. At 28 d after injection the right ventricular systolic pressure was significantly decreased from 50 +/- 4 mm Hg in animals injected with the null-transfected cells to 33 +/- 3 mm Hg in animals injected with the NOS-transfected cells (P < 0.01). These results suggest that a cell-based strategy of ex vivo transfection may provide an effective nonviral approach for the selective delivery of foreign transgenes to pulmonary microvessels in the treatment of pulmonary vascular disease.

show abstract

Gene therapies for pulmonary hypertension—from experimental trials to bedside aspects

Meng

Liu

2009

European Journal of Cardio-Thoracic Surgery

View full text Add to dashboard Cite

Accompanying the continuously deepening understanding of the mechanism of pulmonary hypertension that many genes are found to be aetiologically involved in its development, burgeoning literature manifest that gene therapies aimed at correcting these genetic defects have the ability to restore deficient pulmonary gene expression, over-express biologically active gene products, reverse established disease and regenerate pulmonary vasculature, and may constitute a promising therapeutic strategy for pulmonary hypertension. Therefore, to provide new information to basic scientists and clinical investigators, we present a review that attempts a clear description of the therapeutic potential of gene therapy in the treatment of pulmonary hypertension.

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Long-term Continuous Intravenous Infusion of Prostacyclin for Severe Primary Pulmonary Hypertension.

Cited by 5 publications

References 19 publications

Bosentan Improved Syncope in a Hemodialysis Patient With Pulmonary Hypertension and Mild Aortic Stenosis

Bosentan Improved Syncope in a Hemodialysis Patient With Pulmonary Hypertension and Mild Aortic Stenosis

Cell-Based Gene Transfer to the Pulmonary Vasculature

Gene therapies for pulmonary hypertension—from experimental trials to bedside aspects

Contact Info

Product

Resources

About