Catheterization of pulmonary artery in rats with an ultraminiature catheter pressure transducer

Deten, Alexander; Millar, Huntly; Zimmer, Heinz‐Gerd

doi:10.1152/ajpheart.00315.2003

Cited by 24 publications

(22 citation statements)

References 21 publications

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“…In our hemodynamic measurements, the measured values of PASP and PADP in normal rats were about 36 and 18 mmHg, respectively, which was near the reported values that the PASP and PADP in rats were 34 and 24 mmHg, respectively. 22) Similar values were reported by van Albada et al 23) However, some other investigators reported that the PASP was 21 mmHg and the PADP was 10 mmHg in rats, respectively.…”

Section: Discussionsupporting

confidence: 83%

G.ALPHA.q-Protein Carboxyl Terminus Imitation Polypeptide (GCIP)-27 Inhibits Right Ventricular Hypertrophy Induced by Monocrotaline in Rats

Yang

Zhang

et al. 2009

Biological & Pharmaceutical Bulletin

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Right ventricular (RV) remodeling has been associated with many diseases, such as pulmonary hypertension (PH), left ventricular (LV) pathology, Chagas' disease, and arrhythmogenic right ventricular cardiomyopathy, in which the disease progression may lead to further right ventricle (RV) changes, including hypertrophy, dilatation, and subsequently to variable alterations in RV hemodynamic status. 1) Although the proportionately limited information is related to RV function, its impairment in various disease states, and its impact on the outcome of those diseases suggests that the RV is an important contributor and that further understanding of these issues is of pivotal importance.2)It has been well known that some Gq protein-coupled receptor agonists, such as angiotensin II (Ang II), endothelin-1 (ET-1) and phenylephrine can trigger hypertrophic responses in cultured myocytes, 3,4) and transgenic mice with cardiac overexpression of Gaq present with myocardial hypertrophy. 5)The facts are consistent with the conclusion that in the signal transduction pathway inducing cardiac hypertrophy, the Gq protein and its downstream effectors play a key role, 6) and Gq protein Gaq is thought to locate at the convergent point in the signal transduction pathway leading to cardiac hypertrophy. 7,8) Although some anti-hypertension agents can alleviate cardiac hypertrophy to some extent, the effects of these drugs with a single target are limited, 9) due to the compensatory role of other factors. Theoretically, an inhibition on the Gq signaling pathway may have more satisfactory effect on the cardiac hypertrophy therapy. In the a-subunit of heterotrimetic G-protein, the carboxyl terminus is surface exposed and, thus, easily accessible for contacting the receptor protein, 10) so the C-terminal portion of Ga is critical for the specificity of G-protein-coupled receptor.11) Therefore, to inhibit Gaq signaling may be an approach to prevent cardiac hypertrophy from overloaded pressure and other pathological stimuli. 12)Gaq protein carboxyl terminus imitation polypeptide (GCIP), a peptide cloned and constructed in our laboratory previously, could inhibit the cardiomyocyte hypertrophy induced by noradrenaline (NA) in rats through acting as a competition candidate of the activated binding sites on Gaq. 13)GCIP-27, the optimized form of GCIP, could inhibit the left ventricular (LV) hypertrophy induced by NA in mice and induced by the aortic stenosis in rats, 14) and could also inhibit the LV remodeling in spontaneously hypertensive rats.15) In addition, GCIP-27 could also prevent the hypertrophic responses in cultured rat cardiomyocytes induced by NA or Ang II.14) However, little is known about the effect of GCIP-27 on RV hypertrophy. Because the pathophysiology of RV remodeling is a complex process and may include unique elements not observed in LV remodeling, and the structure and function between the two chambers are very different, 1) it is necessary to characterize the effect of GCIP-27 on the RV remodeling. The present work is desig...

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Section: Discussionsupporting

confidence: 83%

G.ALPHA.q-Protein Carboxyl Terminus Imitation Polypeptide (GCIP)-27 Inhibits Right Ventricular Hypertrophy Induced by Monocrotaline in Rats

Yang

Zhang

et al. 2009

Biological & Pharmaceutical Bulletin

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“…Two force‐designated groups of 4 valves each were studied—either Cycling and Open, or Cycling and Closed conditions—within a single culture experiment, keeping all other variables common. The rate of fluid flow through each Cycling valve graft was adjusted to achieve a complete valve cycle function at a moderate cycle rate (80 bpm; compared with ≈350‐bpm normal rat heart rate) under a flow rate that approximated the known right ventricular stroke volume (160 μL) of the rat heart5, 6 and a pressure cycle (5–28 mm Hg). Flow rate was monitored with inline ultrasonic flow probes (Transonic Systems Inc., Ithaca, NY).…”

Section: Methodsmentioning

confidence: 99%

Critical Role of Coaptive Strain in Aortic Valve Leaflet Homeostasis: Use of a Novel Flow Culture Bioreactor to Explore Heart Valve Mechanobiology

Maeda

Chalajour

et al. 2016

JAHA

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BackgroundAortic valve (AV) disease presents critical situations requiring surgery in over 2% of the US population and is increasingly the reason for cardiac surgery. Throughout the AV cycle, mechanical forces of multiple types and varying intensities are exerted on valve leaflets. The mechanisms whereby forces regulate leaflet homeostasis are incompletely understood. We used a novel flow bioreactor culture to investigate alteration of AV opening or closure on leaflet genes.Methods and ResultsCulture of rat AV was conducted in a flow bioreactor for 7 days at 37°C under conditions approximating the normal stroke volume. Three force condition groups were compared: Cycling (n=8); always open (Open; n=3); or always closed (Closed; n=5). From each culture, AV leaflets were pooled by force condition and RNA expression evaluated using microarrays. Hierarchical clustering of 16 transcriptome data sets from the 3 groups revealed only 2 patterns of gene expression: Cycling and Closed groups clustered together, whereas Open AV were different (P<0.05). Sustained AV opening induced marked changes in expression (202 transcripts >2‐fold; P<0.05), whereas Closed AV exhibited similar expression pattern as Cycling (no transcripts >2‐fold; P<0.05). Comparison with human sclerotic and calcific AV transcriptomes demonstrated high concordance of >40 Open group genes with progression toward disease.ConclusionsFailure of AV to close initiates an extensive response characterized by expression changes common to progression to calcific aortic valve disease. AV coaptation, whether phasic or chronic, preserved phenotypic gene expression. These results demonstrate, for the first time, that coaptation of valve leaflets is a fundamentally important biomechanical cue driving homeostasis.

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“…Systemic arterial pressure (SAP) was measured in the left carotid artery with a PDP-400 pressure transducer. Another transducer of the same model was used to record pulmonary arterial pressure (PAP) in pulmonary artery via a 1.5 mm catheter passed into arterial lumen across the anterior wall of the right ventricle [6]. The left atrial pressure was measured with a Baxter pressure transducer via a catheter passed into the atrium through its auricle.…”

Section: Methodsmentioning

confidence: 99%

Changes in Pulmonary Hemodynamics Induced by Experimental Myocardial Ischemia in Nitroglycerin- or Acetylcholine-Treated Rabbits

Evlakhov

Poyasov

2014

Bull Exp Biol Med

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The responses of cardiovascular parameters to left-ventricular myocardial ischemia induced under control conditions and after administration of nitroglycerin or acetylcholine were examined in rabbits. In nitroglycerine-treated rabbits, experimental myocardial ischemia produced less pronounced depressor BP shifts in the pulmonary artery than those produced by ischemia in controls (prior to pharmacological treatment) or by experimental ischemia provoked after acetylcholine infusion. Control and experimental ischemia (provoked after nitroglycerin or acetylcholine administration) induced the same drop in pulmonary blood fl ow accompanied with insignificant changes in vascular pulmonary resistance. Experimental ischemia produced smaller pressure increase in left atrium of nitroglycerine-treated rabbits (evidencing a smaller drop in left ventricular contractility) than the control ischemia performed prior to pharmacological treatment, or the experimental ischemia in acetylcholine-treated rabbits, which attested to protective effect of nitroglycerin against ischemia.

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Catheterization of pulmonary artery in rats with an ultraminiature catheter pressure transducer

Cited by 24 publications

References 21 publications

G.ALPHA.q-Protein Carboxyl Terminus Imitation Polypeptide (GCIP)-27 Inhibits Right Ventricular Hypertrophy Induced by Monocrotaline in Rats

G.ALPHA.q-Protein Carboxyl Terminus Imitation Polypeptide (GCIP)-27 Inhibits Right Ventricular Hypertrophy Induced by Monocrotaline in Rats

Critical Role of Coaptive Strain in Aortic Valve Leaflet Homeostasis: Use of a Novel Flow Culture Bioreactor to Explore Heart Valve Mechanobiology

Changes in Pulmonary Hemodynamics Induced by Experimental Myocardial Ischemia in Nitroglycerin- or Acetylcholine-Treated Rabbits

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