Protection against L‐<scp>NAME</scp>‐induced reduction in cardiac output persists even after cessation of angiotensin‐converting enzyme inhibitor treatment

Biwer, Lauren A; Xu, Haodong; Carroll, Chad C.; Hale, Taben M.

doi:10.1111/j.1748-1716.2012.02474.x

Cited by 18 publications

(11 citation statements)

References 44 publications

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“…This finding is in agreement with those of several studies, which have indicated that L-NAME decreases the CO in a normal level of Hct either in the short-term or long-term treatments with L-NAME 25)27)28). Furthermore, in this study, the L-NAME administration led to a reduction in SV even after hemodilution.…”

Section: Discussionsupporting

confidence: 94%

“…By administration through a coronary catheter, using non-selective NOS inhibitors such as N-nitro-L-arginine (L-NNA) in normal dogs an increment in the coronary blood flow was shown 29). In contrast, Biwer et al28) demonstrated that long-term L-NAME-treated rats had not only a decrease in CO and SW but also a decrease in coronary blood flow, which potentially caused cardiac dysfunction. Therefore, it is a point of concern that using PEs in hemodilution with a stage of NOS impairment can lead to an attenuation of the cardiac compensatory mechanism.…”

Section: Discussionmentioning

confidence: 99%

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Nitric Oxide Synthase Inhibition Attenuates Cardiac Response to Hemodilution with Viscogenic Plasma Expander

Chatpun

Cabrales

2014

Korean Circ J

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IntroductionFlow-induced shear stress plays a central role on endothelial response and mechano-signal transduction in the cardiovascular system. The mechanical shear force stimulates endothelial protein ac- Background and Objectives: Increased vascular wall shear stress by elevated plasma viscosity significantly enhances the endothelial nitric oxide synthase (eNOS) activity during an acute isovolemic hemodilution. Also the modulation of plasma viscosity has effects on the cardiac function that were revealed if a left ventricular (LV) pressure-volume (PV) measurement was used. The aim of this study was to assess cardiac function responses to nitric oxide synthase (NOS) inhibitors with the presence of an elevated plasma viscosity but a low hematocrit level. Furthermore, systemic parameters were monitored in a murine model. Original Article Materials and Methods:As test group five anesthetized hamsters were administered with N(G)-nitro-L-arginine methyl ester (L-NAME), NOS inhibitor, whereas five other hamsters were used as control group without L-NAME infusion. The dosage of L-NAME was 10 mg/kg. An isovolemic hemodilution was performed by 40% of estimated blood volume with 6% w/v dextran 2000 kDa, high viscosity plasma expanders (PEs) with viscosity 6.34 cP. LV function was measured and assessed using a 1.4 Fr PV conductance catheter. Results:The study results demonstrated that NOS inhibition prevented the normal cardiac adaptive response after hemodilution. The endsystolic pressure increased 14% after L-NAME infusion and maintained higher than at the baseline after hemodilution, whereas it gradually decreased in the animals without L-NAME infusion. The admission of L-NAME significantly decreased the maximum rate of ventricular pressure rise (+dP/dtmax), stroke volume and cardiac output after hemodilution if compared to the control group (p<0.05). Conclusion:This finding supports the presumption that nitric oxide induced by an increased plasma viscosity with the use of a high viscosity PE plays a major role in the cardiac function during an acute isovolemic hemodilution. (Korean Circ J 2014;44(2):105-112)

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Synthase Inhibition Attenuates Cardiac Response to Hemodilution with Viscogenic Plasma Expander

Chatpun

Cabrales

2014

Korean Circ J

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“…This could be due to species differences or that the vessels used in the present study are from more distal regions of the vasculature or that the transient nature in vivo is caused by a stimulus which is not present in the ex vivo setting. This opportunity to study ANG II vasoregulation ex vivo may be valuable, as its blockade prevents the chronic effects of long-term nitric oxide synthase inhibition (Biwer et al 2013), a fascinating phenomenon which has also been observed in the kidney (Helle et al 2009(Helle et al , 2010. We were able to harvest about 10 arterioles from each dissected right ventricle; all positively identified as pre-capillary by attached capillaries.…”

Section: Discussionmentioning

confidence: 99%

A low‐cost, scalable technique to study distal coronary arteriole function

2014

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“…That is, a transient ACE inhibitor treatment induced protective effects that persisted even after stopping treatment and restoration of the renin-angiotensin system. Importantly, NOS inhibition induced focal regions of cardiomyocyte loss as well as coronary artery injury in both naïve and previously treated rats (3). Thus, the reduction in inflammation and fibrosis in rats previously treated with an ACE inhibitor appears to reflect a modified response to myocardial injury.…”

mentioning

confidence: 86%

“…It has thus been suggested that targeting fibroblast survival may be a mechanism by which these drugs are effective in limiting cardiac fibrosis. We have shown that prior transient (i.e., 2-wk treatment followed by a 2-wk washout period) ACE inhibition in young adult male SHRs to be protected against a future cardiac insult induced by the nonspecific NOS inhibitor N -nitro-L-arginine methyl ester (L-NAME) (3,13). This protection was characterized by a preservation of cardiac output (3), a reduction in outer wall collagen deposition, and decreased densities of proliferating cells and macrophages in the LVs of rats that had been previously treated with an ACE inhibitor (13).…”

mentioning

confidence: 99%

Persistent change in cardiac fibroblast physiology after transient ACE inhibition

D’Souza

Biwer

Madhavpeddi

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Transient angiotensin-converting enzyme (ACE) inhibition induces persistent changes that protect against future nitric oxide synthase (NOS) inhibitor-induced cardiac fibrosis and inflammation. Given the role of fibroblasts in mediating these effects, the present study investigates whether prior ACE inhibition produced persistent changes in cardiac fibroblast physiology. Adult male spontaneously hypertensive rats (SHRs) were treated with vehicle (C+L) or the ACE inhibitor, enalapril (E+L) for 2 wk followed by a 2-wk washout period and a subsequent 7-day challenge with the NOS inhibitor N(ω)-nitro-l-arginine methyl ester. A third set of untreated SHRs served as controls. At the end of the study period, cardiac fibroblasts were isolated from control, C+L, and E+L left ventricles to assess proliferation rate, collagen expression, and chemokine release in vitro. After 7 days of NOS inhibition, there were areas of myocardial injury but no significant change in collagen deposition in E+L and C+L hearts in vivo. In vitro, cardiac fibroblasts isolated from C+L but not E+L hearts were hyperproliferative, demonstrated increased collagen type I gene expression, and an elevated secretion of the macrophage-recruiting chemokines monocyte chemoattractant protein-1 and granulocyte macrophage-colony stimulating factor. These findings demonstrate that in vivo N(ω)-nitro-l-arginine methyl ester treatment produces phenotypic changes in fibroblasts that persist in vitro. Moreover, this is the first demonstration that transient ACE inhibition can produce a persistent modification of the cardiac fibroblast phenotype to one that is less inflammatory and fibrogenic. It may be that the cardioprotective effects of ACE inhibition are related in part to beneficial changes in cardiac fibroblast physiology.

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Protection against L‐NAME‐induced reduction in cardiac output persists even after cessation of angiotensin‐converting enzyme inhibitor treatment

Cited by 18 publications

References 44 publications

Nitric Oxide Synthase Inhibition Attenuates Cardiac Response to Hemodilution with Viscogenic Plasma Expander

Nitric Oxide Synthase Inhibition Attenuates Cardiac Response to Hemodilution with Viscogenic Plasma Expander

A low‐cost, scalable technique to study distal coronary arteriole function

Persistent change in cardiac fibroblast physiology after transient ACE inhibition

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