Cardiac Protection (cardiac + protection)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Testosterone protects rat hearts against ischaemic insults by enhancing the effects of ,1 -adrenoceptor stimulation

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2008
S Tsang
Background and purpose: Testosterone alleviates symptoms in patients with ischaemic heart disease. Androgen receptors are present in the heart, and testosterone upregulates gene expression of cardiac ,1 -adrenoceptors. We hypothesize that testosterone may confer cardioprotection by interacting with adrenoceptors. Experimental approach: In isolated perfused hearts and ventricular myocytes from orchidectomized rats without or with testosterone (200 ,g/100 g) replacement, we first determined the effect of ischaemia/reperfusion in the presence of noradrenaline (10,7 M). Then we determined the contribution of interactions between testosterone and ,1 - or ,1 -adrenoceptors in cardiac injury/protection (infarct size, release of lactate dehydrogenase, viability of myocytes, recovery of contractile function and incidence of arrhythmias) upon ischaemia/reperfusion by pharmacological manipulation using selective adrenoceptor agonists (,1 -adrenoceptor agonist: phenylephrine 10,6 M; non-selective ,-adrenoceptor agonist: isoprenaline 10,7 M) and antagonists (,1: prazosin or benoxathian 10,6 M; ,1: CGP 20712A 5 × 10,7 M). We also determined the expression of ,1 and ,1 -adrenoceptor in the hearts from rats with and without testosterone. Key results: Testosterone reduced injury induced by ischaemia/reperfusion and noradrenaline. This was achieved by enhancing the beneficial effect of ,1 -adrenoceptor stimulation, which was greater than the deleterious effect of ,1 -adrenoceptor stimulation (also enhanced by testosterone). The effects of testosterone were abolished or attenuated by blockade of androgen receptors. Testosterone also enhanced the expression of ,1A and ,1 -adrenoceptor. Conclusions and implications: Testosterone conferred cardioprotection by upregulating the cardiac ,1 -adrenoceptor and enhancing the effects of stimulation of this adrenoceptor. The effect of testosterone was at least partly mediated by androgen receptors. British Journal of Pharmacology (2008) 153, 693,709; doi:10.1038/sj.bjp.0707624; published online 24 December 2007 [source]

Remote pharmacological post-conditioning by intrathecal morphine: cardiac protection from spinal opioid receptor activation

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2010
J. LING LING
Background: Intrathecal morphine pre-conditioning attenuates cardiac ischemia,reperfusion injury via activation of central opioid receptors. We hypothesized that intrathecal morphine also post-conditions the myocardium in the rat. Methods: Intrathecal morphine at 0.3 ,g/kg (LMPC), 3 ,g/kg (MMPC) or 30 ,g/kg (HMPC) was administered for 5 min before 120-min reperfusion following 30-min ischemia. Infarct size as a percentage of area at risk (IS/AAR) was determined using triphenyltetrazolium staining. MMPC was repeated following the intrathecal administration of nor BNI, NTD, CTOP, or naloxone methiodide (NM), kappa, delta, mu and non-specific opioid receptor antagonists, respectively. The role of peripheral opioid, adenosine and calcitonin gene-related peptide (CGRP) receptors was examined by the intravenous administration of NM, 8-,-sulfophenyl theophylline (8-SPT) and human CGRP fragment (CGRP8,37), respectively. Results: Morphine post-conditioning at all three doses was cardioprotective (IS/AAR of LMPC=37±4%, MMPC=35±5%, HMPC=32±4%, control=50±5%, P<0.01). The prior administration of opioid receptor antagonists intrathecally, as well as intravenous 8-SPT and CGRP8,37 receptor antagonists, abolished this effect (nor BNI+MMPC=47±7%, NTD+MMPC=49±7%, CTOP+MMPC=45±9%, NM+MMPC=47±6% 8-SPT+MPC=46±5% & CGRP8,37+MPC=53±6%, P=0.63). However, the intravenous administration of NM did not prevent the protective effect (34±4%, P<0.01). Conclusions: Intrathecal morphine administration can induce pharmacological cardiac post-conditioning as it involves opioid receptor centrally but non-opioid receptors peripherally. [source]

The Role of Intra-Aortic Counterpulsation in High-Risk OPCAB Surgery:

JOURNAL OF CARDIAC SURGERY, Issue 4 2003
A Prospective Randomized Study
This prospective and randomized study evaluates the efficacy and safety of pre- and perioperative IABC in high-risk OPCAB. Material: Group A,IABC started prior to induction of anesthesia (n = 15); group B,no preoperative IABC (n = 15). Adult high-risk coronary patients to undergo OPCAB. High risk = (minimum 2) EF < 0.30, left main stenosis, unstable angina, redo. Bailout if hemodynamic instability CPB or IABC in group B. Study endpoints (a) cardiac protection (troponin 1, cardiac index (CI), ECG), (b) inflammatory response (lactate, IL-6), (c) clinical outcome (mortality, morbidity). Emergency operations 33%, re-operation 13%, unstable angina 100%, left main 60% and EF 0.29, without group differences. Results: No bailout group A, 10 in group B, p < 0.0001. Postoperative IABC six (group A) and seven patients (group B), during 6.8 ± 5.1 hours (group A) versus 41.2 ± 25.5 hours (group B), p = 0.0110. Myocardial protection without group differences, but CI significantly better in group A. Inflammatory response significantly less in group A. Clinical outcomes: one death, one MI and two renal failure in group B, none in group A. Intensive care unit (ICU) stay 27 ± 3 hours (group A) versus 65 ± 28 hours (group B), p = 0.0017. LOS 8 ± 2 days (group A) versus 15 ± 10 (group B), p = 0.0351. No IABC related complications. Conclusions: Pre- and perioperative IABC therapy offers efficient hemodynamic support during high-risk OPCAB surgery, lowers the risk of hemodynamic instability, is safe and shortens both ICU and hospital length of stay significantly, and is a cost-effective therapy. (J Card Surg 2003; 18:286-294) [source]

Role of Endothelium/Nitric Oxide and Cyclic AMP in Isoproterenol Potentiation of 17ß-Estradiol-Mediated Vasorelaxation

JOURNAL OF CARDIAC SURGERY, Issue 6 2002
HY Chan
Estrogen exerts vasorelaxation and cardiac protection via multiple cellular mechanisms. Estrogen modifies vasodilatation induced by certain relaxants such as ß-adrenoceptor agonists. However, little is known whether low concentrations of ß-adrenoceptor agonists would also influence the acute relaxant response to estrogen. The present study was designed to investigate the synergistic interaction between isoproterenol and 17ß-estradiol, and to study the role of endothelium and cyclic AMP-dependent pathway in this interaction. Changes in vessel tone of the isolated rat mesenteric artery rings were measured by force-displacement Grass transducer. In 9,11-dideoxy-11,, 9,-epoxy-methanoprostaglandin F2, - preconstricted endothelium-intact rings, 17ß-estradiol induced concentration-dependent relaxation with pD2 of 5.074 ± 0.043. Pretreatment of endothelium-intact rings with isoproterenol (1-3 × 10 -9 M, 1-h incubation time) significantly enhanced 17,-estradiol-induced relaxation. Longer incubation (2.5 h) did not produce further amplifying effect. This effect was inhibited by Rp-cGMPS triethylamine (3 × 10 -6 M), and disappeared in the presence of 3 × 10 -5 M NG -nitro-L-arginine methyl ester or in the endothelium-denuded rings. The effect of isoproterenol was partially antagonized by propranolol (3 × 10 -6 M), ICI 118,551 (3 × 10 -6 M) but not by atenolol (10 -5 M). None of three ,-adrenoceptor antagonists affected 17ß-estradiol-induced relaxation in the absence of isoproterenol. Rp-cAMPS triethylamine (3 × 10 -6 M) abolished the effect of isoproterenol. Besides, exposure to 3 × 10 -9 M forskolin for 1 h also potentiated the relaxant response to 17,-estradiol. In summary, this isoproterenol enhancement was dependent on the presence of endothelium and abolished by L-NAME via a ,2 -adrenoceptor-mediated cyclic AMP-dependent mechanism. These data also indicate the possible existence of cyclic AMP-dependent nitric oxide-producing pathway in the regulation of the vascular response to vasodilators. (supported by UPGC Direct Grant) [source]

Audit of peri-operative cardiac protection in elective aortic aneurysm repair was successfully continued throughout the postoperative

ANAESTHESIA, Issue 4 2007
D. McIntosh
No abstract is available for this article. [source]

Comparison of high-density and low-density lipoprotein cholesterol subclasses and sizes in asian indian women with caucasian women from the framingham offspring study

CLINICAL CARDIOLOGY, Issue 5 2005
Narendra C. Bhalodkar M.D.
Abstract Background: Asian Indian women have a higher rate of coronary artery disease (CAD) than do other ethnic groups, despite similar conventional risk factors and lipid profiles. Smaller high-density lipoprotein cholesterol (HDL-C) particle size is associated with reduced cardiac protection or even an increased risk of CAD. Exceptional longevity correlates better with larger HDL-C particle sizes. Hypothesis: Higherrates of CAD among Asian Indian women may partly be explained by the differenes in the prevalence of atherogenic HDL-C and low-density lipoprotein cholesterol (LDL-C) sizes and their subclass concentrations among Asian Indian women compared with Caucasian women. Methods: We measured HDL-C concentrations and sizes by nuclear magnetic resonance spectroscopy in 119 relatively healthy Asian Indian women and compared them with those of 1,752 Caucasian women from the Framingham Off spring Study (FOS). Results: Asian Indian women were significantly younger (47.9 ± 11.2 vs.51.0 ± 10.1 years, p = 0.0001), leaner (body mass index 24.0 ± 4.7 vs. 26.0 ± 5.6, p = <0.0002), less likely to be postmenopausal (32 vs. 54%, p =< 0.0001), or smoke (< 1 vs. 20%, p = < 0.0001);nevertheless, prevalence of CAD was higher in Asian Indian women (4.2 vs. 1%, p = 0.0006). Asian Indian women had similar HDL-C (53 ±13 vs. 53 ± 13 mg/dl, p = 0.99), smaller HDL-C particle size (8.9 ± 0.35 vs. 9.4 ± 0.44 nm, p = < 0.0001), highertotal cholesterol (209 ± 40 vs. 199 ± 42 mg/dl, p = 0.01), and similar triglyceride (120 ± 77 vs. 108 ± 110 mg /d, p = 0.24) levels. Low-density lipoprotein cholesterol, particle concentrations and sizes, as well as prevalence of pattern B were similar. Conclusions: Compared with the FOS, Asian Indian women have significantly smaller overall HDL particle size and similar levels of HDL-C, which may reflect impaired, reverse cholesterol transport. Total cholesterol was higher, whereas triglyceride and LDL-C levels were similar. This may partly explain the higher CAD rates in Asian Indian women. Further large scale, prospective, long-term studies are warranted. [source]