Transient receptor potential vanilloid 1 inhibitors block laparotomy‐ and opioid‐induced infarct size reduction in rats

Heymann, Helen; Wu, Yun; Lu, Yao; Qvit, Nir; Gross, Garrett J.; Gross, Eric R.

doi:10.1111/bph.14064

Cited by 21 publications

(21 citation statements)

References 53 publications

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“…Morphine, a major analgesic drug used to alleviate severe pain accompanied with AMI, was shown to protect the heart against I/R injury, and this protection was partially mediated by TRPV1 receptors since TRPV1 receptor antagonists (capsazepine or P5, a peptide analgesic and TRPV1 inhibitor), prior to coronary occlusion, abrogated the cardioprotective effects of morphine [ 88 ].…”

Section: The Capsaicin-sensitive Sensory Nerves and The Trpv1 Recementioning

confidence: 99%

Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies

Szabados

Gömöri

Pálvölgyi

et al. 2020

IJMS

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Cardiovascular diseases, including coronary artery disease, ischemic heart diseases such as acute myocardial infarction and postischemic heart failure, heart failure of other etiologies, and cardiac arrhythmias, belong to the leading causes of death. Activation of capsaicin-sensitive sensory nerves by the transient receptor potential vanilloid 1 (TRPV1) capsaicin receptor and other receptors, as well as neuropeptide mediators released from them upon stimulation, play important physiological regulatory roles. Capsaicin-sensitive sensory nerves also contribute to the development and progression of some cardiac diseases, as well as to mechanisms of endogenous stress adaptation leading to cardioprotection. In this review, we summarize the role of capsaicin-sensitive afferents and the TRPV1 ion channel in physiological and pathophysiological functions of the heart based mainly on experimental results and show their diagnostic or therapeutic potentials. Although the actions of several other channels or receptors expressed on cardiac sensory afferents and the effects of TRPV1 channel activation on different non-neural cell types in the heart are not precisely known, most data suggest that stimulation of the TRPV1-expressing sensory nerves or stimulation/overexpression of TRPV1 channels have beneficial effects in cardiac diseases.

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Section: The Capsaicin-sensitive Sensory Nerves and The Trpv1 Recementioning

confidence: 99%

Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies

Szabados

Gömöri

Pálvölgyi

et al. 2020

IJMS

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“…Myocardial ischemia and reperfusion injury model used in this study have been described in detail previously. 15,16,19 Anesthesia was induced in the animals by intraperitoneal administration of pentobarbitone (50 mg/kg) and when required, supplemented by doses of 25 mg/kg at 60 to 90 minutes intervals. A tracheostomy was performed, using a tube made from polyethylene that is then connected to an animal respirator.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…Previous studies have suggested that direct TRPV1 activation could produce cardioprotective effects against myocardial ischemia and reperfusion injury. [14][15][16] Animal models suggest TRPV1 inhibition blocks IPC-induced cardioprotection, suggesting blockade of the channel for pain relief may abrogate an endogenous cardioprotective mechanism. However, excessive TRPV1 stimulation also results in cell death.…”

Section: F I G U R E 3 Determination Of Trpv1 Expression Inmentioning

confidence: 99%

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The timing of propofol administration affects the effectiveness of remote ischemic preconditioning induced cardioprotection in rats

Chen

Wang

et al. 2020

J of Cellular Biochemistry

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The cardioprotection of remote ischemic preconditioning (RIPC) is abolished under propofol maintained anesthesia. Transient receptor potential vanilloid 1 (TRPV1) channel is present in the heart, and its activation could induce cardioprotection. Therefore, we tested whether the anesthetic propofol administration phase interfered with the RIPC‐induced cardioprotection, and RIPC‐induced cardioprotection via the cardiac TRPV1 channel. Male Sprague‐Dawley rats were subjected to myocardial 30 minutes of ischemia followed by 2 hours of reperfusion. RIPC consisted of three cycles of 5‐minute ischemia/reperfusion applied to a hindlimb. Propofol infusion at 12 mg/kg/h was commenced either at 10 minutes before the start of RIPC in the P‐pre + RIPC group, or immediately after myocardial ischemia at the onset of reperfusion (P‐post + RIPC) while performing RIPC. These two propofol infusion regimes were applied to another two grou bs without RIPC (P‐pre and P‐post groups). Infarct size (IS) was assessed by triphenyltetrazolium staining. Heart TRPV1 expression was detected by Western blot and immunofluorescence. RIPC significantly reduced myocardial IS compared with the control group (36.7 ± 3% versus 57.2 ± 4%; P < .01). When propofol was started before RIPC, the IS sparing effect of RIPC was completely abolished. However, propofol infusion starting immediately after myocardial ischemia did not affect RIPC‐induced cardioprotection. TRPV1 expression significant increase after RIPC, then propofol inhibited the TRPV1 activation of RIPC if given before RIPC but not after. Our results suggest that the timing of propofol administration is critical to preserve the cardioprotection of RIPC. Propofol might cancel RIPC‐induced cardioprotection via the cardiac TRPV1 receptor.

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“…The recent paper by Heymann et al . () explores this important interface: the central and peripheral implications of pain management, on the one end to eliminate pain and on the other to insure that peripheral organs are not detrimentally impacted. Opioids were thought to be the magic bullet to positively impact both systems; however, given the current opioid crisis with increasing levels of addiction and misuse, there is a call within the pain management community to develop alternatives to opioids for pain management.…”

Section: Nomenclature Of Targets and Ligandsmentioning

confidence: 99%

No pain, no gain: balancing central versus peripheral benefits of analgesics in the age of the opioid crisis

Patel

Roth

2018

British J Pharmacology

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Transient receptor potential vanilloid 1 inhibitors block laparotomy‐ and opioid‐induced infarct size reduction in rats

Abstract: Inhibiting the TRPV1 channel blocks laparotomy- or morphine-induced cardioprotection. Impaired organ protection may be a potential pitfall of using TRPV1 inhibitors for pain control.

Cited by 21 publications

References 53 publications

Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies

Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies

The timing of propofol administration affects the effectiveness of remote ischemic preconditioning induced cardioprotection in rats

No pain, no gain: balancing central versus peripheral benefits of analgesics in the age of the opioid crisis

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