Extent of ischemic stimulus and plasma β-endorphin levels in silent myocardial ischemia

Hikita, Hiroyuki; Etsuda, Hirokuni; Takase, Bonpei; Satomura, Kimio; Kurita, Akira; Nakamura, Haruo

doi:10.1016/s0002-8703(98)70039-0

Cited by 15 publications

(8 citation statements)

References 20 publications

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“…Changes in E levels were not associated with the presence or absence of pain during exercise-induced myocardial ischemia (Heller et al 1987). Elevation of E level was observed in patients with coronary heart disease during "silent myocardial ischemia" induced by exertion (Hikita et al 1998).…”

Section: The Evect Of Exercise In Various Diseasesmentioning

confidence: 94%

The effect of physical therapy on beta-endorphin levels

Bender¹,

Nagy²,

Barna

et al. 2007

Eur J Appl Physiol

115

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Beta-endorphin (betaE) is an important reliever of pain. Various stressors and certain modalities of physiotherapy are potent inducers of the release of endogenous betaE to the blood stream. Most forms of exercise also increase blood betaE level, especially when exercise intensity involves reaching the anaerobic threshold and is associated with the elevation of serum lactate level. Age, gender, and mental activity during exercise also may influence betaE levels. Publications on the potential stimulating effect of manual therapy and massage on betaE release are controversial. Sauna, mud bath, and thermal water increase betaE levels through conveying heat to the tissues. The majority of the techniques for electrical stimulation have a similar effect, which is exerted both centrally and--to a lesser extent--peripherally. However, the parameters of electrotherapy have not yet been standardised. The efficacy of analgesia and the improvement of general well-being do not necessarily correlate with betaE level. Although in addition to blood, increased brain and cerebrospinal fluid betaE levels are also associated with pain, the majority of studies have concerned blood betaE levels. In general, various modalities of physical therapy might influence endorphin levels in the serum or in the cerebrospinal fluid--this is usually manifested by elevation with potential mitigation of pain. However, a causal relationship between the elevation of blood, cerebrospinal fluid or brain betaE levels and the onset of the analgesic action cannot be demonstrated with certainty.

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Section: The Evect Of Exercise In Various Diseasesmentioning

confidence: 94%

The effect of physical therapy on beta-endorphin levels

Bender¹,

Nagy²,

Barna

et al. 2007

Eur J Appl Physiol

115

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“…Plasma enkephalin and ␤-endorphin are increased during acute myocardial ischemia in rats (40). Several clinical studies (5,7,27) have demonstrated that, compared with ␤-endorphin in the femoral arterial blood, coronary sinus concentrations are dramatically higher (15 Ϯ 4 vs. 75 Ϯ 17, femoral vs. coronary) in patients experiencing myocardial ischemia and/or infarction who are treated with transluminal angioplasty. Second, anatomic studies (13,24,29,42,59) have demonstrated that -, ␦-, and -opioid receptors are located on small-, medium-, and large-diameter sensory neurons in the DRG, nodose, and trigeminal ganglia of animals and humans.…”

Section: Discussionmentioning

confidence: 99%

“…Leukocytes that accumulate in the area of coronary arterial plaques release large quantities of opioids when they are activated during plaque disruption (36,38,46). Clinical studies (5,7,27) have documented increased concentrations of coronary opioid peptides in patients with unstable angina pectoris or undergoing coronary angioplasty. Hence, myocardial ischemia leads to the production and release of opioid peptides that have the potential to contribute to the regulation of cardiac spinal afferent nerve activity during ischemia.…”

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confidence: 99%

Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia

Longhurst

2013

American Journal of Physiology-Heart and Circulatory Physiology

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Fu LW, Longhurst JC. Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia. Am J Physiol Heart Circ Physiol 305: H76-H85, 2013. First published May 3, 2013 doi:10.1152/ajpheart.00091.2013.-Thinly myelinated A␦-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) sensory nerve fibers are activated during myocardial ischemia to transmit the sensation of angina pectoris. Although recent observations showed that myocardial ischemia increases the concentrations of opioid peptides and that the stimulation of peripheral opioid receptors inhibits chemically induced visceral and somatic nociception, the role of opioids in cardiac spinal afferent signaling during myocardial ischemia has not been studied. The present study tested the hypothesis that peripheral opioid receptors modulate cardiac spinal afferent nerve activity during myocardial ischemia by suppressing the responses of cardiac afferent nerve to ischemic mediators like bradykinin and extracellular ATP. The nerve activity of single unit cardiac afferents was recorded from the left sympathetic chain (T2-T5) in anesthetized cats. Forty-three ischemically sensitive afferent nerves (conduction velocity: 0.32-3.90 m/s) with receptive fields in the left and right ventricles were identified. The responses of these afferent nerves to repeat ischemia or ischemic mediators were further studied in the following protocols. First, epicardial administration of naloxone (8 mol), a nonselective opioid receptor antagonist, enhanced the responses of eight cardiac afferent nerves to recurrent myocardial ischemia by 62%, whereas epicardial application of vehicle (PBS) did not alter the responses of seven other cardiac afferent nerves to ischemia. Second, naloxone applied to the epicardial surface facilitated the responses of seven cardiac afferent nerves to epicardial ATP by 76%. Third, administration of naloxone enhanced the responses of seven other afferent nerves to bradykinin by 85%. In contrast, in the absence of naloxone, cardiac afferent nerves consistently responded to repeated application of ATP (n ϭ 7) or bradykinin (n ϭ 7). These data suggest that peripheral opioid peptides suppress the responses of cardiac sympathetic afferent nerves to myocardial ischemia and ischemic mediators like ATP and bradykinin. sympathetic afferent nerves; opioid receptors; myocardial ischemia; naloxone ACTIVATION of thinly myelinated A␦-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) afferent nerves during myocardial ischemia is responsible for the transmission of information from the heart to the brain that ultimately elicits the perception of cardiac pain and evokes excitatory cardiaccardiovascular reflex responses (19,22,39). For many years, attention has been focused on characterizing the excitatory effects elicited by a number of ischemic mediators on cardiac spinal afferent nerve activity during myocardial ischemia. In contrast, inhibitory influences of ischemic mediators on cardiac spinal...

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“…Several treadmill studies have indicated that elevated ß-endorphin levels may delay or prevent the onset of angina. (12)(13)(14) Other investigations, however, including efforts to "unmask" silent ischaemia with naloxone have contradicted this finding and at present the role of opioids in unrecognised ischaemia and myocardial infarction has not been clearly established. (15,16) Evidence from mental stress experiments also suggests that silent ischaemic events may be associated with distinct patterns of brain activity.…”

Section: Neuropsychiatric Factorsmentioning

confidence: 99%

A Study of Clinical Profile of Unrecognised Myocardial Infarction

Evuru¹,

Rao²

2017

jemds

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BACKGROUND Atypical and silent myocardial infarctions were grouped together as unrecognised myocardial infarction. The prognosis for patients with unrecognised myocardial infarction is as serious as that of recognised myocardial infarction. It is difficult to choose methods by which to identify these patients and to take decisions about secondary prevention and medical treatment. Detailed knowledge about this disease entity is therefore important and must include a thorough understanding of which patient subgroups are especially vulnerable.The aim of the study is to study the presenting symptoms listed as those of unrecognised myocardial infarction in patients attending NRIMCH with no chest pain. MATERIALS AND METHODSTwenty-two patients over the age of 40 years with these symptoms were studied. All investigations including serial ECG, cardiac enzymes and echocardiogram were done and the outcome assessed. RESULTSFemales dominated the study. Out of 22 patients, 50% presented with breathlessness, 45.45% with sweating, 36.36% with abdominal pain, 31.82% with cough and expectoration, 27.27% with fever, 22.73% with nausea and vomiting, 13.64% with oedema, 18.18% with loose stools, 9.09% each with palpitation and hemiplegia, 4.55% each with giddiness, bleeding per rectum and coma. Four died during the study period. CONCLUSIONIt is recommended that an ECG and cardiac enzymes at least be a part of clinical workup offered to all patients with any symptom, however, atypical that might indicate a myocardial infarction.

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Extent of ischemic stimulus and plasma β-endorphin levels in silent myocardial ischemia

Cited by 15 publications

References 20 publications

The effect of physical therapy on beta-endorphin levels

The effect of physical therapy on beta-endorphin levels

Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia

A Study of Clinical Profile of Unrecognised Myocardial Infarction

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