Possible role of cardloaortic reflexes in postcoronary bypass hypertension

Fouad, Fetnat M.; Estafanous, Fawzy G.; Bravo, Emmanuel L.; Iyer, Kamalnath A.; Maydak, John H.; Tarazi, Robert C.

doi:10.1016/0002-9149(79)90215-7

Cited by 54 publications

(6 citation statements)

References 20 publications

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“…For instance, during left‐ventricular outflow obstruction, there is particularly strong stimulation of cardiac vagal afferents, leading to reflex cardioinhibition and occasionally syncope and collapse 1,2. During or after cardiopulmonary bypass, sympathetic cardiac afferents are stimulated and remarkable hypertensive emergencies can occur 3–6. Conversely, in patients with congestive heart failure, the activity of cardiac afferents, particularly the atrial afferents, appears to be blunted, and normal reflex processes that could promote a diuresis, and thereby reverse the volume overload, are not brought into action in an appropriate fashion 2,7,8.…”

Section: Introductionmentioning

confidence: 99%

“…1,2 During or after cardiopulmonary bypass, sympathetic cardiac afferents are stimulated and remarkable hypertensive emergencies can occur. [3][4][5][6] Conversely, in patients with congestive heart failure, the activity of cardiac afferents, particularly the atrial afferents, appears to be blunted, and normal reflex processes that could promote a diuresis, and thereby reverse the volume overload, are not brought into action in an appropriate fashion. 2,7,8 Myocardial ischemia is still another condition when both vagal and sympathetic cardiac-afferent systems are activated.…”

Section: Introductionmentioning

confidence: 99%

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Cardiac Sympathetic Afferent Activation Provoked by Myocardial Ischemia and Reperfusion

Longhurst

Tjen‐A‐Looi

2001

Annals of the New York Academy of Sciences

128

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Cardiac sympathetic afferents are known to reflexly activate the cardiovascular system, leading to increases in blood pressure, heart rate, and myocardial contractile function. During myocardial ischemia, these sensory nerves also transmit the sensation of pain (angina pectoris) and cause tachyarrhythmias. The authors' laboratory has been interested in defining the mechanisms of activation of this neural system during ischemia and reperfusion. During these periods, reactive oxygen species, particularly hydroxyl radicals, are produced from the breakdown of purine metabolites and lead to stimulation of sympathetic (and vagal) ventricular chemosensitive nerve endings. For example, stimulation with hydrogen peroxide leads to a small reflex increase in blood pressure from the predominant sympathetic afferent activation that is reduced by simultaneous activation of cardiac vagal afferents (known to exert predominantly depressor reflexes). Central integration of these two opposing reflexes likely occurs at several regions of the brain stem, including the nucleus tractus solitarii, where neural occlusion occurs during simultaneous cardiac sympathetic and vagal‐afferent stimulation. Activation of platelets also appears to play a role during myocardial ischemia, leading to local release of serotonin (5HT), which, through a 5HT3 mechanism, stimulates sympathetic afferents. Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins. Prostaglandins sensitize cardiac sympathetic afferents to BK. Thus, stimulation of cardiac sympathetic afferents during ischemia and reperfusion and the resulting reflex events form a multifactorial process resulting from activation of a number of chemical pathways in the myocardium.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cardiac Sympathetic Afferent Activation Provoked by Myocardial Ischemia and Reperfusion

Longhurst

Tjen‐A‐Looi

2001

Annals of the New York Academy of Sciences

128

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“…14 Another cardiogenic mechanism that has received recent attention concerns the adrenergic stimulation of the myocardium in patients with postcoronary bypass hypertension. 4 However, while the almost uniform observation of postcardiac transplantation hypertension is assuredly cardiogenic (as defined most broadly), early studies involving cardiac homotransplantation demonstrated that reinnervation of the transplanted heart occurred within 6 weeks. Thus, the heart may not remain completely denervated.…”

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confidence: 99%

The heart in hypertension: unresolved conceptual challenges. Special lecture.

Fröhlich

1988

Hypertension

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SUMMARY Much has been learned over the past 25 years concerning the role of the heart in hypertension. In a multiplicity of areas a great deal has been clarified but a number of issues remain unresolved. This personal overview outlines some of these challenging areas for investigation, including questions relating to the cardiogenlc reflexes, mechanisms underlying total body autoregulation that may involve not only the adaptation of arterioles but also venoconstriction in hypertension, postcapUIary constriction also involving the efferent glomerular arterioles, the mechanisms underlying the development and regression of hypertrophy as well as the function of the hypertropnied and "regressed hypertrophy" heart, and the precise hemodynamic actions of atrial natriuretic factor.

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“…According to our routine a nonpulsatile, low flow/ low pressure perfusion technique was used. This implies a blood pressure in the range 30-60 mmHg and a flow reduction to [25][26][27][28][29][30][31][32][33][34][35] ml . kg-' during hypothermia, with the most pronounced reduction in patients with the highest blood pressure.…”

Section: Anaesthesia and Extracorporeal Circulation ( Ecc)mentioning

confidence: 99%

Thoracic epidural analgesia in aortocoronary bypass surgery I: haemodynamic effects

Stenseth

Bjella

Berg

et al. 1994

Acta Anaesthesiol Scand

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Tachycardia and hypertension may cause myocardial ischaemia in patients with coronary heart disease going through major surgery. Thoracic epidural analgesia (TEA) has been reported to be beneficial in this situation. The haemodynamic effects of TEA in aortocoronary bypass surgery were investigated in 30 male patients < 65 years old and with ejection fraction > 0.5. They were randomized into 3 groups: the high dose fentanyl (HF) group receiving high-dose fentanyl (55 micrograms.kg-1) anaesthesia, the HF+TEA group receiving the same fentanyl dose+TEA with 10 ml bupivacaine 5 mg.ml-1 followed by 4 ml every hour, and the low dose fentanyl (LF) + TEA group receiving low-dose fentanyl (15 micrograms.kg-1) anaesthesia+TEA. Haemodynamic parameters, the use of vasoactive and inotropic drugs and fluid balance were followed during the operation and for 20 h postoperatively. Before bypass the only significant difference between groups was a higher mean pulmonary arterial pressure in the HF+TEA group and a lower systemic vascular resistance (SVR) in the LF+TEA group, both compared to the HF group. 89% of epidural group patients needed small doses of ephedrine whereas more HF group patients were given nitroglycerine. During bypass SVR and mean arterial pressure (MAP) were significantly higher and pump flow lower in the HF group compared to the LF+TEA group. More ketanserin to HF group patients and methoxamine to epidural group patients were given. After bypass heart rate increased in all groups. Lower MAP 0.5 h after bypass and higher filling pressures in the early post bypass period in the epidural groups, most pronounced in the HF+TEA group, were noted.(ABSTRACT TRUNCATED AT 250 WORDS)

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Possible role of cardloaortic reflexes in postcoronary bypass hypertension

Cited by 54 publications

References 20 publications

Cardiac Sympathetic Afferent Activation Provoked by Myocardial Ischemia and Reperfusion

Cardiac Sympathetic Afferent Activation Provoked by Myocardial Ischemia and Reperfusion

The heart in hypertension: unresolved conceptual challenges. Special lecture.

Thoracic epidural analgesia in aortocoronary bypass surgery I: haemodynamic effects

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