Effects of anesthesia and sleep on circulatory response to carotid sinus nerve stimulation

Vatner, S. F.; Franklin, Dean; Braunwald, Eugene

doi:10.1152/ajplegacy.1971.220.5.1249

Cited by 113 publications

(67 citation statements)

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“…Pentobarbital is known to decrease both baroreflex (3,15) and chemoreflex function in adult dogs (4). It is also known to increase baseline heart rate, which is in accordance with our findings in fetal sheep.…”

Section: Discussionsupporting

confidence: 92%

Effect of Drugs on Chemoreceptor Responsiveness in Fetal Sheep

et al. 1995

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This study was designed to examine the effects of the drugs ketamine, morphine, pentobarbital, and propranolol on fetal chemoreceptor responsiveness. Eleven fetal lambs (gestational age 125-133 d) were chronically instrumented with a catheter in a hindlimb artery and vein and a forelimb artery; a carotid arterial oximeter catheter was placed in six of these fetuses. An inflatable cuff occluder was placed around the maternal hypogastric artery. Acute fetal hypoxemia was induced repeatedly by reducing uterine blood flow. Fetal heart rate, arterial pressure, and carotid arterial oxygen saturation were monitored continuously before and after administering ketamine, morphine, pentobarbital, or propranolol to the fetus. The ratio Aheart rate/AO, saturation has been shown previously to be a reproducible index of chemoreflex response. The differences in baseline values and changes with drugs were compared by multiple regression analysis coded by effects. Chemoreflex response was markedly attenuated by ketamine and morphine but not by pentobarbital or propranolol. Because the cardiovascular response to hypoxemia is blunted by some drugs, caution should be exercised in interpreting heart rate responses to hypoxemia in the fetus when these drugs have been administered to the mother. (Pediatr Res 38: 938-943, 1995) Abbreviation AHRIAsat = ratio of the decrease in heart rate to the decrease in 0, saturation Acute fetal hypoxemia causes a bradycardic response (I), sponse to acute hypoxemia that is quantitative and reproducible which we have previously shown is due to stimulation of (2). peripheral chemoreceptors. The sensitivity of fetal chemoreceptors determines the severity of the bradycardic response. Chemoreceptor sensitivity depends on baseline oxygenation; METHODS the lower the baseline oxygenation, the more marked is the bradycardic response (2). Fetal chemoreceptor sensitivity may also change with the use of anesthetic agents; both baroreceptor function (3) and chemoreceptor function (4) in dogs are attenuated by pentobarbital. Fetal heart rate monitoring is frequently used for the assessment of fetal well being. Because drugs are often used during labor, it is important to know whether they influence chemoreceptor function, and thus alter the heart rate response to hypoxemia.In this study, we examined the effect of ketamine, morphine, and pentobarbital and of a P-adrenoreceptor blocker (proprano-101) on chemoreceptor responsiveness in unanesthetized fetal sheep. Chemoreceptor responsiveness was determined by measuring the heart rate response to acute hypoxemia. We have shown that the change of heart rate in response to a change in arterial oxygen saturation is an index of chemoreceptor re-

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Section: Discussionsupporting

confidence: 92%

Effect of Drugs on Chemoreceptor Responsiveness in Fetal Sheep

et al. 1995

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“…The finding in this study that CSNS does not involve a substantial inotropic response mediated by the sympathetic nervous system in conscious animals is in accord with a previous work from this laboratory (11) and that of Scher and Young (37) which showed the chronotropic changes that occur with elevation of arterial pressure (37) or with CSNS (11) to be mediated primarily by an increase in vagal restraint and to a much lesser extent by a reduction in sympathetic tone. In the latter study when the animals were tested after general anesthesia, the vagal component was minimal and a profound sympathetic component appeared (11).…”

Section: Bilateral Carotid Artery Occlusionsupporting

confidence: 92%

“…In the latter study when the animals were tested after general anesthesia, the vagal component was minimal and a profound sympathetic component appeared (11). These findings that baroreceptor-induced cardiac slowing is primarily parasympathetically mediated have been extended to conscious man as well (38).…”

Section: Bilateral Carotid Artery Occlusionmentioning

confidence: 81%

“…However, there is little information regarding the carotid sinus control of the myocardial contractile state in the intact conscious animal, in which all circulatory control mechanisms are intact. We have previously observed that general anesthesia radically alters the coronary, peripheral vascular, and chronotrophic responses to carotid sinus nerve stimulation (CSNS)1 (11), and have also demonstrated that it substantially depresses the myocardial contractile state, resulting in an augmented response to l Abbreviations used in this paper: BCO, bilateral carotid artery occlusion; CSNS, carotid sinus nerve stimulation; D, diameter; dD/dt, rate of change of diameter; dP/dt, rate of change of pressure; LV, left ventricular; PI, isolength systolic pressure; V, velocity of contraction; Vt*0, isolength velocity of myocardial shortening.…”

Section: Introductionmentioning

confidence: 99%

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Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Vatner¹,

Higgins²,

Franklin³

et al. 1972

J. Clin. Invest.

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A B S T R A C T The effects of bilateral carotid artery occlusion (BCO) and carotid sinus nerve stimulation (CSNS) on left ventricular (LV) pressure (P), diameter (D), velocity of contraction (V), rate of change of pressure (dP/dt), and cardiac output were studied in conscious dogs instrumented with ultrasonic diameter gauges, miniature pressure gauges, and aortic electromagnetic flow transducers. The effects of BCO and CSNS were also studied after autonomic blockade and were compared to similar alterations in pressure produced by norepinephrine, methoxamine, and nitroglycerin. When heart rate was maintained constant with atrial stimulation, BCO had little effect on ventricular contractility, increasing isolength systolic pressure (LV Pis.) by 36% while isolength velocity of myocardial shortening (Vt..) decreased by 12% and (dP/dt)/P fell by 8%. These effects could be explained largely by vasoconstriction, since elevating systolic pressure with methoxamine produced similar results, while norepinephrine increased Vt.. by 36% and (dP/dt)/P by 56%S. CSNS produced directionally opposite results from BCO; it decreased Pi.8 by 15%, Vt.0 increased by 11%, while (dP/dt)/P remained almost constant. These effects may be explained largely by vasodilatation since reducing systolic pressure to the same level with nitroglycerin produced similar results. When peripheral vasoconstriction was minimized by phenoxybenzamine pretreatment, BCO produced a slight positive inotropic effect (Ptso increased by 8%o, Vt.. by 4%, and (dp/ This study was presented in part at the 44th Annual Scientific Sessions of the American Heart Association, Anaheim, Calif., November 1971. An

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“…Several investigators (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) have pointed out that observations in open-chest models are confounded by the effects of anesthesia, surgical trauma, abnormal hemodynamic conditions, excessive levels of circulating catecholamines, and other factors. Certain conclusions derived from open-chest preparations have subsequently been found not to be applicable to conscious animals (9,10,15,17,18,20). We have recently observed (21 ) that the severity of myocardial stunning after a 15-min coronary occlusion is greatly exaggerated in the barbiturate-anesthetized open-chest dog, i.e., approximately half of the postischemic depression of contractility observed in this model is not present in the awake dog.…”

Section: Introductionmentioning

confidence: 99%

Demonstration of free radical generation in the "stunned" myocardium in the conscious dog and identification of major differences between conscious and open-chest dogs.

et al. 1993

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IntroductionConscious dogs undergoing a 15-min coronary occlusion were given a-phenyl N-tert-butyl nitrone (PBN) and the local coronary venous plasma was analyzed by electron paramagnetic resonance spectroscopy. A prolonged myocardial release of PBN radical adducts was observed, which exhibited a burst in the initial minutes of reflow (peaking at 3 min) and then abated but continued for 1-3 h after reperfusion. Recent studies using spin trapping techniques ( 1-7) support the hypothesis that oxygen-derived free radicals contribute to the pathogenesis of postischemic myocardial dysfunction (myocardial "stunning" [8]). These studies have shown that free radicals are generated in various animal models ofstunned myocardium ( 1, 2, 7), and that the generation ofthe radicals is inhibited by the same antioxidants that attenuate postischemic dysfunction (3-7).

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Effects of anesthesia and sleep on circulatory response to carotid sinus nerve stimulation

Abstract: Effects of anesthesia and sleep on circulatory response to carotid sinus nerve stimulation.

Cited by 113 publications

References 0 publications

Effect of Drugs on Chemoreceptor Responsiveness in Fetal Sheep

Effect of Drugs on Chemoreceptor Responsiveness in Fetal Sheep

Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Demonstration of free radical generation in the "stunned" myocardium in the conscious dog and identification of major differences between conscious and open-chest dogs.

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