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Biomedical subjects

J de Champlain

Publications and source records attributed to J de Champlain.

At least 109 records · Page 6Linked to original sources
PubMed1989

Sympatho-adrenal and cardiovascular responses during hand-grip in human hypertension.

Circulating norepinephrine and epinephrine levels were correlated with echocardiographic indices of cardiovascular function during isometric exercise (hand-grip at 30% of maximum force for 3 minutes) in 19 patients with mild essential hypertension and 9 normotensive subjects. At the end of the third minute of exercise, plasma norepinephrine and epinephrine, blood pressure and heart rate, increased significantly and similarly in both groups of patients. In contrast, peripheral resistance tended to increase in hypertensives but tended to decrease in normotensives. Moreover, indices of ventricular function increased in normotensives but decreased in hypertensives. At the end of the exercise, systolic and diastolic blood pressures were directly correlated with epinephrine levels in normotensives but were correlated only with norepinephrine levels in hypertensives. On the other hand, norepinephrine and epinephrine levels were inversely correlated with changes in indices of left ventricular performance in hypertensive patients only. These results demonstrate that during isometric exercise, the increase in blood pressure in normotensives is associated with a sympatho-adrenal activation of cardiac performance and contractility, while in hypertensives the increase in blood pressure results mainly from an increase in peripheral resistance associated with a reduction in cardiac performance and contractility, despite a similar sympatho-adrenal activation in both groups. These differences in the hemodynamic responses may be compatible with the hypothesis of beta-adrenoceptor desensitization or structural alterations of the cardiovascular system in hypertensive patients.

Adrenal Glands↗
PubMed1988

Local modulation of adrenal catecholamines release by beta-2 adrenoceptors in the anaesthetized dog.

The release of adrenal catecholamines into the adrenal vein elicited by splanchnic nerve stimulation, was evaluated in the presence of a beta-adrenoceptor agonist and both beta-1 and beta-2 adrenoceptor antagonists in anaesthetized and vagotomized dogs. Stimulations (0.5 V pulses of 2 ms duration for 3 min at 1 Hz) were applied before and after the i.v. infusion of the beta-adrenoceptor agonist, isoproterenol (0.1 microgram/kg/min). While maintaining the infusion of isoproterenol, either ICI 118551 (0.3 mg/kg), a selective beta-2 adrenoceptor antagonist, or 204-155 (0.2 mg/kg), a selective beta-1 adrenoceptor antagonist (Sandoz Co., Dorval, PQ, Canada), were injected intravenously and the stimulation was repeated. The results show that isoproterenol increased significantly both pre-stimulation basal levels and the stimulated release of catecholamines. These potentiated responses were significantly reversed by ICI 118551, but not by 204-155. These results suggest that the release of adrenal catecholamines is locally modulated by a positive feedback mechanism through activation of beta-2 adrenoceptors.

Adrenal Medulla↗
PubMed1988

Neurohumoral and hemodynamic changes in congestive heart failure: lack of correlation and evidence of compensatory mechanisms.

The objective of this study was to assess the hemodynamic and neurohumoral (plasma renin activity, aldosterone, epinephrine, norepinephrine, vasopressin, and atrial natriuretic peptide) determinants of systemic vascular resistance in 35 patients with stable congestive heart failure. In the supine position, although activation of the various neurohumoral systems tended to occur in the same patients, there was little correlation between activation of any of the neurohumoral systems, as reflected by circulating levels, and systemic vascular resistance. There was also little correlation between changes in circulating neurohormones and changes in either mean arterial pressure or systemic vascular resistance in the standing position. Acutely reducing the activity of the renin-angiotensin system with the use of captopril did not improve the correlation between other neurohumoral and hemodynamic variables. In fact there was no correlation between the effects of acute captopril therapy and baseline renin values. These results support the concept that activation of one or another vasoconstrictor neurohumoral system varies from patient to patient and that the effects of their activation are tempered by activation of parallel vasodilator systems and by attenuation of neurohormone release and effector organ response.

Adaptation, Physiological↗
PubMed1988

Effects of chronic dietary lithium on phosphatidylinositol pathway in heart and arteries of DOCA-salt hypertensive rats.

The sensitivity of the phosphatidylinositol (PI) pathway was evaluated in slices of atria (A), ventricles (V), and mesenteric artery (MA) in normotensive (NT) and DOCA-salt hypertensive (DOCA-HT) rats. During norepinephrine (NE) activation, the PI reactivity was two to three times greater in A, V, and MA of HT rats compared to NT rats. The long-term (2 weeks) administration of dietary lithium (Li) reduced the activation of PI by NE in left A and right V but caused no changes in MA of HT rats. The Li-treated hypertensive rats were also characterized by a lower systolic blood pressure and a lower ratio of ventricular weight/body weight. Plasma epinephrine (E) levels that were higher in HT rats were normalized in DOCA-HT + Li-treated rats, while the NE levels remained elevated in the DOCA-HT + Li group.

Animals↗
PubMed1988

Modulation of adrenal catecholamine release by DA2 dopamine receptors in the anaesthetized dog.

1. The effects of DA2 agonist, quinpirole (50 micrograms/kg, i.v.) and a DA2 antagonist, domperidone (50 micrograms/kg, i.v.) on the release of adrenal catecholamines were evaluated in the anaesthetized and vagotomized dog. 2. Stimulations (5 V pulses of 2 ms duration for 3 min) of the splanchnic nerve at frequencies of 1, 3 and 5 Hz were applied randomly before and after injection of the drug. 3. The results show that quinpirole reduces significantly the release of adrenaline at 1 and 3 Hz but not at 5 Hz, while the release of noradrenaline is reduced at 1 Hz but not at 3 and 5 Hz. Inversely, domperidone potentiates significantly the release of both catecholamines at 3 and 5 Hz, but not at 1 Hz. 4. There was no change in basal release of adrenal catecholamines, adrenal blood flow or heart rate after both drug treatments. 5. The mean arterial pressure was not affected by domperidone treatment but there was a significant reduction in basal mean arterial pressure after the injection of quinpirole. 6. There was no change in any of these parameters during electrical stimulation. 7. Therefore, these results strongly suggest that DA2 dopamine receptors are present at the level of the adrenal medulla and that their activation could mediate an inhibitory modulation on the adrenal catecholamines release within a certain range of electrical stimulation.

Adrenal Glands↗
PubMed1988

In vivo modulation by alpha 2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog.

In this study, the reversal of the potentiating effect of idazoxan, a selective alpha 2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective alpha 2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i.v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 micrograms/kg). The alpha 2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the alpha 2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of alpha 2-blockade can be reversed by activation of those receptors by a selective alpha 2-agonist.

Adrenal Glands↗
PubMed1988

Coronary sinus norepinephrine concentrations during ventricular tachycardia induced by left stellate ganglion stimulation in dogs.

Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and alpha-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p less than 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.

Animals↗
PubMed1988

In vivo interactions between prejunctional alpha 2- and beta 2-adrenoceptors at the level of the adrenal medulla.

The combined effect of a beta 2-antagonist and an alpha 2-agonist on the release of adrenal catecholamines was studied in the anaesthetized and vagotomized dog. The electrical stimulation of the splanchnic nerve (5-V pulses of 2 ms duration for 3 min at a frequency of 3 Hz) produced a significant rise in adrenal catecholamine release in the adrenal vein. Intravenous injection of a beta 2-antagonist significantly reduced this response and a subsequent injection of an alpha 2-agonist further reduced the release of catecholamines. However, if the alpha 2-agonist is injected first, the release is not different compared with the control stimulation, and the subsequent injection of the beta 2-antagonist also did not modify the release in response to electrical stimulation. These results suggest that the blockade of presynaptic beta 2-receptors reduces the release of adrenal catecholamines without interfering with the activation of the alpha 2-adrenoceptors. In contrast, the pretreatment with the alpha 2-agonist, which does not modify the release of catecholamine at 3 Hz, seems to interfere with the inhibitory effect of the beta 2-antagonist.

Adrenal Medulla↗
PubMed1987

Effects of exercise training on plasma catecholamines and blood pressure in labile hypertensive subjects.

Plasma catecholamine concentrations (norepinephrine, NE; epinephrine, E) were measured along with heart rate (HR) and blood pressure (BP) at rest in supine (20 min) and standing (10 min) positions and in response to cycle ergometer exercise (5 min; 60% estimated maximal aerobic power) in 12 hypertensive patients before and after 20 weeks of aerobic training on cycle ergometer (six males, one female) or by jogging (five males). In a control group of labile hypertensive patients (five males, two females), estimated maximal aerobic power as well as HR and BP at rest in the supine and standing positions and in response to exercise were not modified from the first to the second evaluation (43 +/- 4 vs 43 +/- 5 ml.kg-1.min-1). In comparison estimated maximal aerobic power significantly increased in both training groups (cycle: 38 +/- 4 to 43 +/- 4; jogging: 38 +/- 3 to 46 +/- 4 ml.kg-1.min-1). However HR and BP were not modified following training, except for small reductions in systolic (18.9 to 18 kPa: 142 to 135 mmHg) and diastolic pressures (13.3 to 12 kPa: 100 to 90 mmHg) (p less than 0.05) at standing rest in the cycle group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

The release of catecholamines from the adrenal medulla and its modulation by alpha 2-adrenoceptors in the anaesthetized dog.

The adrenal nerve of anaesthetized and vagotomized dogs was electrically stimulated (10 V pulses of 2 ms duration for 10 min) at frequencies of 1, 3, 10, and 25 Hz. There was a correlation between the frequency of stimulation and the plasma concentrations of epinephrine, norepinephrine, and dopamine in the adrenal vein, mainly after the 1st min of stimulation and the maximal concentration was reached sooner with higher frequencies of stimulation. Moreover, the relative percentage of catecholamines released in response to the electrical stimulation was not changed by the frequency of stimulation. To test the hypothesis that a local negative feedback mechanism mediated by alpha 2-adrenoceptors exists in the adrenal medulla, the effects of the systemic administration of clonidine (alpha 2-antagonist) on the concentrations of catecholamines in the adrenal vein were evaluated during the electrical stimulation of the adrenal nerve (5 V pulses of 2 ms duration for 3 min) at 3 Hz. Moreover, the effects of the systemic injections of more specific alpha 2-agonist and antagonist (oxymetazoline and idazoxan) were tested on the release of catecholamines in the adrenal vein in response to electrical stimulation of the splanchnic nerve at 1 and 3 Hz frequencies. The injection of 0.5 mg/kg of yohimbine caused a significant increase in the concentrations of epinephrine and norepinephrine in the adrenal vein induced by the electrical stimulation of the adrenal nerve and the injection of 15 micrograms/kg of clonidine had no effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1987

Abnormal regulation of the sympathoadrenal system in deoxycorticosterone acetate-salt hypertensive rats.

With the use of circulating norepinephrine (NE) and epinephrine (E) levels, the sympathoadrenal activity as well as its local modulation by adrenoceptors were studied in normotensive (NT) and DOCA-salt hypertensive (HT) rats. In anesthetized hypertensive rats, plasma NE levels were higher, whereas in conscious animals both NE and E levels were found to be increased, suggesting an increased basal sympathoadrenal tone in these animals. The finding of a close correlation between blood pressure levels and NE levels suggests that the elevation of blood pressure may be linked to sympathetic system activity in this experimental model of hypertension. The reactivity of the sympathoadrenal system was also found to be increased in DOCA HT rats. Following a bilateral carotid occlusion of 1 min, which specifically activates the adrenal medulla, the elevation of E levels was found to be potentiated in intact or vagotomized HT rats. Moreover, in response to prolonged or acute hypotension in anesthetized and conscious animals, the elevation in plasma NE and E levels was found to be markedly potentiated in DOCA HT rats. The local modulating adrenoceptor-mediated mechanisms of the sympathoadrenal system appeared to be altered in this model of hypertension. Although it was possible to demonstrate that the E response to carotid occlusion can be greatly potentiated by administration of an alpha2-antagonist (yohimbine) and completely abolished by an alpha2-agonist (clonidine) in NT rats, the E response was found to be unaffected by the same treatments in HT rats, suggesting a reduced sensitivity in the alpha2-mediated inhibitory modulation of the adrenal medulla. Moreover, the acute treatment with a beta-blocker (sotalol) lowered circulating NE levels and blood pressure only in HT rats, suggesting the possibility of a more sensitive beta-receptor-mediated presynaptic facilitatory mechanism on sympathetic fibers of these animals. Finally, it was observed that the functional balance which exists between the activities of sympathetic fibers and the adrenal medulla in normotensive animals appears to be impaired in DOCA HT rats. In conclusion, the present studies suggest that the increased sympathoadrenal tone and reactivity may be due, in part, to a variety of dysfunctions in local adrenoceptor modulatory mechanisms of the sympathoadrenal system in DOCA hypertensive rats.

Adrenal Medulla↗
PubMed1987

Effects of yohimbine and desipramine on cardiac noradrenaline release and ventricular arrhythmias during acute coronary artery occlusion and reperfusion in anesthetized dogs.

Effects of yohimbine (YHMB, an alpha 2-antagonist) and desipramine (DMI, a neuronal uptake inhibitor) were compared on cardiac noradrenaline (NA) release either upon left ansa subclavia nerve stimulation during acute occlusion of the left anterior descending coronary artery (LAD) or upon subsequent LAD reperfusion without stimulation in anesthetized dogs. In control dogs, before LAD occlusion, coronary sinus (CS) NA output increased from 5.4 +/- 1.0 to 26.8 +/- 4.0 ng/min (p less than 0.05) upon stimulation (2 Hz, 30 s). The response to stimulation remained unchanged 25 min after LAD occlusion. During reperfusion 60 min after occlusion, the output of CS-NA and lactate increased from 6.1 +/- 0.8 to 51.3 +/- 19.4 ng/min (p less than 0.05) and from 2.7 +/- 0.5 to 6.7 +/- 1.3 mg/min (p less than 0.05), respectively. In dogs treated with YHMB, the stimulation-induced increase in NA output was potentiated at least fourfold (p less than 0.05) either before or during LAD occlusion, but not during reperfusion. In dogs receiving DMI, stimulation-induced CS-NA output was enhanced to a similar extent (approximately twofold, p less than 0.05) either before or during occlusion, while reperfusion-induced NA output was markedly potentiated by approximately ninefold (p less than 0.05). Maximum dP/dt of left ventricular pressure remained unchanged upon reperfusion in all groups. The total arrhythmic ratio in the drug-treated groups did not significantly differ from the ratio in control dogs upon either stimulation or reperfusion. The data suggest that an abrupt increase in NA output upon reperfusion may result from a washout of NA locally accumulated in the ischemic and (or) peri-ischemic region during the preceding occlusion period, and that NA thus released does not have substantial hemodynamic effects. The results indicate that in the presence of YHMB or DMI, the potentiated increase in NA release in response to either nerve stimulation during LAD occlusion or to reperfusion without stimulation did not aggravate ventricular arrhythmia, most probably owing to the antiarrhythmic properties of these substances.

Anesthesia↗
PubMed1987

Red blood cell catecholamine levels in normotensive and DOCA-salt hypertensive rats.

Under basal conditions in anesthetized rats, significant concentrations of free norepinephrine (NE), epinephrine (E), and dopamine (DA) were detected in red blood cell (RBC) lysate. These concentrations were not proportional to their respective plasma concentrations and thus RBC-to-plasma concentration ratios were different for each catecholamine (CA). DA was by far the most concentrated amine inside the RBC. An acute increase in plasma NE and E levels, induced by hemorrhagic hypotension in normotensive (NT) rats, did not result in any modification of the RBC CA content. However, chronic elevation of the NE plasma levels in bilaterally adrenalectomized rats and in deoxycorticosterone acetate (DOCA)-salt hypertensive rats (DOCA-salt HT) were associated with increased NE levels in the RBC. In addition, the large elevation in plasma E concentrations following hemorrhagic hypotension in DOCA-salt HT rats, as well as the greater plasma NE response to hypotension in adrenalectomized animals, were accompanied by increases in the respective RBC amine concentrations. During a steady-state intravenous infusion of tritiated NE, we observed a slow accumulation of radioactivity inside the RBC, indicating that CA can enter the RBC from the plasma. Moreover, catechol methyltransferase activity was measured in the cytosolic fraction of the RBC of both NT and DOCA-salt HT rats suggesting that, once inside the RBC, the catecholamines can be metabolized.

Adrenalectomy↗
PubMed1987

Abnormalities in the regulation of sympathetic activity in human hypertension.

Various biochemical, pharmacologic, and physiologic techniques were used to evaluate the sympathetic tone and reactivity in labile and sustained hypertension in humans. The results of these studies suggest the existence of an important subgroup of hypertensive patients characterized by increased basal sympathetic tone and reactivity to standing. Such abnormalities could be the result of various dysfunctions, involving the activity of central and peripheral cardiovascular sympathetic fibers, the presynaptic modulation of sympathetic fibers (including the interaction with the parasympathetic system), the inactivation of circulating norepinephrine, and the sensitivity of the efferent cells. The increase in circulating norepinephrine in a group of hypertensive patients seems to reflect a functional increase in the sympathetic tone as shown by the presence of hyperkinetic cardiac functions in hyperadrenergic patients (elevated catecholamine levels), while cardiac functions are normal in normoadrenergic patients (catecholamine levels within normal range). Moreover, the better hypotensive response, combined with normalization of the basal and reactive circulating norepinephrine levels following beta-blockade in hyperadrenergic hypertensive patients, strongly supports the participation of the sympathetic system in the maintenance of hypertension in those patients. The identification and characterization of this subpopulation of patients may be helpful in the development of more rational therapeutic approaches and could eventually permit us to devise better predictors of outcome in hypertension.

Blood Pressure↗
PubMed1986

Persistent effects of a marathon run on the pituitary-testicular axis.

Plasma levels of testosterone (T), LH, FSH, prolactin (PRL), cortisol (F), dehydroepiandrosterone sulfate (DHAS), noradrenaline (NA), NA sulfate (NAS), adrenaline (A) and A sulfate (AS) were measured in 7 adult males before and immediately after a marathon run as well as every morning for 5 days after the run. While plasma T levels fell significantly on the first and the second postmarathon day, those of LH rose significantly during the first 3 postrun days. Plasma PRL and F values increased significantly only at the end of the marathon. Plasma levels of NA and NAS rose significantly at the end of the run and again on days 2 and 5 postmarathon, respectively. A similar pattern was observed for A and AS except for the second peak of free A. These results show that a strenuous physical exercise leads to a persistent relative insensitivity to LH of the testicular T biosynthetic machinery, while the feedback mechanisms operating at the hypothalamic-pituitary level are normal. Furthermore, they suggest that catecholamines may be responsible for the prolonged inhibitory effect of stress on T biosynthesis.

Adult↗
PubMed1986

Increased basal and reactive plasma norepinephrine and epinephrine levels in awake DOCA-salt hypertensive rats.

The sympatho-adrenal basal tone and reactivity were studied using plasma norepinephrine (NE) and epinephrine (E) levels in awake DOCA-salt hypertensive rats. In those animals, basal NE and E levels were about twice greater than those found in normotensive rats. Moreover, plasma NE levels could be significantly correlated with mean arterial pressures in both groups of animals. Following a hemorrhagic hypotension, elevation in NE and E levels tended to be greater in hypertensive rats. These studies suggest that the basal activity of the sympatho-adrenal system is increased and that its reactivity might be potentiated in DOCA-salt hypertension.

Animals↗