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Biomedical subjects

J B Stoker

Publications and source records attributed to J B Stoker.

At least 19 recordsLinked to original sources
PubMed2006

Nuclear magnetic moment of the 57Cu ground state.

The nuclear magnetic moment of the ground state of (57)Cu(Iota(pi) = 3/2(-), T(1/2) = 196.3 ms) has been measured to be /mu((57)Cu)/ = (2.00 +/- 0.05)mu(N) using the beta-NMR technique. Together with the known magnetic moment of the mirror partner (57)Ni, the spin expectation value was extracted as = -0.078 +/- 0.13. This is the heaviest isospin mirror T = 1/2 pair above the (40)Ca region for which both ground state magnetic moments have been determined. The discrepancy between the present results and shell-model calculations in the full f p shell giving mu((57)Cu) approximately 2.4mu(N) and approximately 0.5 implies significant shell breaking at (56)Ni with the neutron number N = 28.

Journal Article↗
PubMed2003

The activity of single vasoconstrictor nerve units in hypertension.

AIM: It has long been established from controlled experiments in anaesthetized animals that it is more accurate to quantify the mean frequency of efferent sympathetic nerve activity from single unit than from multi-unit bursts recordings. More recently, sympathetic nerve hyperactivity has been reported in patients with essential hypertension (EHT) when using microneurographic recordings from peripheral efferent nerves. This review will focus on the mean frequency of single unit of muscle sympathetic nerve activity (s-MSNA) in relation to that of multi-unit bursts (MSNA) as obtained by microneurography in EHT. RESULTS: We have shown that the resting levels of s-MSNA and MSNA were increased in uncomplicated EHT, white coat hypertension and in EHT complicated by left ventricular hypertrophy. There was a relatively greater increase in s-MSNA than in MSNA in mild hypertension and in complicated EHT. We also found that both s-MSNA and MSNA were increased to a similar extent in conditions known to affect reflexes emanating from the heart and influencing sympathetic output, such as acute myocardial infarction. In other preliminary studies, the increase of s-MSNA in response to the discomfort of cold pressor test was greater than that of MSNA and this difference was abolished by the centrally sympatholytic agent moxonidine. CONCLUSION: These results are consistent with the hypothesis that an increase in the mean frequency of central sympathetic discharge to the periphery (greater s-MSNA than MSNA) is involved in the pathogenesis and complications of EHT. Target organ damage may in turn lead to an increase in overall sympathetic output (excessive MSNA increase) through the operation of peripheral reflex mechanisms.

Animals↗
PubMed2001

Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive.

OBJECTIVES: This study was designed to examine whether the occurrence of left ventricular hypertrophy (LVH) in moderate to severe essential hypertension (EHT) was associated with alteration in peripheral sympathetic drive. BACKGROUND: In hypertension, LVH is an independent predictor of increased morbidity and mortality. The reported mechanisms leading to LVH remain unclear but include hemodynamic and humoral factors. The sympathetic nervous system may be important, particularly as catecholamines have been shown to have trophic properties. We tested the hypothesis that sympathetic activity measured using microneurography could be different in patients with hypertension depending on the presence of LVH. METHODS: We examined 28 subjects with moderate to severe EHT (stages 2 to 3; Joint National Committee [JNC]-VI classification). Fourteen had echocardiographic evidence of LVH (EHT + LVH), while the other 14 subjects (EHT) did not. Subjects were matched in terms of age, body mass index and levels of arterial blood pressure. Peripheral muscle sympathetic nerve activity was measured from both multiunit bursts (MSNA) and single unit (s-MSNA) vasoconstrictor impulses via the peroneal nerve. RESULTS: The mean frequency of s-MSNA and MSNA was greater in the EHT + LVH group than it was in the EHT group (mean +/- SEM; 75.9 +/- 6.9 impulses/100 beats vs. 52.1 +/- 2.9 impulses/100 beats, p < 0.001 and 64.2 +/- 5.7 bursts/100 beats vs. 48.9 +/- 2.8 bursts/100 beats, p < 0.05). CONCLUSIONS: These results indicate that, in subjects with moderate to severe hypertension, the presence of LVH is associated with higher sympathetic discharge, evidenced by an increase in unitary firing frequency and also by fiber recruitment.

Action Potentials↗
PubMed2001

Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.

BACKGROUND: Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE). It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low. The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women. METHODS AND RESULTS: Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats). MSNA followed a similar trend. Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN. After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS. In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure. CONCLUSIONS: Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group. The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.

Action Potentials↗
PubMed2001

Mechanisms of the renal vasodilation caused by insulin in anesthetized pigs.

The present study was planned to determine the mechanisms involved in the renal vasodilation caused by insulin. Changes in flow caused by the intravenous infusion of 0.004 IU/kg/min of insulin at constant heart rate, aortic blood pressure, left ventricular contractility and blood levels of glucose and potassium in the left renal artery were assessed using an electromagnetic flowmeter. In ten pigs, infusion of insulin caused an increase in renal blood flow which averaged 12.8% of the control values. After hemodynamic variables had returned to control values, insulin infusion was repeated in five pigs following blockade of alpha-adrenergic receptors with injection of phentolamine into the renal artery and in the other five pigs following blockade of nitric oxide formation with injection in the same artery of Nomega-nitro-L-arginine methyl ester (L-NAME). After blockade of alpha-adrenergic receptors, insulin infusion caused an increase in renal blood flow which averaged 18.1% of the control values, being significantly enhanced with respect to the increase previously obtained in the same pigs. On the contrary, after blockade of nitric oxide formation insulin infusion caused a decrease in renal blood flow which averaged 6.5% of the control values. These responses were respectively abolished by the subsequent injection into the renal artery of L-NAME and phentolamine. The present study showed that the renal vasodilation caused by insulin in the anesthetized pig was the result of two opposite effects which involved a predominant vasodilation mediated by the release of nitric oxide from the endothelium and a sympathetic vasoconstrictor mechanism mediated by alpha-adrenergic receptors.

Animals↗
PubMed2001

The effect of progesterone on coronary blood flow in anaesthesized pigs.

The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h(-1) of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h(-1). The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of N(omega)-nitro-L-arginine methyl ester (L-NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L-NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide.

Animals↗
PubMed2001

Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects.

A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean+/-S.E.M.) from 42+/-4 to 58+/-5 impulses/100 beats (P<0.01) and from 36+/-4 to 51+/-5 bursts/100 beats (P<0.001). There were corresponding increases in calf vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.

Action Potentials↗
PubMed2000

Chronic I(1)-imidazoline agonism : sympathetic mechanisms in hypertension.

Evidence exists for a state of sympathetic hyperactivity in essential hypertension, and moxonidine, a new central sympathetic inhibitor, has been introduced for its treatment. Acute administration of moxonidine lowers peripheral sympathetic neural output. This study examined the effect of chronic moxonidine therapy, at increasing therapeutic doses, on resting peripheral sympathetic activity and vascular resistance and their responses to physiological reflex maneuvers. Twelve newly diagnosed patients with essential hypertension were studied sequentially at least 1 month apart, initially on no therapy, then on 200 microg, and finally on 400 microg of oral moxonidine daily. Changes in heart rate, arterial blood pressure, calf vascular resistance, and peripheral sympathetic drive were assessed at rest and during reflex maneuvers. Peroneal microneurography was used to quantify peripheral sympathetic vasoconstrictor activity by single-unit and multiunit techniques. Moxonidine therapy progressively reduced resting mean arterial pressure (P<0.0001) without affecting heart rate. At 200 microg daily, there was a significant reduction in sympathetic nerve activity (P<0.001) and calf vascular resistance (P<0.01). At 400 microg daily, further reductions were smaller and insignificant. Responses to cold stimulus and isometric handgrip exercise showed a similar pattern, with the greatest magnitude of change at 200 microg daily. In patients with essential hypertension, chronic moxonidine therapy inhibited resting sympathetic vasoconstrictor drive and also its reflex responses. The magnitude of inhibition became less as the therapeutic dose was increased, suggesting that moxonidine may be more effective under conditions of high sympathetic activity.

Aged↗
PubMed1999

Single-unit sympathetic discharge : quantitative assessment in human hypertensive disease.

Background-Reports demonstrating sympathetic hyperactivity in hypertension with the use of microneurography have been inconsistent. One possible reason is that previous studies have assessed muscle sympathetic nerve activity (MSNA) from integrated voltage waves ("bursts") recorded from multiunit discharges. We studied single units with defined vasoconstrictor properties (s-MSNA) to further characterize sympathetic output in hypertensive disease. Methods and Results-We examined 74 subjects with a wide range of arterial blood pressure that were considered to be either normal (NT), high normal (HN), or stages 1 to 3 essential hypertension (EHT-1, EHT-2/3). All had their peripheral sympathetic activity measured from both multiunit bursts and single-unit vasoconstrictor impulses. There was a significant correlation between s-MSNA and MSNA, and results of variability studies were similar. The EHT-1 and EHT-2/3 groups had greater s-MSNA and MSNA than did the matched NT group (always P<0. 01). The HN group also had greater s-MSNA and MSNA than did the NT group (mean+/-SEM; 43+/-5 vs 29+/-2 impulses/100 beats, P<0.05; 36+/-4 vs 24+/-2 bursts/100 beats, P<0.05). In addition, the EHT-1 group had significantly greater s-MSNA than did the EHT-2/3 group (63+/-6 vs 51+/-3 impulses/100 beats, P<0.05), which could not be demonstrated with MSNA bursts. Conclusions-Quantification from single vasoconstrictor units has provided additional evidence in established essential hypertension of increased central sympathetic output. Furthermore, in the mild or early stages of hypertension, this technique has provided new evidence of augmented sympathetic output compared with more severe hypertension.

Action Potentials↗
PubMed1998

Sympathetic nerve discharge in normal pregnancy and pregnancy-induced hypertension.

BACKGROUND: Microneurographic assessment of processed bursts that represent multi-unit nerve discharge has suggested that sympathetic hyperactivity occurs in pregnancy induced hypertension and pre-eclampsia in comparison with normal pregnancy. OBJECTIVE: To examine the differences between peripheral sympathetic outputs in pregnancy-induced hypertension and normal pregnancy by directly measuring single impulses of neural discharge. DESIGN: We compared the sympathetic neural discharge at rest and its reflex responses in subjects with pregnancy-induced hypertension and normal pregnancy and re-examined their progress at least 6 weeks post partum. The patients with pregnancy-induced hypertension were hospital in-patients for whom the diagnosis could be strictly defined and the normally pregnant women were recruited to match the former. METHODS: Standard microneurography was performed to quantify single impulses of action potentials, together with the processed multi-unit bursts from fibres innervating the leg muscles. We measured neural discharge with vascular vasoconstrictive properties, heart rate and finger arterial blood pressure at rest and their responses to standard isometric hand-grip exercise and cold pressor tests. RESULTS: As expected, patients with pregnancy-induced hypertension (n = 13) had higher levels of finger arterial blood pressure than did women with normal pregnancies (n = 11). The number of single impulses of action potentials (per min and per 100 cardiac beats) in resting patients with pregnancy-induced hypertension was more than three times greater than that in resting women with normal pregnancies, and the number of multi-unit bursts was twofold greater. After delivery of their child, sympathetic activity and heart rate in nine patients decreased, but finger arterial blood pressure decreased in patients with pregnancy-induced hypertension only. CONCLUSIONS: From results of cross-sectional and longitudinal studies, pregnancy-induced hypertension is associated with a greater resting sympathetic output than that of women with normal pregnancies. Follow-up data after parturition suggest that this hyperactivity is not the only cause of hypertension.

Electrophysiology↗
PubMed1988

Changes in myocardial ischaemia during isosorbide dinitrate or indoramin therapy in patients with stable angina using relations between the ST segment and heart rate.

The effect of isosorbide dinitrate or indoramin on myocardial ischaemia was examined in patients with stable angina pectoris. In a prospective trial, randomization resulted in 8 and 9 patients, respectively, given isosorbide dinitrate in a dose of 30-90 mg daily, and indoramin in a dose of 75-225 mg daily; 2 of these patients were serially examined during the two types of therapy. Changes in myocardial ischaemia were assessed by exercise testing using 12 standard electrocardiographic leads and a bipolar lead CM5. Individual and group comparisons showed that isosorbide dinitrate resulted in an increase in ST segment depression, the maximal ST/heart rate slope and the ratio of net ST segment depression to increases in heart rate (at least P less than 0.01). In contrast, with indoramin therapy there were no significant changes in these indices. The results in these patients suggest that isosorbide dinitrate leads more consistently to increases in the severity of myocardial ischaemia than indoramin, although this effect on ischaemia is apparently less than the benefit of these agents on exercise performance.

Adult↗
PubMed1988

Aortic valve disease and the ST segment/heart rate relationship: a longitudinal study before and after aortic valve replacement.

The ST segment/heart rate relationship or maximal ST/HR slope has been validated as an index of myocardial ischemia in selected populations of patients with angina pectoris. The present study involved patients selected as having aortic valve disease unaccompanied by angiographic coronary artery narrowing. In each of seven patients, so far examined, a slope value and ST segment depression of greater than 1 mm were obtained which, according to previous experience, indicated myocardial ischemia equivalent to coronary heart disease. After aortic valve replacement, there was a significant reduction in heart size as assessed using the cardiothoracic ratio, and the amplitude of QRS complex on the electrocardiogram. The slope was abolished (two patients) or markedly reduced (five patients), and the decrease in the seven patients was statistically significant. ST segment depression could be obtained in one patient. This study has shown the occurrence of maximal ST/HR slope in patients without large coronary artery disease who have aortic valve disease and cardiac enlargement.

Aortic Valve↗
PubMed1987

Use of the maximal ST/HR slope to estimate myocardial ischaemia after recent myocardial infarction.

Fifty two patients were examined 4-6 weeks after myocardial infarction to assess whether factors other than coronary artery narrowing affect the maximal ST/HR slope which is used as an index of myocardial ischaemia. The slope was compared with indices of myocardial scarring or cardiac enlargement derived from x ray and echocardiographic and angio-cardiographic investigations. In 35 (67%) patients the slope failed to predict the severity of myocardial ischaemia attributable to coronary artery narrowing: in 14 (27%) patients the slope overestimated the findings of coronary angiography and in 21 (40%) patients the slope underestimated the findings of coronary angiography. In the remaining 17 (33%) patients the slope accorded with the assessment of myocardial ischaemia by coronary angiography. Underestimation by the slope was associated with significantly poorer left ventricular function and a lower ejection fraction, indicating a greater degree of myocardial scarring. To assess whether overestimation was related to cardiac enlargement with better preservation of ventricular function a follow up examination was performed six months after infarction. In the overestimated group 11 patients were followed up and seven of them showed a reduction in the maximal ST/HR slope which correlated with a reduction in the cardiothoracic ratio. This suggested that cardiac enlargement had contributed to myocardial ischaemia. The results suggest that if the maximal ST/HR slope is an index of exercise induced myocardial ischaemia after recent infarction, it is subject to the influences of coronary artery narrowing as well as those of scarring and cardiac enlargement.

Adult↗
PubMed1986

Assessment of the effect of nifedipine on myocardial ischaemia by using the ST segment/heart rate slope.

Nifedipine is used in patients with stable angina of effort and any resulting change in symptoms is attributed to several effects of nifedipine. However, there have been indications in such patients that one effect of nifedipine could be an increase in the severity of myocardial ischaemia, and the present report involves a trial the results of which could explain this effect. In the present trial, the effect of nifedipine on myocardial ischaemia was assessed by using the maximal ST/heart rate slope. This slope was used as an index of myocardial ischaemia because, in our hands in patients with angina, an increase or a decrease in the value of the slope respectively indicated an increase or a decrease in the severity of myocardial ischaemia as assessed by coronary arteriography. The maximal ST/heart rate slope was obtained at least twice in each of 23 patients with stable angina, with and without nifedipine; two patients were examined twice and three other patients were examined after an increased dose. Nifedipine resulted in an increase in the slope in 24 of the 28 comparisons, no change in three and a decrease in one comparison; there was a statistically significant (P less than 0.005; n = 28; paired t-test) increase in the maximal ST/heart rate slope. A further increase in the slope was obtained by increasing the dose of nifedipine in two out of three patients. The increase in the maximal ST/heart rate slope occurred in the absence of any effect of nifedipine on the initial level of ST segment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

The effect of indoramin on exercise performance in mild hypertension.

The alpha 1-adrenoceptor antagonist indoramin is proposed to reduce arterial blood pressure without a concomitantly significant increase in heart rate (HR). The present study involves assessment of the effect of alpha 1-adrenoceptor antagonism in patients with mild hypertension on the HR/oxygen consumption (Vo2) relationship, which has previously been shown to indicate improvement in cardiorespiratory fitness following exercise training. A total of 16 patients with a systolic blood pressure of 140-200 mm Hg and diastolic blood pressure of 95-110 mm Hg were examined. A double-blind, placebo-controlled study design was utilized. Following initial observations, the patients were randomized into one group (a) of seven patients who were given a placebo, indoramin, and finally placebo, and a second group (b) of nine patients who were given the two agents in the reverse order, i.e., indoramin, placebo, indoramin; each intervention lasted for 2 weeks and indoramin was given in a dose of 75 mg/day. Indoramin caused a reduction in the elevation of the computed regression line relating HR to Vo2 (a shift to the right), such that at the same HR a greater Vo2 was attained in 11 of the 16 patients in comparison with the baseline exercise test. Pooled results showed a shift of the HR/Vo2 regression line to the right when indoramin was compared with baseline (p less than 0.05) or placebo. In the same patients, indoramin caused a decrease in arterial blood pressure during exercise relative to baseline or placebo periods, and a decrease in the HR during exercise relative to baseline period, but not when compared with placebo periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1984

Assessment of aortocoronary bypass grafting using exercise ST segment/heart rate relation.

The maximal rate of progression of ST segment depression relative to increases in heart rate (maximal ST/HR slope) has recently been shown to be an accurate index of the presence and the severity of coronary heart disease in patients with angina. The value of this new exercise test was assessed in patients undergoing aortocoronary bypass. The maximal ST/HR slope and the results of coronary angiography were obtained in each of 46 patients before aortocoronary bypass surgery and in 26 of the 46 patients six months after the operation. At each stage of the investigation the maximal ST/HR slope detected without false results the absence and the number of significantly diseased vessels as shown by angiocardiography. As in previous findings the ranges of the maximal ST/HR slope showed no overlap between the four groups of patients: those with no significant disease and those with single, double, or triple vessel disease. In each of the 46 patients in whom the maximal ST/HR slope was determined before operation and three months afterwards the slope was lower after operation than before, indicating improvement. Follow up examinations showed that the maximal ST/HR slopes accurately detected the number of patent grafts used to bypass significantly diseased coronary arteries. Furthermore, the development of a significant narrowing or occlusion in any vein graft caused an increase in the maximal ST/HR slope which was equivalent to the value of single vessel disease. It is suggested that the maximal ST/HR slope may be used reliably in individual patients to indicate restoration of adequate blood supply to the myocardium after successfully aortorcoronary bypass surgery and the to detect in the period of six months after the operation the degree of severity of coronary heart disease whether it is caused by occlusion of the graft of significant disease of the coronary arteries.

Adult↗