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Biomedical subjects

S Julius

Publications and source records attributed to S Julius.

At least 163 records · Page 9Linked to original sources
PubMed1984

Blood pressure elevation during hindquarter compression in dogs is neurogenic.

In a previous paper we reported that in pigs and dogs hindlimb compression causes large blood pressure increases which appear to be neurogenic. The present studies explore the utility of this non-invasive pressor model by determining the duration of the blood pressure increase, and by providing definitive evidence that the pressor response is neurogenic. All studies were done in chloralose-anaesthetized mongrel dogs. Prolonged experiments were performed in five experimental and four control dogs. Pressor responses could be elicited over a period of 9 h. The blood pressure increase during the 9th h was +30 +/- (s.e.m.) 6/32 +/- 5 mmHg (P less than 0.001 by paired t-test). The blood pressure in control animals did not change. Short-term hormonal and haemodynamic responses were analysed in 10 dogs. After 20 min hindlimb compression, mean blood pressure was elevated by 41.2 +/- 8.0 mmHg (P less than 0.001), plasma norepinephrine increased by 717 +/- 133 pg/ml (P less than 0.01) and plasma renin rose by 3.4 +/- 1.0 ng/ml/h (P less than 0.05). The pressure elevation was due to a 37% increase in total vascular resistance (P less than 0.01). Spinal anaesthesia at L4-L5 level in nine dogs caused a 70% reduction of blood pressure increase during lower body compression (P less than 0.001) and totally abolished plasma renin and norepinephrine increases. The infrarenal aorta and lower vena cava were occluded in eight dogs. After the ligation, there was a small rise in mean blood pressure (13.1 +/- 3.7 mmHg, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Stroke volume--pulse pressure relationships in borderline hypertension: a possible indicator of decreased arterial compliance.

Resting invasive haemodynamic measurements were performed on 354 volunteers, 168 normals, and 186 with borderline hypertension. To test the hypothesis that patients with borderline hypertension would have a decrease in the compliance of their arterial system, the relationship of stroke volume (SV) and stroke volume index (SVI) to pulse pressure (PP) in the two groups was examined. Theoretically, as compliance decreases, there should have been a stronger relationship between SV or SVI and PP. In the sample studied, SV and SVI were significantly related to PP in borderline hypertensive patients (P less than 0.005), but not in normotensive patients. When the samples were divided into tertiles of low, middle, and high SV, the borderline hypertensive patients had higher PP with higher SV (P less than 0.01), while the normals did not. It is concluded that there appear to be significant differences between normals and patients with borderline hypertension in the relationship of SV and SVI to PP. This can be interpreted as evidence to support the existence of an abnormality in arterial compliance in borderline hypertension.

Adult↗
PubMed1983

Use of clonidine and propranolol as monotherapy in borderline hypertension.

The effect of clonidine (average 0.24 mg/day) and propranolol (average 105 mg/day) on home blood pressure readings in 16 patients with borderline hypertension was investigated in a randomized, double-blind, placebo crossover design. Patients could detect small but significant decreases of blood pressure with both active compounds (-8/-5 with propranolol and -11/-7 with clonidine). The larger mean blood pressure decrease from clonidine vs propranolol was significant (p less than 0.015). Small doses of sympatholytic agents might control the blood pressure in patients with borderline hypertension, and the home blood pressure technique is a convenient tool to detect and monitor such changes. Biochemical predictors of the responsiveness to clonidine were investigated. There was no difference in placebo norepinephrine and renin values between better and lesser responders to clonidine. Plasma norepinephrine fell with clonidine treatment, but with no relationship to the blood pressure response. Plasma norepinephrine response to clonidine might reflect not only the central withdrawal of sympathetic tone, but also, in part, the effect of clonidine on peripheral presynaptic alpha 2-receptors.

Adult↗
PubMed1983

Cardiopulmonary mechanoreceptors and renin release in humans.

We investigated the hemodynamic determinants of the reflex release of renin to changes in posture and blood volume distribution in healthy humans to determine the relative contribution of arterial and cardiopulmonary mechanoreceptors to the reflex release of renin under physiological circumstances. In the first experiments, we induced a selective decrease of right atrial pressure by inflation of cuffs around the thighs. Renin increased and returned toward baseline on decompression. The renin increase was neurogenic because plasma norepinephrine increased, the response was abolished by beta blockade, and renin did not increase in patients with denervated transplanted kidneys. The second experiments were performed with tilting and later filling a pressure suit to counteract the effect of tilting on gravitational pooling of the blood. Tilting elicited increases of renin and norepinephrine; filling the suit abolished these increases. Right atrial pressure fell with tilting and rose after filling the suit. Because the neck was elevated above the heart equally in both conditions, it is concluded that the increase and decrease of renin reflected decrease and increase of the stretch of cardiopulmonary receptors. The third experiments were performed by elevating the upper trunk with the legs remaining in a horizontal position (sitting). This caused a heart-to-neck pressure difference and an increased sympathetic outflow through unloading arterial baroreceptors. Norepinephrine increased but renin did not. Cardiopulmonary receptors exhibit an important influence on the reflex release of renin.

Blood Pressure↗
PubMed1983

Borderline hypertension.

Blood pressures over 130 mm Hg systolic and 80 mm Hg diastolic are associated with a significantly increased risk of cardiovascular morbidity and mortality as well as an increased risk of progression to later established hypertension. An average blood pressure based on repeated determinations is a better predictor of target organ damage in hypertensive individuals than an isolated casual clinic blood pressure. Careful clinical assessment of the patient with borderline hypertension can identify those at highest risk for progression to established hypertension and those at greatest risk for cardiovascular morbidity and mortality. We cannot currently recommend pharmacologic therapy for the vast majority of patients with blood pressures between l30/80 and l140/90 mm Hg. Although nonpharmacologic therapy is frequently met with a high degree of noncompliance, there is evidence that modest reductions in salt intake and weight often result in significant reductions in blood pressure. Many patients with borderline hypertension, when appraised of these facts, will comply and attempt to reach these limited goals. Repeated self-determination of blood pressures at home is ideally suited to many patients with borderline hypertension in defining current average blood pressure, detecting future progression, and evaluating the effects of nonpharmacologic interventions.

Alcohol Drinking↗
PubMed1982

Usefulness of home BP determination in treating borderline hypertension.

This study explores whether home BP self-determination can be used to assess the effect of treatment in patients with borderline hypertension. Sixteen untreated patients underwent a double-blind trial of propranolol hydrochloride (average dose, 105 mg), clonidine hydrochloride (0.24 mg), and placebo. Home BP readings decreased with both active compounds (-8/-5 with propranolol and -11/-7 with clonidine). During placebo, the readings increased to levels identical to untreated values. This study demonstrates that patients with borderline hypertension are consistently capable of detecting small average changes in home BP. It is also shown that sympatholytic monotherapy can be effectively used to lower the BP in such patients.

Adult↗
PubMed1982

Increased platelet catecholamine content in pheochromocytoma: a diagnostic test in patients with elevated plasma catecholamines.

Platelet catecholamine content was determined by radioenzymatic assay in 16 patients with elevated plasma norepinephrine or epinephrine or both and a clinical picture suggesting pheochromocytoma. Twenty-two normal subjects served as controls. Pheochromocytoma was documented in 10 patients, all of whom had markedly elevated platelet catecholamines. The other six patients had no tumor, and their platelet catecholamine levels were normal. Platelet catecholamines tended to return to normal more slowly than plasma catecholamines after removal of the pheochromocytoma, suggesting that platelets were rich in stored catecholamines. Determination of platelet catecholamine content is a helpful aid to the diagnosis of pheochromocytoma in patients with suggestive but not diagnostic elevations of the plasma catecholamine concentration.

Adolescent↗
PubMed1982

Vasodilators in the treatment of hypertension.

Vasodilators lower the blood pressure by decreasing total peripheral resistance. The hemodynamic changes depend on the mix between arteriolar and venous dilatation. Since the compensatory responses are blunted with sympatholytic agents and diuretics, vasodilators can be applied effectively in the treatment of hypertension. Hydralazine and prazosin are used as step III drugs in combination with beta-adrenergic blockers and diuretics. Only hypertensive patients whose blood pressure is not controlled by standard antihypertensive drugs should receive minoxidil or captopril. Hypertensives receiving minoxidil usually require a loop diuretic such as furosemide, in addition to a beta-blocker. Captopril is usually combined with a thiazide diuretic and frequently also with a beta-adrenergic blocker. For hypertensive emergencies diazoxide must be injected intravenously as a bolus. It is contraindicated in patients with dissecting aortic aneurysm or left ventricular failure. Sodium nitroprusside is effective in most cases of hypertensive crisis and must be administered intravenously under continuous observation.

Calcium Channel Blockers↗
PubMed1982

Lead, hypertension, and the renin-angiotensin system in rats.

Rats were exposed continuously to Pb in utero and after birth by giving their mothers, during pregnancy and lactation, drinking water containing 0, 100, or 500 ppm Pb (as Pb acetate) and then continuing this regimen after weaning. Male rats received 100 ppm developed a significant elevation of systolic blood pressure (152 +/- 3.7 mm Hg vs. 135 +/- 5.6 for controls) at 3 1/2 months and remained hypertensive until sacrifice at 6 months; 500 ppm rats remained normotensive. Both 100 ppm and 500 ppm females remained normotensive. At 6 months, PRA was significantly reduced in the 100 ppm male group but was normal in the 500 ppm group. There were dose-dependent decreases in the AII/PRA ration and in renal renin. Pulmonary converting enzyme activity was not changed by Pb exposure. Blood [Pb] was 40 and 71 mug/dl, respectively, and kidney [Pb] was 4.8 and 22.9 mug/gm. Renal histology was normal in the 100 ppm group. We conclude that doses of Pb which produce blood [Pb] seen in many people are capable of inducing modest hypertension in male rats; higher doses fail to do so. The hypertension is associated with a reduction in PRA and All and therefore is unlikely to be due to hyperactivity of the RAS. (J Lab Clin Med 99:354, 1982.)

Aging↗
PubMed1981

Reliability of echocardiography in assessing cardiac output. A comparative study with a dye dilution technique.

Because of the potential benefits froma noninvasive technique in assessing cardiac output, we compared cardiac output estimates from left ventricular echocardiograms with results obtained simultaneously by a standard technique, dye dilution in 10 healthy normal volunteers. During rest, cardiac outputs by echocardiographic and dye dilution techniques were reproducible and not significantly different. Increases in cardiac output produced by intravenous infusion of isoproterenol (15 ng/kg/min for 4 min) were accurately estimated by echocardiography in subjects whose stroke volume increased less than 40%, but were significantly underestimated when stroke volume increased more than 40%. Decreased cardiac output produced by intravenous propranolol (0.2 mg/kg) was comparable by both methods. Although echocardiography accurately estimated mean cardiac output for the group it over- or underestimated cardiac output in individual subjects. We propose that echocardiography can reliably estimate cardiac output in groups at rest and when stroke volume changes less than 40%.

Cardiac Output↗
PubMed1981

Withdrawal of endogenous sympathetic drive lowers blood pressure in primary aldosteronism.

We were able to observe the effect of withdrawal of endogenous sympathetic drive in a hypertensive patient with an aldosterone-secreting adrenal adenoma. Acute stimulation of both carotid sinus nerves lowered blood pressure to normotensive or hypotensive levels by reducing peripheral resistance. When chronic carotid sinus nerve stimulation was discontinued, peripheral resistance and blood pressure increased. These data suggest that the sympathetic nervous system is important in the maintenance of hypertension in established primary aldosteronism.

Carotid Sinus↗
PubMed1981

Evidence against an interaction of angiotensin II with the sympathetic nervous system in man.

Animal experiments indicate that angiotensin II can, under some circumstances stimulate the sympathetic nervous system at a number of different sites. In order to determine whether such a relationship of the renin-angiotensin and sympathetic nervous system exists in man, we increased (by intravenous infusion), or decreased (by administering the oral converting enzyme inhibitor captopril) circulating angiotensin II levels and monitored plasma adrenaline and noradrenaline responses. Angiotensin II infusions did not increase plasma catechol-amines, and lowering of angiotensin II by captopril treatment in patients with severe hypertension or congestive heart failure failed to alter plasma adrenaline or nor-adrenaline levels. Whether physiological levels of angiotensin II are capable of interacting directly with the sympathetic nervous system in man remains to be demonstrated.

Adult↗
PubMed1981

Efficacy of an oral angiotensin-converting enzyme inhibitor (captopril) in severe hypertension.

The antihypertensive effect of captopril was assessed during short- and long-term periods in ten patients with elevated blood pressure readings that were uncontrollable by standard therapy (supine diastolic blood pressure of greater than 100 mm Hg with a regimen of propranolol hydrochloride, hydralazine hydrochloride, and hydrochlorothiazide). When given alone, captopril therapy was unable to normalize the blood pressure in any patient. The addition of hydrochlorothiazide to the captopril therapy normalized the blood pressure in one patient and sharply improved the blood pressure in four others. The blood pressure in the remaining patients responded inadequately to this combination. The addition of propranolol to captopril and hydrochlorothiazide reduced the blood pressure further in most cases (seven on the ten patients had normal blood pressure readings while they received these three drugs). In four patients, the blood pressure response to the added propranolol was unrelated to changes in plasma angiotensin II concentration. Captopril was helpful in the management of refractory hypertension in most cases.

Administration, Oral↗
PubMed1980

Borderline hypertension. Hypertension seminars at Ostra Hospital, Göteberg, Sweden.

Borderline hypertension was the topic of one of the "Hypertension seminars" arranged by the Hypertension Section at the Ostra Hospital, Göteborg, Sweden. On that occasion Professor Stevo Julius, Ann Arbor, Michigan USA, was an invited guest. During the seminar, various aspects of borderline hypertension were discussed, e.g. the natural history, hemodynamics and management of this condition. The present review is based on these discussions.

Adolescent↗
PubMed1980

Practical management of borderline hypertension.

Patients with borderline hypertension are at a higher risk to develop sustained hypertension and its sequelae, higher cardiovascular morbidity and mortality. However, this excess risk is not overwhelming. Aggressive antihypertensive medication for all patients with borderline hypertension is not warranted. Only patients who are at highest risk for hypertension and its complications should be given small doses of antihypertensive monotherapy. The objective of the treatment is to lower blood pressure without side effects. Patients who are not chosen for treatment must be continuously managed. The management includes following the blood pressure trends, dietary sodium restriction, and control of overweight.

Adolescent↗
PubMed1979

Effect of systemic autonomic inhibition on the hemodynamic response to antihypertensive therapy with timolol.

To evaluate the role of systemic autonomic tone in the hemodynamic response to beta-inhibitors, the hemodynamic effects of long-term timolol therapy were studied in hypertensive patients under two sets of conditions: at rest and after pharmacologic systemic autonomic inhibition (SAI). Hemodynamic studies were performed in every subject at the end of a 4-week placebo period and again at the end of a 9-week treatment period. The antihypertensive effect of timolol was associated with decreased cardiac output and unchanged peripheral resistance at rest and with unchanged cardiac output and decreased peripheral resistance after SAI. The hemodynamic response to SAI during the two studies was also markedly different. The findings provide evidence of increased alpha-adrenergic component of systemic autonomic tone during long-term therapy with timolol.

Adult↗