Search PubMed⌕ Search

Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 325 records · Page 18Linked to original sources
PubMed1975

Splanchnic blood flow in essential hypertension and in hypertensive patients with renal artery stenosis.

Splanchnic blood flow (SBF) was measured simultaneously with cardiac output (dye dilution) and intrarterial blood pressure by constant infusion of indocyanine green in 11 control subjects, 13 patients with essential hypertension (EH) and seven hypertensive patients with renal artery stenosis (RAS). The cardiac index (CI) was lower (P less than 0.05) in patients with EH (3.17 plus or minus 0.07 L/min/m-2) (mean plus or minus SEM) than in control subjects (3.43 plus or minus 0.09). Associated with the lower CI was a significantly (P less than 0.01) lower SBF (0.797 plus or minus 0.02 L/min/m-2 vs 0.889 plus or minus 0.04). Patients with RAS presented with higher (P less than 0.01 vs EH, nonsignificant vs control subjects) cardiac index (3.66 plus or minus 0.17) and even lower SBF (0.749 PLUS OR MINUS 0.02). Furthermore, there was a negative correlation (r = - 0.652) between the mean arterial pressure and the SBF when results for all patients were considered. The correlation remained (r = - 0.568) in the EH group and the slope of regression line was not different from that for all subjects. The CI and SBF were weakly correlated (r = 0.423) in control subjects and patients with EH, whereas in patients with RAS, a negative correlation was found (r = - 0.778). This study indicates that the SBF, although significantly decreased in patients with EH, remains proportional to the CI in control subjects and in essential hypertensive patients. No redistribution of CI in regard to the splanchnic circulation occurs in EH. In contrast, in patients with RAS a dissociation of CI and SBF occurs and the fraction of the CI which passes through the splanchnic vascular bed is markedly reduced. The close correlation between mean arterial pressure and SBF suggests that both parameters are influenced by a common pathophysiological factor.

Abdomen↗
PubMed1975

Labile (borderline) hypertension--new aspects of a common disorder.

Labile hypertension in patients under 50 years of age (the non-atherosclerotic form) was found to be characterized by higher urinary excretion of catecholamines and particularly of homovanillic acid; when further analyzed it was shown to be a heterogeneous entity with two types of patients clinically and biochemically distinguishable from each other, from control subjects and from patients with stable hypertension. Reactivity to assuming an upright posture distinguishes one type of labile hypertension having a normal postural pulse rate response from another having an excessive postural increase in pulse rate. The first group also showed normal responses of plasma norepinephrine concentration and of urinary cyclic AMP to posture. The group with excessive pulse rate response, in contrast, showed a decrease in plasma norepinephrine and an excessive increase of urinary cyclic AMP excretion in response to upright posture. The results suggest that not only circulating catecholamines but also the reactivity of their target tissues (as probably reflected by cyclic AMP measurements) are important in bringing about signs of adrenergic excess. The hypothesis that cyclic AMP changes reflect beta-adrenergic receptor reactivity is strongly favoured by data indicating qualitative differences in cyclic AMP responses to beta-adrenergic stimulation or inhibition between control subjects and those labile hypertensive patients with clinical signs of excessive sympathetic reactivity. The study stresses the need for more precise definition of labile hypertension, for dynamic clinical and biochemical correlative studies, and for consideration not only of the circulating hormones but also of the "second messengers" (such as cyclic AMP and cyclic GMP) which reflect the cellular action of hormones. Blood pressure is a very labile parameter in health and disease. In one sense, therefore, hypertension can be considered "labile" in every hypertensive patient. Usually, however, labile (or borderline) hypertension is regarded as characterized by a blood pressure over 140/90 mmHg, falling below these values with physical and emotional rest. This clinical entity, which affects some 20% (variously estimated between 16 and 30%) of the adult population, gives rise to uncertainties in both definition and prognosis. In some patients labile hypertension represents the precursor of a fixed hypertensive state, whereas in many others it remains labile throughout life, never progressing to the stable phase nor becoming associated with hypertensive cardiovascular disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Catecholamines↗
PubMed1975

Diurnal variation of plasma vasopressin in man.

Plasma arginine vasopressin (PAV) concentration was determined by radioimmunoassay during the diurnal cycle in 8 recombent healthy male subjects. Two subjects were studied again 3 weeks later while receiving 1 mycles. In 8 out of 10 cycles, a nocturnal increase in PAV was found; there was a progressive rise during the night in 5 subjects and a peak occurred at 2400 or 3400 h. In 1 subject no variation was detected and in another, the pattern was compleetly different. The mean PAV in the 10 cycles was significantly (P less than 0.001) higher during the night than during the day. Dexamethasone did not modify the pattern of variation, but induced a significant (P less than 0.001) decrease in PAV. Hematocrit remained stable throughout the study as did osmolality, except at 2000 h, when a significant (P less than 0.001) increase (5 mOsm) on average occurred in every subject. Blood sugar, sodium or chloride did not account for the observed rise in osmolality and no simultaneous change in PAV occurred. A rise in PAV explains, to some extent, the known nocturnal decrease in urine output. Diurnal variations in PAV must be taken into account in clinical investigations involving vasopressin.

Adult↗
PubMedDate not supplied

Hypertension and the heart.

It has been clearly demonstrated that left ventricular (LV) hypertrophy is a strong blood pressure independent risk factor for cardiovascular morbidity and mortality in the general population, in primary and secondary hypertension and in cardiac patients. LV hypertrophy in arterial hypertension develops in response to an increased afterload, but underlying pathophysiological mechanisms include a variety of non-haemodynamic factors. Due to the prognostic importance of LV hypertrophy, normalisation of LV mass emerged as a desirable goal of antihypertensive treatment. Indeed, several prospective studies now indicate that regression of LV hypertrophy reduced cardiovascular complications. As a consequence, the question was raised whether certain antihypertensive drugs differ in their ability to reduce LV mass. Several comparative studies and meta-analyses have been carried out to resolve this issue. The available data seem to indicate that angiotensin-converting enzyme (ACE)-inhibitors and calcium channel blockers were more potent than beta-blockers in their ability to reduce LV hypertrophy, with diuretics in the intermediate range. The role of new antihypertensive agents such as angiotensin II AT1-receptor blockers appears similar to the one of ACE-inhibitors, since in some studies angiotensin II AT1-receptor blockers were superior to beta-blockers and diuretics. Various aspects of LV hypertrophy including its prevalence, determinants, prognosis and regression are discussed in this article.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Efficacy and safety of angiotensin II receptor blockers in elderly patients with mild to moderate hypertension.

The role of the renin-angiotensin-aldosterone system in the pathogenesis of hypertensive disease has long been recognized, and the interruption of this cascade with angiotensin-converting enzyme-I has been beneficial in the management of hypertension. Recently, a new class of drugs, the angiotensin receptor blockers, emerged, enlarging the antihypertensive armamentarium. Since elderly patients are more prone to adverse drug reactions, in this paper we review several trials, most of which were of short duration, on the efficacy and safety of angiotensin receptor blockers in the geriatric population with mild to moderate hypertension. These studies established that the drugs are well-tolerated, safe, and in most instances as efficacious as other classes of antihypertensive medications. Combination therapy with angiotensin receptor blockers and hydrochlorothiazide was additive, without any significant effect on the safety profile.

Aged↗
PubMedDate not supplied

Antiadrenergic therapy: special aspects in hypertension in the elderly.

The effect of antiadrenergic treatment with methyldopa was studied in 17 patients with established essential hypertension who were subdivided with respect to age in a group younger (n = 10; mean age, 47 +/- 2.4 (SEM) years; and a group older than 60 years of age (n = 7, mean age, 67 +/- 2.8 SEM). The fall in arterial pressure was associated with a significant (p less than 0.05) decrease in cardiac output and heart rate in patients over 60 years of age and no change in total peripheral resistance, whereas a (nonsignificant) fall in resistance occurred in younger patients. In both age groups, a significant (p less than 0.05 and less than 0.01, respectively) decrease in plasma norepinephrine levels was observed, whereas epinephrine and dopamine showed no changes. Pre- and posttreatment values of mean arterial pressure correlated directly with plasma norepinephrine values (r = 0.35 p less than 0.05). Regardless of whether cardiac output was reduced or remained unchanged, renal blood flow, plasma and total blood volume did not change in either group with antiadrenergic treatment. Further, reflexive cardiac changes (responses to isometric exercise and upright tilt) remained qualitatively unchanged. It is concluded that antiadrenergic treatment with methyldopa lowers arterial pressure additionally by decreasing circulating norepinephrine levels. The antihypertensive effect is associated with a fall in peripheral resistance in the younger and a decrease in cardiac output in the older patients, and does not compromise renal blood flow or cardiac reflexive responses.

Aged↗
PubMedDate not supplied

The problem of obesity and hypertension.

Hypertension and obesity are two disorders that have been closely related, each occurring in greater frequency with the other than in an otherwise normal population. Although a causal relationship has not been established between the two, their coincidence carries increased risk of cardiovascular morbidity and mortality. This report summarizes the pathophysiological studies from our laboratory concerning their interrelationship and offers a rational hypothesis for the mechanisms underlying this enhanced risk. Patients with hypertension demonstrate an increased total peripheral resistance that explains hemodynamically the rising arterial pressure with advancing vascular disease. In response to this increased afterload imposed upon the heart, the left ventricle adapts itself structurally through a process of concentric hypertrophy. In addition, in most patients with essential hypertension, plasma volume progressively contracts and renal vascular resistance increases in proportion to the rise in arterial pressure and total peripheral resistance. In contrast, in obesity-hypertension there is a superimposed factor of volume overload upon the hemodynamic abnormality. The result is an additional cardiac stimulus for eccentric hypertrophy due to the increased ventricular preload. This factor enhances left ventricular stroke work and its attendant myocardial oxygen demands, thereby providing a dual overload on cardiac function that can explain the increased risk of heart failure related to these associated conditions. In contrast to the compounding adverse hemodynamic effects on the heart, there does not seem to be an additive hemodynamic effect of obesity on hypertensive renal vascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Hemodynamic and cardiac effects of centrally acting antihypertensive drugs.

The centrally acting alpha-adrenergic receptor agonist compounds have been available for treatment of hypertension for more than 25 years. Through studies of these compounds during this time, new knowledge has been made available not only on their mechanisms of antihypertensive action but also on the role of the adrenergic nervous system in essential hypertension. This discussion primarily reviews work from this laboratory on the cardiovascular actions of these compounds but reflects the general information from other quarters. In general, reduction of arterial pressure induced by these agents is associated with a cardiac output that remains relatively unchanged and with organ blood flows that are preserved. As a result of the reduced pressure, cardiac function is improved; and in recent studies, cardiac mass may be reduced. Associated with the reduced arterial pressure is an expanded plasma volume that is associated with a reduced blood viscosity, hematocrit, and plasma renin activity, but which may be at the expense of some return of arterial pressure toward pretreatment levels. The latter usually requires the addition of diuretic therapy. Current studies in our laboratory concern the performance of the heart following regression of ventricular hypertrophy both at reduced as well as increased ventricular afterloads.

Adrenergic alpha-Agonists↗