Showing papers by "Giuseppe Mancia published in 1983"

Blood pressure and heart rate variabilities in normotensive and hypertensive human beings.

Abstract: Blood pressure and heart rate variabilities were studied in 89 ambulant normotensive or essential hypertensive subjects in whom blood pressure was recorded intra-arterially for 24 hours (Oxford method) under standardized living conditions. Data were analyzed beat to beat by a computer to provide mean values of the 48 half hours of the 24-hour period. Variabilities were assessed by the standard deviation and variation coefficients separately obtained for each half hour, as well as by the standard deviations and variation coefficients obtained by averaging the 48 mean values. In each subject, blood pressure and heart rate varied markedly either among or within half hours, indicating the existence of relatively longand short-term variabilities during the 24 hours. When averaged for all subjects, the long-term variabilities showed only one systematic component, i.e., the marked reduction occurring during sleep. Sleep was further responsible for a marked reduction in the short-term blood pressure and heart rate variabilities. These variabilities showed marked (though nonsystematic) modifications, even outside sleep, which were positively related to the blood pressure and heart rate means. Modifications in blood pressure and heart rate means and short-term variabilities were also positively related to each other. All these features were common to normotensives and hypertensives. In hypertensives, the absolute long and short-term blood pressure variabilities were greater than in normotensives, but the percent blood pressure variabilities were similar. Heart rate variabilities (both absolute and percent) were similar in normotensive and hypertensive subjects. Heart rate variabilities were also similar whether the subjects had impaired or preserved baroreflex control of heart rate (vasoactive drug technique). These findings uncover a number of factors that are associated with and responsible for blood pressure and heart rate variabilities in human beings. The nature of these factors suggest a primary role of central nervous mechanisms in the production of these phenomena and in the overall cardiovascular modulation, with no substantial difference between conditions of normal and chronically elevated blood pressure. (Circ Res 53: 96-104, 1983)

Arterial Baroreflexes in Humans

Abstract: The sections in this article are: 1 Techniques 1.1 Carotid Sinus Massage 1.2 Electrical Stimulation of Carotid Sinus Nerves 1.3 Section or Anesthesia of Carotid Sinus Nerves and Vagi 1.4 Occlusion of Common Carotid Arteries 1.5 Neck Chamber 1.6 Vasoactive Drugs 1.7 Nonselective Techniques 2 Arterial Baroreceptor Control of Heart Rate 2.1 Autonomic Mediation 2.2 Other Properties 2.3 Relationship to Base-Line R-R Interval 2.4 Relationship to Respiratory Cycle 3 Arterial Baroreceptor Control of Atrioventricular Conduction and Ventricles 4 Carotid Baroreceptor Control of Blood Pressure 5 Carotid Baroreceptor Influence on Cardiac Output and Total Peripheral Resistance 6 Arterial Baroreceptor Control of Regional Circulations 7 Arterial Baroreceptor Control of Veins 8 Set Point of Carotid Baroreflex 9 Aortic Baroreflexes 10 Factors That Modify Arterial Baroreceptor Control of Circulation 10.1 Age 10.2 Exercise 10.3 Mental Stress 10.4 Sleep 10.5 Anesthesia 10.6 Central Blood Volume and Posture 11 Pathological States 11.1 Hypertension 11.2 Heart Disease 11.3 Carotid Sinus Syndrome 11.4 Other Pathological Conditions 12 Modification of Arterial Baroreflexes by Drugs 12.1 β-Adrenergic Antagonists 12.2 Cardiac Glycosides 12.3 Antihypertensive Drugs

Cardiopulmonary Baroreflexes in Humans

Abstract: The sections in this article are: 1 Techniques 1.1 Lower-Body Negative Pressure 1.2 Congesting Cuffs and Hemorrhage 1.3 Elevation of Legs and Lower-Body Positive Pressure 1.4 Head-Out Water Immersion 1.5 Upright Tilting and Respiratory Maneuvers 2 Cardiopulmonary Baroreceptor Control of Forearm Vascular Resistance and Sympathetic Nerve Activity 3 Cardiopulmonary Baroreceptor Control of Splanchnic Circulation 4 Cardiopulmonary Baroreceptor Control of Venous Tone 5 Cardiopulmonary Baroreceptor Control of Heart Rate 6 Cardiopulmonary Baroreceptor Control of Renin and Vasopressin 6.1 Renin Release 6.2 Vasopressin Secretion 7 Interaction of Cardiopulmonary, Carotid, and Somatic Reflexes 8 Myocardial Ischemia and Infarction 8.1 Mechanisms of Bradycardia and Hypotension With Inferoposterior Infarction 8.2 Mechanisms of Tachycardia and Hypertension With Anterior Myocardial Infarction 9 Pathological States 9.1 Bradycardia and Hypotension During Coronary Arteriography 9.2 Chronic Heart Failure 9.3 Hypertension 9.4 Syncope

Methods for assessing blood pressure values in humans

Abstract: In clinical medicine and epidemiology, measurements of blood pressure largely rely upon the use of cuff inflation and Korotkoff sounds. Although still the most practical, this method has been recognized to have important limitations. This paper focuses on two limitations of the cuff method that have been found while recording 24-hour intraarterial blood pressure in free-living normotensive and hypertensive patients. First, the 24-hour blood pressure is characterized by large long- and short-term variabilities whose magnitudes vary according to the patient's basal blood pressure and age. This is likely to reduce the possibility that a few isolated cuff measurements are accurate and representative of the patient's average blood pressure. Second, during cuff blood pressure assessment by the doctor (and to a lesser degree by the nurse), the patient's blood pressure normally rises due to an alarm reaction, with a large peak within the first 4 minutes and a subsequent decline. The magnitude of the peak rise, as well as its large and unpredictable difference among subjects may be responsible for seriously and variably overestimating the blood pressure. A 10-minute wait from the beginning of the doctor's visit usually avoids this inconvenience. Finally, the paper briefly considers alternative methods to the cuff method, including invasive intraarterial 24-hour recording in ambulatory subjects, which provides a large amount of information but is impractical, and noninvasive automatic blood pressure devices, which offer a promising practical approach but must wait for technical validation.

Plasma catecholamines do not invariably reflect sympathetically induced changes in blood pressure in man.

Abstract: 1. Plasma concentrations of noradrenaline and adrenaline were measured radioenzymatically in nine subjects during 4 min pressor and depressor responses (intra-arterial measurements) induced by increasing and reducing sympathetic vasoconstrictor tone via carotid baroreceptor deactivation and stimulation (neck chamber technique). 2. During the pressor response (15 ± 3 mmHg, mean ± se) plasma noradrenaline and adrenaline showed various changes in the different subjects and on average were not significantly increased above control. During the depressor response (−9 ± 2 mmHg) plasma noradrenaline and adrenaline also showed various changes in the subjects and were on average not significantly reduced below control. 3. In contrast the same subjects all showed an increase in noradrenaline and adrenaline (average 76 and 117%) at the fourth minute of a tilting manoeuvre with- a return to pretilting values no more than 4 min after resumption of the supine position. 4. These results suggest that the moderate and/or restricted alterations in sympathetic tone produced by manipulating a single baroreflex, though capable of affecting blood pressure, are not reflected by alterations in plasma catecholamines. To modify these humoral indices significantly, the more drastic or more diffuse alterations in sympathetic activity that may be produced by manipulating low as well as high pressure reflexogenic areas are needed.

Mechanisms of antihypertensive action of beta-adrenergic blocking drugs: evidence against potentiation of baroreflexes

Abstract: A possibility that can be advanced to explain the antihypertensive effect of beta-blocking drugs is that they act through the baroreflex control of the cardiovascular system. In 38 essential hypertensive patients we measured 1) The lengthening and shortening in R-R interval caused by stimulation or deactivation of arterial baroreceptors (vasoactive drug technique); 2) The fall and rise in blood pressure caused by stimulation and deactivation of carotid baroreceptors (neck chamber); 3) The rise in forearm vascular resistance caused by deactivation of cardiopulmonary receptors (lower body suction). The study was made before and after 6-10 days' administration of nadolol (80-360 mg once a day) or acebutolol (200-600 mg t.i.d.). Nadolol and acebutolol similarly reduced blood pressure and heart rate. Either drug increased heart rate responses to arterial baroreceptor manipulation but the increase fell short of statistical significance. Blood pressure and vasomotor responses to carotid baroreceptor and cardiopulmonary receptor manipulation were also not significantly modified by beta blockade. The baroreceptor control of heart rate and blood pressure showed a modification, however, insofar as a resetting towards the lower blood pressure values occurred. These findings demonstrate that arterial baroreceptor and cardiopulmonary receptor control of circulation is not potentiated by beta-blocking drugs, and that therefore this mechanism cannot account for their antihypertensive effect. The resetting of the baroreflex that occurs during beta blockade may, however, contribute to maintain the hypotension obtained.

Modification of the baroreceptor control of atrio-ventricular conduction induced by digitalis in man

Abstract: Several studies in animals and in man have suggested that the inhibitory influence of baroreceptors on heart rate and peripheral circulation is enhanced by digitalis. Because the atrio-ventricular node represents a key site for the clinical action of digitalis we studied how baroreceptor control of atrio-ventricular conduction is modified by digitalis at therapeutical doses. In eight subjects heart rate was kept constant by atrial pacing to assess neural influences on atrio-ventricular conduction rate without the modifications caused by simultaneous changes in cardiac cycle length. Arterial baroreceptors were stimulated by increasing or reducing blood pressure (intra-arterial recording), via an iv bolus of phenylephrine or nitroglycerine. The baroreflex sensitivity was assessed in ms·mmHg−1 as the slope of the linear regressions relating the rise or fall in systolic blood pressure to the lengthening or shortening in St- (atrial stimulus artifact) Q interval (ECG recording). The study was performed before and 45 min after iv administration of digitalis (0.8 mg of Lanatoside C®). Baroreflex sensitivity during baroreceptor stimulation was 2.9±1.1 ms·mmHg−1(mean ±SE) before digitalis, whereas after digitalis a significantly and markedly greater value of 5.6±1.5 ms·mmHg−1 was found. Baroreflex sensitivity during baroreceptor deactivation was 0.9±0.1 ms·mmHg−1 before digitalis, and was not significantly affected by the drug. Thus in man the baroreceptor control of atrio-ventricular conduction is strikingly potentiated by digitalis although this potentiation is only evident in the upper portion of the stimulus-response curve of the reflex. This phenomenon may be one of the mechanisms that account for the beneficial slowing in atrioventricular conduction rate that is produced by digitalis in several clinical conditions.