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Biomedical subjects

T G Pickering

Publications and source records attributed to T G Pickering.

At least 235 records · Page 13Linked to original sources

Situational variations of blood pressure in ambulatory hypertensive patients.

Blood pressure and heart rate were recorded at 15-min intervals for 24 hr in 60 untreated patients with uncomplicated mild essential hypertension using a new automatic noninvasive portable recorder. During the recording, the patients went about their normal daily routine, of which they kept a detailed record. The data were analyzed for five different recording situations: in the clinic, at work, at home, asleep, and average of the entire 24-hr period. Twenty-four hour readings were also compared with previously obtained casual readings. Clinic readings were correlated with the average 24-hr values, but for individual patients clinic pressures were relatively poor predictors of 24-hr pressures. Pressures recorded in the clinic were also greater than average 24-hr values. Similar degrees of correlation were found between clinic, home, work, and sleep pressures. Pressures recorded in the clinic were similar to pressures at work but higher than at home or asleep. In contrast, heart rate was similar in all conditions except during sleep, when it was lower. Previously measured casual pressures were also correlated with the clinic readings, with systolic values being similar, but diastolic values higher in the clinic during the 24-hr recording. For patients with clinic diastolic pressures in the range 90-104 mm Hg, 24-hr pressures varied from 75 to 100 mm Hg. We conclude that pressures measured casually in the clinic do not accurately reflect average 24-hr pressures and that ambulatory recording is helpful in the evaluation of mildly hypertensive patients.

Adult↗

Ambulatory monitoring in the evaluation of blood pressure in patients with borderline hypertension and the role of the defense reflex.

The differences between blood pressure (BP) readings taken in the clinic and during normal daily activities were assessed in two studies using a noninvasive ambulatory BP monitor (Avionics). In the first study 30 untreated hypertensive patients (17 with borderline pressures, average diastolic less than or equal to 95, and 13 established hypertensives, diastolics above 95) and 5 normotensive subjects had 30 readings taken in the physician's office and 30 while at home. Conventional sphygmomanometer BPs were also recorded in the office. In the borderline group home BPs were significantly lower than clinic BPs, whereas this difference was less marked for the established and normotensive group. In the second study BP was measured every 15 minutes for 24 hours in 25 normal subjects, 25 borderline and 25 established hypertensives, and readings categorized according to four recording situations: physician's office, work, at home, and sleep. BPs in all groups were highest at work and lowest asleep, and directional changes were similar. Both hypertensive groups showed higher BPs in the physician's office than at home, while normal subjects showed no difference. BPs recorded in the physician's office were good predictors of 24 hour average BP in normal and established hypertensive subjects, but not in the borderline group: in such patients 24 hour monitoring may be of particular value in evaluating the need for treatment.

Adolescent↗

Plasma catecholamines and cardiovascular responses during converting enzyme inhibition in normotensive and hypertensive man.

The hemodynamic and plasma catecholamine responses to isometric exercise and head up tilt were investigated in normotensive and hypertensive subjects during normal and low sodium intake and before and during the administration of the converting enzyme inhibitors teprotide or captopril. Although teprotide and captopril decreased significantly the mean arterial pressure during both sodium intakes the normal pattern of hemodynamic response to hand grip and head up tilt was preserved. Moreover changes of plasma catecholamines during hand grip and head up tilt were not affected either by teprotide or captopril. When following the administration of teprotide or captopril fainting occurred either in the seated position or during head up tilt it was associated not only with a decrease in arterial pressure but also with a concurrent reduction in cardiac output and/or hypovolemia. It is concluded that converting enzyme inhibition does not impair significantly the cardiovascular responses which are mediated via the sympathetic nervous system either in normotensive or in hypertensive subjects.

Adult↗

Politics and the medical profession.

For most of this century--particularly in the '40s, '50s and '60s--the emphasis among politicians and social planners has been on the provision of more and better health services. However, in the '70s a dramatic change of emphasis occurred and today most discussion of health care policy seems to relate to cost containment. Inevitably this has led to conflict. Aspects of conflict relating to the provision of health care will be discussed.

Australia↗

The vasoconstriction-volume spectrum in normotension and in the pathogenesis of hypertension.

A body of evidence has been reviewed indicating that all hypertensive phenomena ranging from mild disorders to fulminant malignant hypertension can be profitably analyzed by assessing the relative contribution of two final determinants of the arterial blood pressure--the vasoconstriction and volume components. Renin-sodium profiling and the separate application of specific pharmacologic probes provide the basic tools for identifying the relative contribution of the two components. For an equal degree of hypertension, volume forms appear to exhibit better organ flow than the more vasoconstricted forms. This bidimensional analysis has provided new understanding of the pathophysiological mechanisms of the spectrum of human hypertensive diseases of practical value for the evaluation, diagnosis, and treatment of individual patients. Beyond this, the analytical scaffold identifies some key questions for future research.

Aldosterone↗

Direct relationship between blood pressure and blood viscosity in normal and hypertensive subjects. Role of fibrinogen and concentration.

Blood pressure and components of blood viscosity were measured in 49 normal subjects and in 49 untreated patients with essential hypertension. Blood viscosity values measured at six different shear rates were significantly correlated with blood pressure (r = 0.432 to 0.505, p less than 0.001). Blood viscosity was higher in hypertensive patients. This was due to both higher plasma viscosity (1.29 +/- 0.08 standard deviation versus 1.24 +/- 0.05 centipoise (cPs), p less than 0.001) and increased hematocrit values (44.4 +/- 4 percent versus 41.5 +/- 3 percent, p less than 0.005). When blood viscosity was evaluated in subgroups of normal and hypertensive subjects with matched hematocrit values, it remained higher in the hypertensive patients, and the relationship between blood pressure and viscosity was still significant. Regardless of the hematocrit value, fibrinogen levels were elevated in hypertensive patients (p less than 0.006) and, in association with the increased globulin concentration, fibrinogen was largely responsible for the increased plasma viscosity in hypertensive patients. Since the viscosity of defibrinated blood was similar in normal and hypertensive subjects with matched hematocrit values, the elevated fibrinogen level also affected whole blood viscosity. Defibrinated blood viscosity and arterial pressures were not correlated. These studies demonstrate a direct correlation between blood pressure and blood viscosity among normotensive and hypertensive subjects. This relationship is, in part, due to the rheologic effects of an elevated fibrinogen level and to an increased hematocrit value. The basis for hyperfibrinogenemia in hypertensive patients is unclear.

Adult↗

Hemodynamic effects of the converting enzyme inhibitor teprotide in normal- and high-renin hypertension.

The hemodynamic effects of the converting enzyme inhibitor teprotide (SQ 20881) were investigated in five patients with normal plasma renin activity who were normotensive during the study (group I), in five patients with hypertension and normal plasma renin activity (group II), and in five patients with hypertension and high plasma renin activity (group III). No significant hemodynamic changes were observed during teprotide administration in group I. In group II there was a decrease in mean arterial pressure by 10 +/- 2% (p < 0.005) that was associated with a decrease by 16 +/- 7% (p < 0.05) in stroke volume and cardiac output, possibly due to venodilatation and without a concurrent change in total peripheral resistance. In group III the larger decrease of 19 +/- 4% (p < 0.005) in mean arterial pressure was due to a decrease by 30 +/- 3% (p < 0.005) in peripheral resistance. In this group stroke volume and cardiac output increased by 13 +/- 2% (p < 0.025). There were no compensatory changes in heart rate despite the decrease in mean arterial pressure and vasodilatation. These results indicate that teprotide decreases arterial pressure by a dual hemodynamic mechanism. Cardiac output is increased by teprotide in patients with high-renin hypertension who exhibit the greatest decrements in peripheral resistance.

Adult↗

Baroreceptor activation reduces reactivity to noxious stimulation: implications for hypertension.

The hypothesis was tested that an acute rise of blood pressure may reduce reactivity to noxious stimuli through a baroreceptor-mediated reduction of cerebral arousal. When blood pressure was raised by an infusion of phenylephrine, rats showed less running to terminate or avoid noxious stimuli than during saline infusions. This effect was not seen in rats with denervated baroreceptors. The results suggest that a rise of blood pressure could have motivational consequences significant for human hypertension.

Animals↗

Renin profiling for diagnosis and treatment of hypertension.

Recent research shows that the renin-angiotensin-aldosterone axis either maintains or causes some or all of the high blood pressure of most patients and demonstrates anew that renin-sodium profiling defines this involvement. Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions. For the remaining majority with essential hypertension, renin profiling exposes the relative participation of either vasoconstriction or volume factors, thereby guiding simpler, more specific, and predictably effective antirenin or antivolume treatments. Renin profiling identifies those in whom treatment should begin with a beta-blocker as opposed to a diuretic while not infrequently also providing baseline information about severity and prognosis in individual patients.

Adrenergic beta-Antagonists↗

Contrasting effects of acute beta blockade with propranolol on plasma catecholamines and renin in essential hypertension: a possible basis for the delayed antihypertensive response.

Blood pressure, heart rate, plasma renin activity, plasma norepinephrine and plasma epinephrine were determined in 11 patients with essential hypertension at rest before and 15, 30, 45, and 60 minutes after an intravenous infusion of 0.12 mg./Kg. propranolol given over five minutes. After propranolol mean blood pressure was unchanged; heart rate decreased by 14 per cent within 15 minutes and showed no further changes. Plasma renin activity decreased progressively by 48 per cent 60 minutes after propranolol, whereas plasma norepinephrine and epinephrine were always higher after propranolol than control values. Increases in norepinephrine were statistically significant at 30, 45, and 60 minutes (respectively 49, 39, and 45 per cent, P less than 0.005 at least) and those of epinephrine even at 15 minutes (respectively 60, 82, 62, and 94 per cent P less than 0.01 for all). These results indicate that acute beta blockade with propranolol incudes increases in circulating plasma norepinephrine and epinephrine which might be consequent to rapidly induced hemodynamic changes. This augmented sympathetic activity might explain why propranolol, when acutely infused, does not decrease blood pressure despite effective cardiac and renin blockade.

Adrenergic beta-Antagonists↗