Critical care technicians: letting nurses be nurses. Interview by Michael Villaire.
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Critical Care↗
Biomedical subjects
B Stanek
Publications and source records attributed to B Stanek.
[A case of serum cholinesterase anenzymia].
A report is given on a 66-year-old man suffering from serum cholinesterase anenzymia. The following tests were performed to characterize the genetic pseudo-cholinesterase variants: plasma cholinesterase activity using benzoyldicholine as substrate (according to Kalow) and dibucaine and sodium fluoride as inhibiting substances. In addition, polyacrylamide density gradient gel electrophoresis followed by esterase staining technique (Mascall) was used for the electrophoretic separation of cholinesterase isoenzymes. Similarly, the only daughter's and the granddaughter's sera were analyzed. Determination of activity and inhibitor numbers indicated that the propositus had the homozygote "silent gene" genotype (A = 2, DN = 0, FN = 0). The granddaughter showed an isoenzyme constellation within normal ranges (A = 128, DN = 80, FN = 58); for the daughter apparently normal values were also found for activity and inhibitor numbers (A = 73, DN = 82, FN = 58). Figure 1 shows the results of electrophoretic separation from the sera tested and Fig. 2 results obtained by densitometric assessment. Electrophoretic separation and the zymogram obtained from the propositus' serum show only sample peak and albumin fractions. In contrast, the granddaughter's serum turned out to be absolutely normal. In the daughter's sample, however, three cholinesterase components normally found in serum were missing, as also shown by densitometry. Despite apparently normal activity and rather insignificant inhibitor numbers, gradient gel electrophoresis clearly revealed her to be a heterozygote carrier of the silent gene Es variant. As our data are in accordance with results obtained by other investigators, this observation cannot be regarded as exceptional.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Felodipine is more effective than hydrochlorothiazide when added to a beta-blocker in treating elderly hypertensive patients.
This randomized, double-blind, parallel-group study compared felodipine and hydrochlorothiazide (HCT) given in addition to a beta-blocker in 134 elderly hypertensive patients aged 56-79 years (mean of 66 +/- 5 years). In the felodipine-treated group (n = 57), supine blood pressure (BP) was reduced from 171 +/- 16/101 +/- 6 mm Hg at randomization to 147 +/- 12/86 +/- 6 mm Hg after 8 weeks, whereas in the HCT-treated group (n = 66), BP was reduced from 170 +/- 4/101 +/- 5 to 151 +/- 16/89 +/- 9 mm Hg. The reduction in diastolic blood pressure (DBP) was significantly greater in the felodipine than in the HCT group (p less than 0.003). In the felodipine-treated group, 87% of the patients were controlled (DBP less than or equal to 90 mm Hg) compared with 58% in the HCT group (p less than 0.001). Reported adverse events were generally mild. Six patients withdrew from the study due to adverse events, five in the felodipine group and one in the HCT group.
Adrenergic beta-Antagonists↗
The white-coat effect and self-recording of blood pressure.
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Blood Pressure Determination↗
Increase in bicycloprostaglandin E2 metabolite in congestive heart failure in response to captopril.
Vasodilating prostaglandins may be increased in patients with chronic congestive heart failure (CHF) to balance out the effects of vasoconstricting forces. Significant increases in plasma levels of bicycloprostaglandin E2 metabolite (PGEm), a chemically stable degradation product of the vasodilating prostaglandin E2, were found in response to captopril (39.4 +/- 7.8 vs. 46.2 +/- 8.2 pg/ml; p less than 0.01). With chronic captopril treatment bicyclo-PGEm remained elevated for 12 h after the last dose after 1 and 2 months (75.5 +/- 5.5; p less than 0.05 and 72.1 +/- 6.3 pg/ml; p less than 0.05, respectively). Upon readministration of captopril during chronic captopril treatment the significant increase of bicyclo-PGEm in response to captopril was sustained, as were changes in plasma renin activity, angiotensin II, and blood pressure. Plasma catecholamines were unchanged with captopril or decreased slightly, vasopressin remained moderately increased throughout. Taken together, the results suggest that vasodilating prostaglandin E2 production might play a part in captopril's beneficial action in chronic congestive heart failure.
Adult↗
[Left heart hypertrophy in arterial hypertension in relation to hemodynamic and humoral factors].
In patients with arterial hypertension hemodynamic as well as humoral factors may influence the development of left ventricular hypertrophy. We therefore investigated in 23 patients with long standing hypertension (11 females, 12 males, age 50 +/- 13 years) wether left ventricular mass as determined by echocardiography interrelates with hemodynamic or humoral parameters. Left ventricular mass measured 161 +/- 51 g/m2 and correlated significantly with patients' age (r = 0.55, p less than 0.05) and systolic blood pressure (159 +/- 21 mm Hg, r = 0.51, p less than 0.05) but not with diastolic blood pressure (99 +/- 15 mm Hg, r = 0.23, not significant). Plasma renin activity was 0.6 +/- 0.6 ng/ml/h and plasma norepinephrine levels measured 371 +/- 168 ng/l. Neither of these humoral parameters correlated significantly with left ventricular mass. It is concluded that in long standing hypertension left ventricular hypertrophy is determined predominantly by the elevation of systolic blood pressure and the patients' age.
Adult↗
Sympatho-adrenal response to hypoglycaemia in infants.
The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
Adrenal Glands↗
Effect of captopril on renin and blood pressure in cirrhosis.
In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction. Captopril caused an increase in plasma renin activity (p less than 0.005) and a decrease in plasma aldosterone (p less than 0.025) from an elevated baseline, and a moderate drop in systolic (p less than 0.025) and diastolic (p less than 0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r = -0.66, p less than 0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r = 0.49, p less than 0.05 for systolic and r = 0.71, p less than 0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels. The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.
Adult↗
Renin-angiotensin-aldosterone system and vasopressin in cyclosporine-treated renal allograft recipients.
Eleven patients, who had undergone renal transplantation and who had hypertension, aged 19-56 years, were treated with cyclosporine and prednisolone. We measured plasma renin activity, aldosterone and vasopressin (RIAs) at the first, second and third week and again 9 to 12 months after transplantation. Plasma renin activity was in the low-normal range throughout (0.31 +/- 0.05, 0.30 +/- 0.03, 0.32 +/- 0.05 ng/ml/h on short- vs. 0.32 +/- 0.04 ng/ml/h on long-term), aldosterone showed a tendency to decrease (114 +/- 27, 72 +/- 18, 71 +/- 11 pg/ml on short- vs. 54 +/- 23 pg/ml on long-term), whereas vasopressin remained moderately increased during the observation period (10.5 +/- 0.8, 10.4 +/- 1.6, 8.9 +/- 0.6 pg/ml on short- vs. 9.6 +/- 1.0 pg/ml on long-term). We then investigated the reactivity of the renin-system in 5 of the patients by stimulating renin release by captopril. Increases in plasma renin activity were only moderate (0.35 +/- 0.03 vs. 0.66 +/- 0.21 ng/ml/h) and blood pressure dropped only slightly (148 +/- 2.0/98 +/- 1.2 vs. 141 +/- 4.6/95 +/- 4.2 mmHg). Levels of plasma aldosterone were significantly suppressed from a low baseline (46.4 +/- 13.5 vs. 25.3 +/- 6.1 pg/ml, p less than 0.05). The increase in vasopressin was unaffected by captopril (9.6 +/- 1.0 vs. 8.8 +/- 0.4 pg/ml). Our results suggest that in renal transplantation patients with good graft function, the activity of the renin system is unaffected by cyclosporine treatment on short- and on long-term. Vasopressin stimulation does not seem to depend on the renin system and might play a role as a vasoconstrictor in the face of a denervated kidney.
Adult↗
Bicyclo-prostaglandin E2 metabolite in congestive heart failure and relation to vasoconstrictor neurohumoral principles.
Vasodilator prostaglandins may play a role in maintaining circulatory homeostasis in patients with congestive heart failure (CHF). Plasma levels of bicyclo-prostaglandin E2 metabolite (PGEm), a chemically stabilized degradation product of the vasodilator prostaglandin E2, were determined in 45 patients with chronic CHF (New York Heart Association class II, III or IV). Mean circulating levels of bicyclo-PGEm were significantly elevated in patients with functional class III (72 +/- 8 pg/ml) or IV CHF (77 +/- 10 pg/ml) compared with control subjects (49 +/- 3 pg/ml) and patients with functional class II CHF (49 +/- 4 pg/ml). Bicyclo-PGEm concentrations correlated with plasma renin activity (r = 0.68, p less than 0.001) and plasma angiotensin II (r = 0.56, p less than 0.001) and plasma noradrenalin levels (r = 0.34, p less than 0.05). An inverse correlation was found between serum sodium concentrations and levels of bicyclo-PGEm (r = 0.46, p less than 0.01) as well as plasma renin activity (r = 0.66, p less than 0.001). Thus, prostaglandin E2 levels in plasma are increased in patients with severe CHF.
Adult↗
Acute and chronic effects of captopril on bicyclo-PGEm, the stable bicyclic end product of prostaglandin E2 in essential hypertension.
Hemodynamic and hormonal actions of acute (50 mg) and chronic (150 mg/day) captopril were tested in 10 patients with essential hypertension. Under short-term conditions blood pressure was reduced, heart rate and plasma adrenaline did not change, plasma angiotensin II and plasma aldosterone decreased. Plasma renin activity, basal plasma noradrenaline and bicyclo-PGEm, a novel stable metabolite of prostaglandin E2, increased after captopril. With chronic captopril treatment blood pressure was reduced after 4 weeks before readministration of captopril, heart rate did not change, plasma renin activity and bicyclo-PGEm remained elevated for 12 h after the last captopril dose. Angiotensin II remained suppressed, aldosterone and plasma catecholamines did not change between doses. Readministration of captopril led to a further reduction in blood pressure. Angiotensin II and aldosterone were further suppressed, bicyclo-PGEm levels increased from a higher baseline. Heart rate and plasma catecholamines did not change. Taken together, the results suggest that prostaglandin E2 is involved in the acute and chronic hypotensive response of captopril in patients with essential hypertension.
Blood Pressure↗
Renin-angiotensin-aldosterone system in cyclosporin A-treated renal allograft recipients.
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Cyclosporins↗
Plasma vasopressin as influenced by acute and chronic blockade of the renin-angiotensin system.
The activation of the renin-angiotensin system that occurs during the development of congestive heart failure (CHF) may be accompanied by continued secretion of vasopressin (AVP) in response to non-osmotic stimuli. Increased supine plasma AVP levels (by radio-immunoassay) were found in 31 patients with moderate to severe CHF (11.49 +/- 1.00 pg/ml s.e.m.) 24 h after the last diuretic dose, which correlated with plasma renin activity (PRA) (r = 0.37, P less than 0.05). However, acute inhibition of converting enzyme with captopril did not decrease plasma AVP levels (14.9 +/- 3.9 versus 14.0 +/- 2.8 pg/ml, n = 8). Indeed, in six out of eight patients, plasma AVP actually increased following captopril - presumably secondary to haemodynamic changes. Readministration of captopril after 4 months of captopril treatment, 12 h after the last dose, again did not change AVP levels (9.58 +/- 1.2 versus 13.1 +/- 1.9 pg/ml), whereas changes in haemodynamics, PRA and angiotensin II were as expected and similar to the first test. These results suggest that the acute haemodynamic action of captopril in CHF is not mediated via suppression of vasopressin, although in some patients with non-osmotic vasopressin, excess activation of the renin-angiotensin-aldosterone system might constitute a factor.
Adult↗
[Age dependence of the response of blood pressure, heart rate and plasma renin activity to captopril in essential hypertension].
The acute effects of the converting enzyme inhibitor captopril on blood pressure, heart rate and plasma renin activity were assessed in 53 patients (aged 20-80 years) with mild to moderate essential hypertension under basal conditions. The systolic blood pressure before captopril was elevated in patients in the forties (p less than 0,01) when compared to the younger patients and was positively correlated to the age before (r = 0.32, p less than 0.05) and after (r = 0.32, p less than 0,05) angiotensin converting enzyme inhibition with captopril 25 mg. the drop in systolic (-13%) and diastolic (-10%) blood pressure was significantly greater in patients in the fifties (p less than 0,025 and p less than 0,05 respectively) when compared to younger and older (p less than 0,1) patients. The response of plasma renin activity paralleled the blood pressure response, while heart rate after captopril was not significantly changed in any group. The lack of age dependence of the blood pressure response to captopril and of reflex tachycardia suggests converting enzyme inhibition to be a valuable adjunct for the treatment of essential hypertension in the elderly.
Adult↗
Acute effects of alinidine on heart rate and blood pressure in healthy subjects and patients with hyperkinetic heart syndrome.
The effects of a single dose of alinidine (0.5 mg/kg i.v.), the N-allyl-derivative of clonidine, on heart rate and blood pressure were investigated in healthy volunteers and in patients with hyperkinetic heart syndrome, at rest and during bicycle exercise. In healthy volunteers plasma catecholamine levels were also determined. Alinidine did not change heart rate at rest in the healthy volunteers but it did significantly reduce exercise-induced tachycardia, whereas blood pressure and plasma catecholamine levels were not significantly affected by alinidine, either at rest or during exercise. In patients with hyperkinetic heart syndrome, alinidine reduced heart rate at rest and during exercise to a similar extent as propranolol (0.1 mg/kg i.v.). The blood pressure did not change with alinidine but it was significantly reduced by propranolol. The observation that an alinidine-induced reduction of heart rate occurs without a concomitant fall in blood pressure, and without a clonidine-like symphatho-inhibitory action, is in line with experimental findings suggesting a specific bradycardic action of alinidine under short-term conditions.
Blood Pressure↗
Acute hypotensive effect of captopril in man modified by prostaglandin synthesis inhibition.
1 A study was carried out to investigate the possible contribution of prostaglandins in captopril-induced hypotension. 2 Healthy volunteers and patients with essential hypertension were given single oral doses of 25 mg and 50 mg captopril respectively before and after cyclo-oxygenase inhibition with indomethacin. 3 The acute hypotensive effect of captopril was not associated with changes in heart rate. As expected, captopril led to an increase in plasma renin activity, decrease in plasma angiotensin II, and decrease in plasma aldosterone concentration. 4 After acute indomethacin pretreatment the acute hypotensive effect of captopril was significantly blunted in volunteers and in the 14 hypertensive patients. Changes in plasma renin activity and angiotensin II were significantly lower from a lower baseline. 5 Prostaglandins may therefore be mediators of the initial captopril effect. The blunting effect of indomethacin should be taken into account under clinical conditions.
Adult↗
[Acute inhibition of angiotensin-converting enzyme by captopril. Hemodynamic and biochemical aspects in normotension and essential hypertension].
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Adult↗
Plasma catecholamines, plasma renin activity and haemodynamics during sodium nitroprusside-induced hypotension and additional beta-blockage with bunitrolol.
The effects of beta-blockade on certain physiological and haemodynamic responses to sodium nitroprusside-induced hypotension have been studied in 5 patients, aged 18--54 years, undergoing inner ear surgery. Samples of blood were collected under premedication, following induction of anaesthesia, during neuroleptanalgesia, during a sodium nitroprusside infusion adjusted to produce a 40% fall in blood pressure, during superimposed beta-blockage with bunitrolol and under stable haemodynamic conditions after discontinuation of sodium nitroprusside. The sodium nitroprusside-induced reduction in blood pressure led to a massive increase in plasma noradrenaline and adrenaline and in plasma renin activity. beta-blockade with bunitrolol did not affect the increased catecholamine concentrations, the increase in plasma renin activity was significantly reduced, the increase in heart rate was reversed, and total peripheral resistance and diastolic blood pressure were further reduced. These changes can be attributed to the intrinsic beta-synmpathomimetic activity of bunitrolol in addition to its beta-blocking effect. Since no adverse effect was observed in this study, combined therapy with sodium nitroprusside and beta-receptor blockade should be employed if the effects of increased sympathetic tone are considered to be undesirable.
Adolescent↗