Vasovagal syncope after infusion of a vasodilator in a heart-transplant recipient.
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Biomedical subjects
Publications and source records attributed to U Scherrer.
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Static muscle contraction activates metabolically sensitive muscle afferents that reflexively increase sympathetic nerve activity and arterial pressure. To determine if this contraction-induced reflex is modulated by the sinoaortic baroreflex, we performed microelectrode recordings of sympathetic nerve activity to resting leg muscle during static handgrip in humans while attempting to clamp the level of baroreflex stimulation by controlling the exercise-induced rise in blood pressure with pharmacologic agents. The principal new finding is that partial pharmacologic suppression of the rise in blood pressure during static handgrip (nitroprusside infusion) augmented the exercise-induced increases in heart rate and sympathetic activity by greater than 300%. Pharmacologic accentuation of the exercise-induced rise in blood pressure (phenylephrine infusion) attenuated these reflex increases by greater than 50%. In contrast, these pharmacologic manipulations in arterial pressure had little or no effect on: (a) forearm muscle cell pH, an index of the metabolic stimulus to skeletal muscle afferents; or (b) central venous pressure, an index of the mechanical stimulus to cardiopulmonary afferents. We conclude that in humans the sinoaortic baroreflex is much more effective than previously thought in buffering the reflex sympathetic activation caused by static muscle contraction.
Vascular studies in humans have advanced the concept that, during orthostatic stress, cardiopulmonary afferents reflexly regulate vascular resistance in the forearm but exert surprisingly little if any effects on vascular resistance in the calf. In contrast, neurophysiological studies have indicated that unloading of cardiopulmonary afferents during lower body negative pressure evokes comparable increases in sympathetic outflow to the muscles of both the forearm and the calf. The aim of this study, therefore, was to determine if alterations in central venous pressure over the physiological range trigger reflex changes in muscle sympathetic outflow that not only are statistically significant but also are large enough to alter vascular resistance in the calf. To accomplish this aim, we measured calf blood flow with plethysmography and simultaneously performed microelectrode recordings of sympathetic outflow to calf muscles in conscious humans during maneuvers designed to alter the loading conditions of the cardiopulmonary afferents. We found that calf vascular resistance increased by 33 +/- 7% (mean +/- SEM, p less than 0.05) during decreases in central venous pressure produced by nonhypotensive lower body negative pressure (LBNP) and decreased by 26 +/- 5% (p less than 0.05) during increases in central venous pressure produced by nonhypertensive infusion of normal saline. These changes in calf resistance were at least as large as the changes in forearm resistance evoked by these maneuvers and were accompanied by parallel changes in peroneal muscle sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of a synthetic atrial natriuretic peptide (h-ANP, 25 amino acids, Wy-47.663) on blood pressure, renal electrolyte excretion, plasma catecholamines, and plasma renin activity was studied in nine patients with cirrhosis of the liver and ascites. The peptide was infused intravenously at 24-h intervals for 2 h in groups of four patients each in two different doses (0.015 and 0.075 micrograms/kg/min or 0.06 and 0.3 micrograms/kg/min). A control experiment with the vehicle was performed in all patients. In three patients h-ANP (1 and 2 micrograms/kg i.v.) was administered as an intravenous bolus injection. Consistent falls in blood pressure were observed during h-ANP infusion only with the two higher doses. The two lower infused doses induced a consistent natriuresis; this renal response was abolished when the two larger doses were used. When given as a bolus, h-ANP had a natriuretic effect comparable to that of the two lower doses of infused h-ANP. Plasma catecholamines and plasma renin activity increased during infusion of the two higher doses of h-ANP. It thus appears that in patients with cirrhosis and ascites, the natriuretic effect of infused h-ANP decreases rather than increases when the doses are raised. Bolus administration of h-ANP may be less prone to trigger counterbalancing responses and side-effects.
Although previous studies in both animals and humans have suggested that cardiac baroreceptors modulate reflex sympathetic vasoconstriction during exercise, more recent studies in conscious animals have not supported this view. To further test this concept in humans, we measured sympathetic nerve discharge with intraneural microelectrodes while we used static handgrip to activate the exercise pressor reflex and nonhypotensive lower-body negative pressure (LBNP) to selectively unload the cardiac baroreflex. In nine healthy subjects, we measured blood pressure, heart rate, central venous pressure, and muscle sympathetic nerve activity (MSNA) from the peroneal nerve (resting leg) during 2 minutes of static handgrip at 20% and 30% of maximal voluntary contraction (MVC) alone and in combination with LBNP at -5 mm Hg. Handgrip alone (exercise reflex) at 20% and 30% MVC caused graded increases in MSNA. LBNP alone (cardiac reflex) did not alter blood pressure or heart rate but decreased central venous pressure by 2.5 +/- 0.1 mm Hg (mean +/- SEM, p less than 0.05) and increased MSNA by 92 +/- 22% over the control value. Most important, handgrip performed during LBNP (interaction of reflexes) caused increases in MSNA that were comparable with the increases during handgrip alone: +114 +/- 32% versus +175 +/- 89% at 20% MVC and +328 +/- 101% versus +431 +/- 110% at 30% MVC (handgrip plus LBNP vs. handgrip alone, p greater than 0.1). Pressor and heart rate responses to handgrip also were unaffected by LBNP. In five additional experiments, comparable findings were obtained when the LBNP was superimposed on handgrip rather than handgrip being superimposed on LBNP. In conclusion, this study provides direct evidence in humans that nonhypotensive LBNP does not augment muscle sympathetic outflow during static handgrip and challenges the concept of an important interaction between cardiac baroreceptor and exercise pressor reflexes during this form of exercise.
In this retrospective analysis, we assessed the usefulness of ambulatory blood pressure monitoring in the evaluation of elderly hypertensive patients. Thirty-eight untreated and 31 treated hypertensives aged 70 years or more had a systolic blood pressure greater than or equal to 160 mmHg and/or a diastolic blood pressure greater than or equal to 95 mmHg in the clinic. All 69 patients underwent blood pressure monitoring during their customary daily activities using a portable semi-automatic blood pressure recorder (Remier M2000). The mean of all blood pressures obtained with this device was taken as the ambulatory recorded blood pressure. Recorded blood pressures were greater than or equal to 160 mmHg systolic and greater than or equal to 90 mmHg diastolic in 17 untreated and 17 treated patients. In these patients, the introduction of antihypertensive therapy, or its modification, markedly reduced blood pressure during a 4-8 month follow-up. A further 21 untreated and 14 treated patients had recorded blood pressures of less than 160/90 mmHg. The treatment status of these patients was left unchanged for 4-8 months of follow-up. Nevertheless, office blood pressure in these groups, with no change in treatment, decreased significantly during the observation period. At the last visit to the outpatient clinic, there was no significant difference in blood pressure between the four subgroups of patients. Thus, ambulatory blood pressure monitoring appears to be useful in the elderly hypertensive patient in detecting those patients whose blood pressure is elevated only in the clinic. Blood pressure profiles obtained outside the clinic may therefore be useful in making therapeutic decisions in the aged hypertensive.
Ambulatory blood pressure (BP) was recorded in hypertensive patients whose physicians had been asked to reduce diastolic pressure measured in the office to 90 mm Hg or less. 34 hypertensive patients with a diastolic pressure measured by their physician of 95 mm Hg or more despite antihypertensive therapy had their treatment changed with the aim of achieving this pre-set goal within 3 months. At the beginning and the end of the study, ambulatory BP was monitored during the daytime with a portable non-invasive recorder. The results of the ambulatory recordings were not made available to the physicians until completion of the study. In half the patients the ambulatory diastolic pressure was already 90 mm Hg or less at the start. In these patients, treatment adjustment did not further decrease ambulatory BP. In contrast, patients who initially had an ambulatory diastolic pressure above 90 mm Hg had a significantly decreased ambulatory BP at the end of the study. Intensifying the therapy of hypertensive patients who have a normal ambulatory BP may result in overtreatment without any real gain in BP control.
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The antihypertensive efficacy and tolerability of bisoprolol and atenolol were compared in the Bisoprolol International Multicenter Study (BIMS). In 104 patients with essential hypertension (21 to 70 years of age and diastolic blood pressures (DBP) of 100-120 mm Hg in the sitting position), after a four-week placebo period, the active drug was given in a random double-blind crossover design (10 to 20 mg bisoprolol, 50 to 100 mg atenolol) for eight weeks each, with a 2 to 6 week placebo wash-out phase between active therapy. All blood pressures were recorded 24 h after drug intake. Of the 104 patients, 10 were withdrawn during the study because of unwanted effects, unsatisfactory blood pressure response, or intercurrent disease, leaving 94 for intraindividual comparisons. After 8 weeks active treatment with individually titrated dose, there were slightly, but significantly greater falls in blood pressure with bisoprolol (p less than or equal to 0.05). Diastolic target pressures of less than or equal to 95 mm Hg were reached in 68% with bisoprolol and 56% with atenolol (p less than or equal to 0.05; Mc Nemar). There was no between treatment group difference in the patients' self-assessed well-being. For both drugs, response rates were greater in patients below the age of 60 years than in those above 60 years. Better antihypertensive responses were observed with bisoprolol in patients regularly smoking cigarettes.
One case of digitoxin-induced thrombopenia with relapse upon reexposure is reported. Cytopenia was each time rapidly reversible upon withdrawal of the medication. During the two episodes, blood digitoxin was superior to the generally accepted value. No thrombopenia was caused by administration of digoxin. The criteria for diagnosis and the difficulty of causal demonstration are discussed. Up to the present the literature has reported 11 cases of cardiotonic-induced thrombopenia. The features of these observations are reviewed.
A report was made of 35 Charnley prostheses implanted between 1962 and 1965. The occurring complications were discussed. In an exceptionally high number of these complications, fracture of the acetabulum proved to be the most important factor. Causes and predisposing factors were presented. Finally, reference was made to the significance of some of the experiences acquired on the basis of the long-term results which were published in this form for the first time.
We present a new approach to cardiovascular analysis based on a well-known signal processing technique, namely, the frequency subband decomposition. The subbands are chosen in accordance with physiological standards: (1) 0-0.04 Hz, (2) 0.04-0.15 Hz, (3) 0.15-0.4 Hz. It is shown that such a pre-processing drastically improves the accuracy of the analysis and introduces a new direction in the understanding of the relationships between cardiovascular signals.