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Biomedical subjects

K Heusser

Publications and source records attributed to K Heusser.

10 recordsLinked to original sources
PubMed2004

Pregnancy-induced sympathetic overactivity: a precursor of preeclampsia.

BACKGROUND: Preeclampsia has been shown to constitute a state of sympathetic overactivity. However, it remains unclear if the sympathetic activity precedes preeclampsia or represents only a secondary phenomenon. To further investigate this issue, we performed a prospective study in pregnant women considered to be at increased risk for preeclampsia owing to preeclampsia during a preceding pregnancy. MATERIALS AND METHODS: Twenty-two women with a history of preeclampsia were longitudinally studied on three occasions: twice during pregnancy (M1: 22 +/- 4, M2: 33 +/- 5 weeks) and once postpartum (M3: 26 +/- 6 weeks postpartum). We measured muscle sympathetic nerve activity (MSNA), forearm blood flow, and blood pressure at rest and during reactive hyperaemia after forearm occlusion. RESULTS: At M1 and M2, none of the subjects was hypertensive, however, muscle sympathetic nerve activity levels were significantly augmented, compared with their postpartum values (M1: 21 +/- 9, M2: 29 +/- 14, M3: 9 +/- 5 bursts min(-1); P < 0.05). Forearm vascular resistance did not significantly change from M1 through M3 (M1: 16 +/- 9, M2: 15 +/- 7, M3: 16 +/- 7 U; P = NS). Gestational muscle sympathetic nerve activity values did not differ significantly among the subjects with subsequent preeclampsia compared with those who remained normotensive [with preeclampsia (n = 6): M1: 21 +/- 5, M2: 27 +/- 6, M3: 7 +/- 4 bursts min(-1); without preeclampsia (n = 16): M1: 21 +/- 11, M2: 30 +/- 16, M3: 9 +/- 6 bursts min(-1); P = NS]. CONCLUSION: Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail.

Adult↗
PubMed2002

Cardiovascular effects of beta-blockers with and without intrinsic sympathomimetic activity. A comparison between celiprolol and metoprolol.

BACKGROUND: Celiprolol, a newer beta-blocking agent, has been reported to have vasodilatory capacity which may be due to partial beta-2-receptor agonistic activity or to alpha-receptor antagonistic or central sympathoinhibitory effects. METHODS: To more critically assess the physiologic effects of celiprolol, we measured sympathetic nerve activity to muscle (MSNA), forearm blood flow (FBF), blood pressure (BP), central venous pressure, and heart rate (HR) in 10 normal volunteers at rest, during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP), and during a cold pressor test (CPT). Responses were compared with those seen with metoprolol and with placebo, i.e. each subject was studied three times. RESULTS: Celiprolol did not alter resting levels of hemodynamics, FBF, and MSNA nor did it alter responses to LBNP or the CPT. In contrast, metoprolol produced significant decreases of FBF and HR, and increases of forearm vascular resistance and BP, but had also no effect on responses to the applied stress tests. CONCLUSIONS: The lack of peripheral vasoconstriction seen after acute administration of celiprolol is most likely due to its partial beta-2-receptor agonistic effect and does not seem to be due to a central or reflex action or to an alpha-blocking effect. Both beta-blockers do not impair fundamental neural mechanisms involved in circulatory homeostasis.

Adrenergic beta-Antagonists↗
PubMed2001

Long-term results after microvascular decompression in essential hypertension.

BACKGROUND AND PURPOSE: In 1998, 8 patients with severe, intractable arterial hypertension and MR tomography-demonstrated neurovascular contact of a looping artery at the root entry zone of cranial nerves IX and X, causing neurovascular compression, underwent neurosurgical decompression. The short-term results showed a normalization of blood pressure with a markedly reduced antihypertensive drug regimen in 7 patients. To determine the longer-term outcome concerning blood pressure and secondary organ damage after neurovascular decompression, we studied these 8 operated patients prospectively for a mean follow-up of 3.5 years after surgical intervention. METHODS: Eight hypertensive patients who had undergone microsurgical decompression were monitored every 6 months after surgery to assess blood pressure (by 24-hour ambulatory pressure readings) and the need for antihypertensive medication. To evaluate secondary organ damage, echocardiographic assessment of left ventricular hypertrophy, fundoscopic assessment of hypertensive lesions, and analysis of renal function and proteinuria were done. RESULTS: Three of the 8 operated patients remained normotensive in the long-term period with decreased antihypertensive medication. Two patients required gradual increases of antihypertensive medication after the first postoperative year, after which arterial blood pressure levels were 10% to 15% lower than preoperative levels. Three patients suffered serious cardiovascular and renal complications, with the incidence of lethal intracerebral hemorrhage in 1 patient and end-stage renal disease in 2 patients, of whom 1 experienced sudden cardiac death. CONCLUSIONS: The long-term results verify that microsurgical decompression is a successful alternative therapy in a certain subgroup of patients with arterial hypertension due to neurovascular compression. However, the relevance of the looping artery in the other cases, who did not improve, is not clear. Prospective studies to elucidate the pathophysiological role of neurovascular abnormalities and arterial hypertension are needed.

Adult↗
PubMed2000

Severely impaired baroreflex-buffering in patients with monogenic hypertension and neurovascular contact.

BACKGROUND: We identified a family with a monogenic syndrome of hypertension, brachydactyly, and neurovascular contact of the brain stem. Neurovascular contact of the ventrolateral medulla may lead to arterial hypertension by interfering with baroreflex function. METHODS AND RESULTS: In 5 patients with monogenic hypertension (18 to 34 years old), we conducted detailed autonomic function tests. Blood pressure during complete ganglionic blockade was 134+/-4.9/82+/-4.1 mm Hg and 90+/-6/49+/-2.4 mm Hg in patients and in control subjects, respectively. During ganglionic blockade, plasma vasopressin concentration increased 24-fold in control subjects and <2-fold in patients. In patients, cold pressor testing, hand-grip testing, and upright posture all increased blood pressure excessively. In contrast, muscle sympathetic nerve activity was not increased at rest or during cold pressor testing. The phenylephrine dose that increased systolic blood pressure 12.5 mm Hg was 8.0+/-2.0 microg in patients and 135+/-35 microg in control subjects before ganglionic blockade and 5.4+/-0.4 microg in patients and 13+/-4.8 microg in control subjects during ganglionic blockade. CONCLUSIONS: In patients with monogenic hypertension and neurovascular contact, basal blood pressure was increased even during sympathetic and parasympathetic nerve traffic interruption. However, sympathetic stimuli caused an excessive increase in blood pressure. This excessive response cannot be explained by increased sympathetic nerve traffic or increased vascular sensitivity. Instead, we suggest that baroreflex buffering and baroreflex-mediated vasopressin release are severely impaired.

Adolescent↗
PubMed2000

Vascular reactivity in patients with preeclampsia and HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome.

OBJECTIVE: Early structural and functional changes in the systemic vasculature have been proposed to play a major pathogenetic role in preeclampsia and HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. The aim of the study was to determine vascular reactivity in patients with preeclampsia with and without HELLP syndrome with respect to those in healthy pregnant control subjects. STUDY DESIGN: Forearm blood flow was measured by strain gauge plethysmography with the venous occlusion technique in 12 hypertensive patients with HELLP syndrome, in 8 patients with preeclampsia without HELLP syndrome, and in 8 healthy normotensive pregnant control subjects. To determine vascular reactivity the forearm blood flow was measured at baseline and after forearm occlusion for a period of 5 minutes (reactive hyperemia). The investigations were repeated 4 to 6 months post partum. Forearm vascular resistance was calculated as the ratio of mean arterial pressure to forearm blood flow. RESULTS: Mean arterial pressure at rest was elevated in patients with preeclampsia (116 +/- 20 mm Hg) and in patients with HELLP syndrome (110 +/- 16 mm Hg) with respect to healthy pregnant control subjects (86 +/- 10 mm Hg; P <.05). Forearm blood flow at rest was not statistically different in patients with preeclampsia (5.1 +/- 2.6 mL/min per 100 mL) and with HELLP syndrome (4.7 +/- 1.5 mL/min per 100 mL) with respect to pregnant control subjects (5.9 +/- 3.1 mL/min per 100 mL); however, forearm vascular resistance at rest was elevated in patients with preeclampsia (25.9 +/- 9.5 units; P <.05) and in patients with HELLP syndrome(24.6 +/- 6.9 units; P <.05) with respect to healthy control subjects (17.0 +/- 6.1 units). During reactive hyperemia the peak forearm blood flow, which is an indicator of maximal vasodilatory capacity, was impaired in patients with preeclampsia (21.9 +/- 8.2 mL/min per 100 mL; P <.05) but not in patients with HELLP syndrome (37.4 +/- 17.5 mL/min per 100 mL) and healthy control subjects (44.9 +/- 15.0 mL/min per 100 mL). Consequently, minimum forearm vascular resistance was higher in women with preeclampsia (6.1 +/- 1.9 units) than in both women with HELLP syndrome (3.5 +/- 1.6 units) and the control subjects (2.8 +/- 2.4 units). CONCLUSION: Despite similarly elevated forearm vascular resistances at rest in patients with HELLP syndrome and in patients with preeclampsia, forearm vascular resistance during reactive hyperemia did not differ significantly from that in healthy control subjects in the women with HELLP syndrome but was increased in women with preeclampsia. Vasodilatory reactivity thus is reduced in preeclampsia but not in HELLP syndrome, which suggests different alterations of the vasculature.

Adult↗
PubMed1999

[The autonomic nervous system and pre-eclampsia].

Alterations in the autonomic cardiovascular control have been implicated to play an important etiologic role in preeclampsia. Earlier assessments of sympathetic nervous system activity by measurements of urinary and plasma levels of catecholamines showed contradictory results, due to serious methodological problems. The microneurographic technique enables the assessment of sympathetic outflow to the vascular bed of skeletal muscles. By the use of this technique it has been shown that preeclampsia represents a state of sympathetic overactivity as compared to healthy pregnant women. Other studies have shown that exogenous stimulation of the celiac ganglion causes a HELLP-syndrome-like disease in pregnant rats and that preeclamptic human plasma increases norepinephrine release in isolated sympathetic neurons of chicken embryos. These data suggest that the autonomic nervous system may play a fundamental role in the etiology of preeclampsia.

Animals↗
PubMed1998

Effects of naloxone on hemodynamic and sympathetic nerve responses to pain in normotensive vs. borderline hypertensive men.

Pain sensitivity decreases with increasing resting blood pressure. This blood pressure-pain interaction may be mediated by endogenous opioids which have been shown to affect both blood pressure and nociception. To test this hypothesis, we measured mean arterial blood pressure (MAP), central venous pressure (CVP), heart rate (HR), muscle sympathetic nerve activity (MSNA), serum catecholamines, and individual pain rating scales during 2 min periods of noxious mechanostimulation (skin fold pinching) in nine young (26 +/- 2 year), male normotensive (NT) subjects and in 12 age and weight matched males with borderline hypertension (BHT). Measurements were performed before and after the i.v. administration of naloxone (0.15 mg/kg) and placebo in a randomized double-blind cross-over trial. In the pre-naloxone trials, pain led to similar changes in MAP, CVP, MSNA and plasma catecholamines in the two groups except for a higher increase in HR in the BHT group as compared to the NT group (3 +/- 1 vs. 1 +/- 1 bpm; P < 0.005). Opioid blockade with naloxone increased MSNA responses to pain in the NT group (from 5 +/- 1 to 9 +/- 1 bursts/min, and, from 100 +/- 23 to 204 +/- 36 units/min, respectively; P < 0.05) but did not significantly affect the MSNA response to pain in the BHT group. Pain induced responses of MAP, CVP, and catecholamines were not altered by naloxone in either group. Overall, there was a highly significant inverse correlation between pain perception and resting blood pressure which was not significantly affected by naloxone. The BHT subjects exhibited a lower pain perception compared to the NT subjects (P < 0.005). Naloxone increased pain rating in the NT group (from 194 +/- 9 to 218 +/- 13; P < 0.005) but not in the borderline hypertensive group (160 +/- 8 vs. 168 +/- 10; P = 0.36). Except for a decreased HR response in the BHT group, placebo had no effect on the responses to pain. Our data do not indicate a major role of the endogenous opioid system for the blood pressure-pain interaction in man. Endogenous opioids affect pain perception and sympathetic nerve activity responses to pain in normotensive men but their activity seems to be attenuated in borderline hypertensive subjects. Therefore, the lower pain sensitivity in human essential hypertension is probably mediated by non-opioid mechanisms.

Adult↗
PubMed1998

Evidence against elevated sympathetic vasoconstrictor activity in borderline hypertension.

The relationship between sympathetic nerve activity and BP in the early stages of essential hypertension remains unclear. To investigate this relationship further, this study measured resting muscle sympathetic nerve activity (MSNA: representing peripheral vasoconstrictor activity), plasma catecholamines, BP, central venous pressure, and heart rate in 20 young (24 +/- 2 SD yr), lean (body mass index, 24.2 +/- 3.0 kg/m2), male subjects with borderline hypertension (BHT) and in 21 male normotensive (NT) control subjects matched for age and body mass index. A cold pressor test was also performed to evaluate sympathetic reflex responsiveness. Resting mean BP and heart rate were significantly higher in the BHT subjects compared with NT subjects (113 +/- 9 versus 89 +/- 9 mmHg; 74 +/- 8 versus 62 +/- 8 bpm; P < 0.0001 each) with no difference in central venous pressure. Resting MSNA levels tended to be lower in the BHT versus the NT group (12 +/- 6 versus 14 +/- 9 bursts/min, P = NS; 16 +/- 8 versus 22 +/- 13 bursts/100 heartbeats, P = 0.05) and did not correlate with either BP or body mass index. Significant positive correlations were found between resting MSNA and plasma norepinephrine levels in both groups (P < 0.05). Hemodynamic and sympathetic nerve responses to the cold pressor test were similar between the BHT and NT subjects. It is concluded that resting MSNA and plasma norepinephrine levels are correlated in young lean NT and BHT men; however, neither of these variables is correlated with BP. Because MSNA was similar in the two groups, the concept that augmented resting MSNA is important in the early developmental phase of essential hypertension must be reevaluated.

Adult↗
PubMed1997

Influence of an alternating 3 Hz magnetic field with an induction of 0.1 millitesla on chosen parameters of the human occipital EEG.

In 62 volunteers it was studied, whether an alternating 3 Hz magnetic field (induction 0.1 mT) vertically applied to the head over a period of 20 min causes changes in EEG parameters. The study's design was a random crossover controlled, blind one. The field was generated by a Helmholtz coils arrangement. The occipital surface EEGs (O1 and O2) were derived against the left earlobe. Significant differences (two-tailed P < 0.05) between sham and real exposure were found for the relative spectral amplitudes of the theta (3.5-7.5 Hz) and beta band (12.5-25.0 Hz) and the theta/beta ratio. These observations can be interpreted as a more pronounced reduction of alertness under the real field condition compared with the control.

Adolescent↗