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Biomedical subjects

M Frisk-Holmberg

Publications and source records attributed to M Frisk-Holmberg.

59 records · Page 4Linked to original sources
PubMedDate not supplied

Haemodynamic and electrodermal correlates of psychogenic stimuli in hypertensive and normotensive subjects.

This study compared tonic and phasic cardiovascular and electrodermal activity in subjects having essential arterial hypertension (HT) with that of sex- and age-matched normotensive (NT) controls. Fourteen subjects of each group were subjected to 'sensory intake' (letter identification) and 'rejection' (mental arithmetic) tasks while recordings were made of: systolic and diastolic arterial blood pressure, hand and forearm blood flows, heart rate, skin conductance level and fluctuations. The rejection task affected more physiological variables in both groups than the intake task did. The reaction pattern was similar in both groups. Except for systolic and diastolic blood pressures tonic cardiovascular and electrodermal activity of the HT group was not different from that of the NT group. The same pattern, although less clear cut, was observed when reactivity was studied. According to analyses based on pressure levels both tasks raised the systolic blood pressure of the HT group, whereas only the rejection task raised systolic blood pressure in the NT group. In contrast, an analyses based on blood pressure changes from base to task indicated that both groups increased systolic blood pressure to both tasks. Since virtually no other differences in reactivity were found, this study offers weak support for the notion that subjects having essential arterial hypertension are pressor hyper-reactors.

Adult↗
PubMedDate not supplied

The antihypertensive mechanism of clonidine in man. Evidence against a generalized reduction of sympathetic activity.

Recording of multi-unit sympathetic activity were made from muscle branches of the peroneal nerve during i.v. bolus injection of 100 to 275 micrograms clonidine in seven hypertensive patients. Blood pressure was reduced in all patients, but sympathetic activity and heart rate could either increase or decrease. When plasma levels of clonidine were low, sympathetic activity tended to increase, and when plasma levels were high, activity tended to decrease. Irrespective of whether mean level of sympathetic activity increased or decreased with the fall in blood pressure level, transient fluctuations of blood pressure continued to cause dynamic baroreflex modulation of the sympathetic outflow. It is suggested that the drug influences sympathetic outflow by a combination of central and peripheral effects.

Adult↗