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Biomedical subjects

G Waldemar

Publications and source records attributed to G Waldemar.

67 records · Page 4Linked to original sources
PubMed1990

The acute effect of captopril on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers.

The present study was undertaken to examine the effect of captopril on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and CO2 reactivity in eight young healthy volunteers. The mean arterial blood pressure (MABP) was measured intraarterially, and CBF was measured by inhaled xenon-1233. The CO2 reactivity was defined as the relative change in CBF per 0.1 kPa change in arterial CO2. During the CO2 reactivity tests, the CBF changes were estimated by the arteriovenous-oxygen-difference method (CBFsat). Median CBF was 52 ml/100 g/min (50-56) and without any significant regional side-to-side asymmetries. No significant change was observed after captopril. The median resting MABP was 90 mm Hg (89-93), and was slightly reduced by 5 mm Hg (4-6) 1 h after an oral dose of captopril (50 mg). CMRO2 was 3.7 ml/100 g/min (3.5-3.8) and was unchanged after captopril. For the entire range of PaCO2 the median slope of the ln(CBFsat) versus PaCO2 regression line was 1.4 (1.3-1.6) at baseline compared to 1.4 (1.3-1.7) after captopril (p = 0.23). Considering the PaCO2 values between 4.0 and 6.5, the CO2 reactivity was 2.4%/0.1 kPa (2.1-2.4) at baseline and increased significantly to 2.9%/0.1 kPa (2.1-3.2) after captopril (p less than 0.05). No side effects were observed. The present study shows an overall unchanged CO2 reactivity; however, with an increased CO2 reactivity of the cerebral vessels for small changes in PaCO2 around the resting value of PaCO2 and a maintained coupling of CBF and CMRO2 after peroral captopril.

Adult↗
PubMed1990

Arterial CO2 tension and cerebral vascular reactivity during the induction of acute hypertension and hypotension in the awake human.

The CO2 reactivity was calculated at mean arterial blood pressure (MABP) values ranging from 40 to 140 mm Hg in 15 normotensive volunteers and in 7 patients with chronic arterial hypertension. The cerebral vascular reactivity (CVR) was estimated from indirect measurements of cerebral blood flow (CBF) by the arteriovenous oxygen saturation method. In all subjects but one of the hypertensive patients, there was a significant linear correlation of CVR with PaCO2 over the total range of MABP. The median CO2 reactivity in the volunteers and in the hypertensive patients was 2.7 and 2.8% CBF/0.1 kPa, respectively (NS). At MABP values corresponding to the plateau of CBF autoregulation (baseline MABP +/- 20%), the median CO2 reactivity was 3.0% CBF/0.1 kPa in both groups. During a cross-sectional correlation analysis of the pooled data from all volunteers, the CO2 reactivity increased with increasing MABP in the range of 50-110 mm Hg. Outside this range there was no correlation of CVR with PaCO2. In conclusion, our results confirmed that during acute hypo- and hypertension, the influence of PaCO2 on the CVR is reduced. The full CO2 reactivity of the cerebral vessel exists only at the plateau of CBF autoregulation.

Journal Article↗
PubMed1990

ACE inhibitors and cerebral blood flow.

Inhibition of angiotensin converting enzyme (ACE) shifts the limits of cerebral blood flow autoregulation towards lower blood pressure values. In patients with chronic arterial hypertension and in patients with chronic heart failure cerebral blood flow is not changed by acute or chronic ACE inhibition, despite, in some cases, pronounced reductions in the mean arterial blood pressure. ACE inhibition does not change ischaemic regional cerebral blood flow in acute stroke. It is concluded that following ACE inhibition cerebral blood flow is maintained at an unchanged level and especially well maintained in case of blood pressure drop.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Cerebral circulation under normal and pathologic conditions.

Autoregulation of the cerebral circulation is the regulating mechanism that keeps cerebral blood flow (CBF) constant within wide limits of arterial pressure. The lower limit is defined as the value of mean arterial pressure below which CBF decreases below the plateau, and the upper limit as the value of mean arterial pressure above which CBF increases above the plateau (60 and 150 mm Hg, respectively). Two possible mechanisms for autoregulation are discussed, myogenic response and metabolic regulation. Stimulation of the sympathetic nervous system and antagonism of the renin-angiotensin system modulate CBF autoregulation by shifting the entire curve toward higher or lower values of arterial pressure, respectively. The autoregulatory curve is shifted toward higher arterial pressures in chronic hypertension. Therefore, the tolerance to acute decreases in arterial pressure is impaired. Concomitantly, the tolerance of the brain to acute increases in arterial pressure is improved. This shift in the limits of autoregulation is due to structural and functional (hemodynamic) changes in the cerebral resistance vessels. These adaptive changes are partly reversible after chronic treatment with antihypertensive agents. The pathophysiology of autoregulation should be taken into consideration before drugs are used to decrease arterial pressure acutely.

Animals↗
PubMed1989

Angiotensin-converting enzyme inhibition and regional cerebral blood flow in acute stroke.

The effect of the angiotensin-converting enzyme (ACE) inhibitor captopril on regional cerebral blood flow (rCBF) was studied in 12 patients within 5 days after their first acute stroke. rCBF was studied by xenon-133 inhalation and single-photon emission computed tomography (SPECT) scan before and 1 h after oral administration of 25 mg captopril. No increase in rCBF was observed in any of the 12 patients included in the study. In only one patient was there a slight redistribution of blood flow in favor of the low-flow area, but the absolute flow value did not increase. Captopril did not cause any significant change in mean hemispheric blood flow, mean arterial blood pressure (MAP), or end-expiratory CO2 fraction (FECO2). The assumption that ACE inhibition might increase cerebral blood flow in the periinfarct zone and preserve some still viable brain tissue could not be verified in the present study.

Acute Disease↗
PubMed1989

Angiotensin converting enzyme inhibition and cerebral circulation--a review.

1. The identification of a vascular wall renin angiotensin system and of angiotensin converting enzyme on the luminal surface of the endothelium in many tissues, including the brain, has stimulated research on the influence of the renin angiotensin system on regional blood flows. 2. In experimental studies inhibition of the angiotensin converting enzyme shifts the limits of cerebral blood flow autoregulation towards lower blood pressure values. 3. In patients with chronic arterial hypertension and in patients with chronic heart failure cerebral blood flow is not changed by acute or chronic angiotensin converting enzyme inhibition, despite in some cases pronounced reductions in the mean arterial blood pressure. Angiotensin converting enzyme inhibition does not change ischaemic regional cerebral blood flow in acute stroke. 4. It is concluded that following angiotensin converting inhibition cerebral blood flow is maintained at an unchanged level. The mechanism may include inhibition of locally produced angiotensin II leading to a selective dilation of larger cerebral arteries with a compensatory constriction of the smaller cerebral arteries.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Angiotensin converting enzyme inhibition and the upper limit of cerebral blood flow autoregulation: effect of sympathetic stimulation.

The effect of stimulation of the cervical sympathetic ganglia on the upper limit of cerebral blood flow (CBF) autoregulation was studied in normotensive Wistar-Kyoto rats (WKY) and in spontaneously hypertensive rats (SHR) following intravenous administration of the angiotensin converting enzyme inhibitor captopril (10 mg/kg). CBF was measured using the intracarotid 133Xe injection method in halothane/nitrous oxide anaesthetized WKY and SHR. Arterial blood pressure was raised stepwise by the intravenous infusion of noradrenaline. Toward the end of the study, Evans blue was injected and the brains examined for gross blood-brain barrier breakdown. In SHR, sympathetic stimulation reextended the upper limit of CBF autoregulation, which was at a mean arterial blood pressure level of 120-139 mm Hg in the control group of eight SHR and above 170 mm Hg in the stimulated group of nine SHR. In the group of nine WKY subjected to sympathetic stimulation, the upper limit of CBF autoregulation was reached at a mean arterial blood pressure level of 110-129 mm Hg as opposed to 90-109 mm Hg in a previous unstimulated group of WKY. In the two groups subjected to sympathetic stimulation, there was no extravasation of Evans blue in any of the brains. In the control group of SHR, in which there had been marked increases in CBF, three out of eight brains had foci with extravasation of the dye. It is concluded that in normotensive and in hypertensive rats sympathetic stimulation attenuates the downward shift of the upper limit of CBF autoregulation, which is known to accompany intravenous administration of captopril.

Animals↗
PubMed1989

Angiotensin converting enzyme inhibition and cerebral blood flow autoregulation in normotensive and hypertensive man.

The acute effect on the lower limit of cerebral blood flow (CBF) autoregulation of an angiotensin converting enzyme (ACE) inhibitor, captopril, was studied in normotensive volunteers and in hypertensive patients. Baseline CBF was measured using xenon-133 inhalation tomography, and changes in CBF were measured using the arterio-venous oxygen difference method. Cerebral blood flow autoregulation was studied in two separate normotensive groups, one group of 12 volunteers serving as a control, and one group of 12 volunteers studied after the administration of captopril 50 mg. In a group of seven hypertensive patients CBF autoregulation was studied before and 1 h after the administration of captopril 25 mg. In the normotensive volunteers the median lower limit of CBF autoregulation was 83 and 74 mmHg in the untreated and the captopril-treated group, respectively, with no significant difference between the two groups. In five of the hypertensive patients the lower limit of CBF autoregulation was lowered by captopril, in median by 22 mmHg. However, in two patients it was increased, by 3 and 13 mmHg, respectively. It is proposed that the shift in the lower limit of CBF autoregulation seen in some of our cases, and which has previously been documented in experimental studies, may be dependent on the activity of the sympathetic nervous system.

Adult↗
PubMed1988

Inhibition of platelet function by low-dose plain and micro-encapsulated acetylsalicylic acid.

The effect of two acetylsalicylic acid (ASA) formulations, plain (Magnyl) and micro-encapsulated (Globentyl), on platelet aggregation, thromboxane formation, and bleeding time was studied in 12 healthy volunteers in a randomized double-blind cross-over study. All subjects were treated with Magnyl and Globentyl (75 mg daily) in periods of 2 weeks, separated by a wash-out period of 2 weeks. Both drugs significantly depressed platelet aggregation and thromboxane formation and prolonged bleeding time without difference in mode of action of the drugs. It is concluded that significant inhibition of platelet activity may be achieved by low-dose ASA treatment with micro-encapsulated as well as with plain formulations.

Adult↗
PubMed1988

Role of angiotensin in autoregulation of cerebral blood flow.

The presence of the renin-angiotensin system (RAS) in extrarenal tissues, namely the vascular wall and brain tissue, is well established. The availability of effective blocking agents, converting-enzyme inhibitors, has made it possible to further elucidate important functions of the extrarenal RAS. We have found that the angiotensin converting-enzyme inhibitor captopril shifts the limits of cerebral blood flow autoregulation to lower blood pressure levels in normotensive and in spontaneously hypertensive rats. This effect may explain our finding of a remarkable preservation of cerebral blood flow, despite significant blood pressure reduction, in patients with chronic heart failure. We suggest that the effect of angiotensin converting-enzyme inhibition on autoregulation of cerebral blood flow is mediated by a dilatation of larger cerebral arteries, which results from inhibition of the vascular tone normally maintained by locally produced angiotensin II.

Angiotensin II↗
PubMed1987

Neurologic symptoms and hysterectomy: a retrospective survey of the prevalence of hysterectomy in neurologic patients.

Eleven percent of the 272 women aged 25-45 years admitted consecutively to a neurologic department in 1980-1984 had undergone hysterectomy. The population was divided into two groups according to the discharge diagnoses. Among women with discharge diagnoses usually associated with no objective neurologic findings, the frequency of hysterectomy was 14%, compared with 5.4% in women discharged with diagnoses indicating organic neurologic disease. Gynecologic and psychiatric admissions were more frequent in the former than in the latter group. Of the 30 hysterectomized women, only six had had malignant or premalignant changes in the uterus, whereas in 22 cases the removed organs had been normal. These results suggest that a somatization disorder might have been the underlying cause for the hysterectomy as well as for the symptoms and complaints leading to referral to the neurologic service. Awareness of this problem is important in order to avoid unjustified surgery.

Adult↗
PubMedDate not supplied

Differential effects of migraine drugs on cerebral blood flow autoregulation.

The effect of the migraine drugs ergotamine and sumatriptan on the cerebral blood flow (CBF) autoregulation was studied in halothane/nitrous oxide-anesthetized normotensive Wistar Kyoto rats. Ergotamine, an ergot alkaloid affecting 5HT, norepinephrine, and dopamine receptors, was administered intravenously as a single dose of 25 microg/kg. Sumatriptan, a selective 5HT1-like receptor agonist, was administered by intravenous infusion of 300 microg/kg/h. CBF was measured with the intracarotid 133Xe-injection method. The blood pressure limits of CBF autoregulation were determined by computerized least sum of square analysis. CBF autoregulation was preserved after both ergotamine and sumatriptan. Ergotamine shifted the lower blood pressure limit of CBF autoregulation towards higher blood pressures from 60 +/- 3 mmHg to 82 +/- 4 mmHg (p<0.01), but did not significantly affect the upper blood pressure limit of CBF autoregulation. Sumatriptan had no significant effects on the blood pressure limits of CBF autoregulation.

Animals↗