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Biomedical subjects

S Strandgaard

Publications and source records attributed to S Strandgaard.

122 records · Page 7Linked to original sources
PubMed1973

Autoregulation of brain circulation in severe arterial hypertension.

Cerebral blood flow was studied by the arteriovenous oxygen difference method in patients with severe hypertension and in normotensive controls. The blood pressure was lowered to study the lower limit of autoregulation (the pressure below which cerebral blood flow decreases) and the pressure limit of brain hypoxia. Both limits were shifted upwards in the hypertensive patients, probably as a consequence of hypertrophy of the arteriolar walls. These findings have practical implications for antihypertensive therapy.When the blood pressure was raised some patients showed an upper limit of autoregulation beyond which an increase of cerebral blood flow above the resting value was seen without clinical symptoms. No evidence of vasospasm was found in any patient at high blood pressure. These observations may be of importance for the understanding of the pathogenesis of hypertensive encephalopathy.

Adult↗
PubMedDate not supplied

Contractility and endothelium-dependent relaxation of resistance vessels in polycystic kidney disease rats.

Hypertension and vascular disease are common complications in autosomal-dominant polycystic kidney disease (ADPKD). The role of changes in morphology and reactivity of resistance vessels in this disease have not previously been studied. Mesenteric resistance arteries were dissected from 8- to 14-week-old heterozygous Han:SPRD polycystic kidney disease (PKD) rats, homozygous normal Han:SPRD littermates (HSPRD) and Sprague-Dawley rats (SD). The morphology, noradrenaline (NA) contractility, endothelium-dependent acetylcholine (ACh) relaxation before and after incubation with L(G)-nitro-L-arginine methyl ester (L-NAME), and endothelium-independent 3-morphollino-sydnonimine (SIN-1) relaxation were studied with the Mulvany-Halpern myograph. Blood pressure and morphology of vessels were the same in all groups of rats, apart from a slightly higher media/lumen ratio in heterozygous PKD rats (p < 0.05). Active wall tension and contractile sensitivity to NA were higher in both heterozygous PKD rats and HSPRD than SD rats (p < 0. 05). The maximum endothelium-dependent relaxation rate was markedly decreased in heterozygous PKD (19 +/- 9%) and HSPRD (34 +/- 12%) compared to SD rats (75 +/- 11%) (p < 0.05). After incubation with L-NAME, ACh-induced relaxation was significantly attenuated in SD rats, less attenuated in HSPRD, and not significantly changed in heterozygous PKD rats. SIN-1-induced endothelium-independent relaxation was similar in all three groups. In conclusion, hyperreactivity to NA and impaired endothelium-dependent relaxation were present in resistance vessels from Han:SPRD rats, especially in animals with PKD. These abnormalities in resistance vessels from PKD rats may be important for the development of hypertension and vascular disease.

Acetylcholine↗
PubMedDate not supplied

Cerebral blood flow during dihydralazine-induced hypotension in hypertensive rats.

The cerebrovascular effects of graded, controlled dihydralazine-induced hypotension were studied in rats with renal hypertension (RHR) and spontaneous hypertension (SHR). Repeated measurements of cerebral blood flow (CBF) were made using the intraarterial 133Xenon injection technique in anaesthetised normocapnic animals. Dihydralazine was administered in single increasing i.v. doses (0.1 to 2 mg/kg), and CBF measured after each dose when a stable blood pressure had been reached. From a resting level of 145 +/- 7 mm Hg in RHR and 138 +/- 11 mm Hg in SHR, mean arterial pressure (MAP) fell stepwise to a minimum of around 50 mm Hg. CBF was preserved during dihydralazine induced hypotension, and remained at the resting level of 79 +/- 13 ml/100 g . min in RHR and 88 +/- 16 ml/100 g . min in SHR. Following 2 hours hypotension at the lowest pressure reached, the rats were sacrificed by perfusion fixation and the brains processed for light microscopy. Evidence of regional ischaemic brain damage was found in 4 of 11 animals: in 2 cases the damage appeared to be accentuated in the arterial boundary zones. Although the lower limit of CBF autoregulation in these rats is around 100 mm Hg during haemorrhagic hypotension, dihydralazine brought MAP to around 50 mm Hg without any concomitant fall in CBF. This was interpreted as being due to direct dilatation of cerebral resistance vessels. The combination of low pressure and direct dilatation may have resulted in uneven perfusion, thus accounting for the regional ischaemic lesions.

Animals↗
PubMedDate not supplied

Chronic antihypertensive treatment in the rat reverses hypertension-induced changes in cerebral blood flow autoregulation.

Cerebral blood flow (CBF) autoregulation was studied in renal hypertensive rats receiving chronic antihypertensive treatment. Young Wistar Kyoto rats (WKY) were made hypertensive by the Loomis procedure i.e. partial infarction of one kidney with contralateral nephrectomy. Systolic tail blood pressure was measured at 2-week intervals throughout the study. After two months, by which time the rats had been severely hypertensive for 5-6 weeks, antihypertensive treatment was begun; reserpine, dihydralazine and hydrochlorothiazide were administered in the drinking water. Blood pressure fell rapidly to normotensive levels and remained so. Following two months of antihypertensive treatment, the lower blood pressure limit of CBF autoregulation was studied during controlled bleeding. In age-matched untreated renal hypertensive WKY, the lower limit of autoregulation was in the mean arterial pressure range 90-109 mm Hg, as compared to 50-69 mm Hg in age-matched normotensive WKY. In contradistinction to the untreated rats, the treated rats had a normal lower limit of autoregulation, i.e. 50-69 mm Hg. It was inferred that the reversal of the functional change in CBF autoregulation reflected reversal of hypertension-induced cerebrovascular hypertrophy/hyperplasia.

Animals↗
PubMedDate not supplied

Studies on the cerebral circulation of the baboon in acutely induced hypertension.

The upper limit autoregulation of cerebral blood flow was investigated in eight young baboons with the intracarotid 133xenon clearance method. Blood pressure was increased by intravenous angiotensin infusion. Autoregulation was effective during blood pressure increase from normotensive levels to a mean pressure of 130 to 139 mm Hg. At this pressure, cerebrovascular resistance reached a maximum. With further blood pressure increase, autoregulation was broken, and the vascular resistance dropped significantly. This flow increase was restricted to the fast component of the 133xenon clearance curve, leaving slow component unchanged.

Animals↗
PubMedDate not supplied

Cerebrovascular CO2 reactivity in normotensive and hypertensive man.

Cerebrovascular reactivity to CO2 inhalation and voluntary hyperventilation was studied in seven normotensive subjects and nine hypertensive patients without clinical or angiographical signs of arteriosclerosis. Cerebral blood flow (CBF) was measured by the intracarotid 133Xe clearance method and calculated as the initial slope index. Three to five CBF measurements were made in each patient in the PaCO2 range of 20 to 55 mm Hg. No difference was observed in reactivity between hypertensive and normotensive patients, either during CO2 inhalation or during hyperventilation. The shape of the CBF:PaCO2 curve suggested a decrease in reactivity below a PaCO2 of 30 to 35 mm Hg in both groups. Above a PaCO2 of 35 mm Hg, exponential regression analysis yielded a mean reactivity of 6 +/- 2%, whereas below a PaCO2 of 30 mm Hg it was about 2%. The rise in CBF during CO2 inhalation was not influenced by the intravenous infusion of a small dose of trimethaphan which blocked the concomitant rise in blood pressure.

Adolescent↗