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Biomedical subjects

D I Barry

Publications and source records attributed to D I Barry.

At least 37 records · Page 2Linked to original sources
PubMed1985

Cerebral blood flow in hypertension.

The most important aspect of cerebral blood flow (CBF) in hypertension is the change that occurs in CBF autoregulation: increased cerebrovascular resistance causes the lower and upper limits of CBF autoregulation to be at higher pressure levels. The mechanism seems to be mainly structural thickening and luminal narrowing of cerebral resistance vessels. These adaptive changes, while protecting the brain against high intravascular pressure, render the brain more susceptible to ischemia at low blood pressure. An obvious consequence of the shift in the lower limit of CBF autoregulation in hypertension is that if the hypertensive patient's blood pressure is lowered acutely to "normal" levels, the pressure is below the patient's lower limit of autoregulation and ischemic damage may result. Basically, antihypertensive drugs can be placed into four groups as regards their effects on the cerebral circulation. First are the drugs without any direct effect: in this case, CBF remains constant until pressure reaches the lower limit of autoregulation and then decreases with any further pressure decrease. Diazoxide is in this category. Second are the drugs that directly dilate the small resistance levels in such a way that CBF is higher than normal at every pressure including pressures below the lower limit of autoregulation. However, perfusion may be uneven and autoregulation may be lost; an example of this kind of drug is dihydralazine. Third are the drugs which by alpha-or ganglion-blockade prevent the sympathetic vasoconstriction of large cerebral arteries (pial and larger), which can compromise CBF during a fall in blood pressure and hence shift the lower limit of autoregulation to a higher pressure than during blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1984

Blood-brain and blood-spinal cord barrier permeability during the course of experimental allergic encephalomyelitis in the rat.

Experimental allergic encephalomyelitis (EAE) was induced in young male Lewis rats. Blood-brain barrier permeability to radiotracers of different molecular sizes was studied at intervals after induction using a tissue sampling technique. The results were correlated to the clinical picture and to the histological appearance of the central nervous system. Significant increase in blood-brain barrier permeability to small molecules was found to precede clinical symptoms by one day in the lumbar spinal cord and to coincide with the onset of clinical disease in other regions. In all regions, increased blood-brain barrier permeability preceded the occurrence of histological lesions (perivascular cellular infiltrates). No permeability increase to large molecules could be demonstrated.

Animals↗
PubMed1984

Effects of captopril on cerebral blood flow in normotensive and hypertensive rats.

Cerebrovascular effects of the angiotensin converting enzyme inhibitor captopril were examined in normotensive and hypertensive rats. Cerebral blood flow was measured with the intracarotid 133xenon injection method in halothane-anesthetized animals. The blood-brain barrier permeability of captopril (determined with an integral-uptake method) was negligible, the permeability-surface area product in most brain regions being 1 X 10(-5) cm3/g per second, that is, three to four times lower than that of sodium ion. When administered into the cerebral ventricles to bypass the blood-brain barrier, captopril had no effect on cerebral blood flow: furthermore, cerebral blood flow autoregulation (studied by raising and lowering blood pressure) was identical to that in controls. In contrast, when given intravenously, captopril had a marked effect on cerebral blood flow autoregulation--both the lower and upper limits of autoregulation being shifted to a lower pressure (by about 20 to 30 and 50 to 60 mm Hg, respectively), and the autoregulatory range was shortened by about 40 mm Hg. This effect may be ascribed to inhibition of converting enzyme in the cerebral blood vessels rather than within the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebrovascular aspects of converting-enzyme inhibition I: Effects of intravenous captopril in spontaneously hypertensive and normotensive rats.

The cerebrovascular effects of converting enzyme inhibition were examined in normotensive and hypertensive rats. Cerebral blood flow was measured using the intracarotid 133xenon injection method in halothane/nitrous oxide anaesthetized animals. The main finding was that following intravenous administration of captopril (10 mg/kg), cerebral blood flow autoregulation was markedly altered. Although cerebral blood flow was unchanged from baseline levels, both the lower and upper limits of autoregulation were reset to lower mean arterial pressure and the autoregulatory plateau shortened. The lower limit was shifted 20-30 mmHg, the upper limit 50-60 mmHg, and the plateau shortened by 20-40 mmHg. The effect was interpreted as being a consequence of compensatory autoregulatory constriction of small resistance vessels in the brain following captopril-induced dilatation of large resistance vessels. It was inferred that locally produced angiotensin II might play a role in the resistance of large cerebral arteries.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebrovascular aspects of converting-enzyme inhibition II: Blood-brain barrier permeability and effect of intracerebroventricular administration of captopril.

The blood-brain barrier permeability to captopril, and the cerebrovascular effects of intracerebroventricular administration of captopril, were studied in normotensive Wistar rats. The blood-brain barrier permeability-surface area product (PS), determined by an integral-uptake method, was about 1 X 10(-5) cm3/g/s in all brain regions studied. This was three to four times lower than the simultaneously determined PS of Na+ and Cl-, both of which are known to have very low blood-brain barrier permeability. Cerebral blood flow, determined by the intra-arterial 133xenon injection method, was unaffected by intracerebroventricular administration of 100 micrograms captopril. Furthermore the lower limit of cerebral blood flow autoregulation during haemorrhagic hypotension was also unaffected, being in the mean arterial pressure range (50-69 mmHg) in both controls and captopril-treated rats. It was concluded that the blood-brain barrier permeability of captopril was negligible and that inhibition of the brain renin-angiotensin system has no effect on global cerebral blood flow. The cerebrovascular effects of intravenously administered captopril (a resetting to lower pressure of the limits and range of cerebral blood flow autoregulation) are probably exerted via converting enzyme on the luminal surface of cerebral vessels.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebral blood flow autoregulation during acute ethanol intoxication in the rat.

Autoregulation of cerebral blood flow (CBF) was studied in anaesthetized rats during acute ethanol intoxication (blood alcohol concentration 2.5 to 3 g/l). For each rat an autoregulation curve was determined: 8-10 CBF measurements were made over the mean arterial pressure range 129 mmHg to 20 mmHg. MAP was raised above the resting level by angiotension II infusion, then lowered by controlled haemorrhage. In control rats, CBF autoregulation was demonstrated within the MAP range 129 mmHg to 70 mmHg: at lower pressure autoregulation was inadequate and CBF fell. In ethanol intoxicated rats CBF autoregulation was demonstrated within the MAP range 129 mmHg to 50 mmHg: at lower pressure CBF fell. Although the lower limit of CBF autoregulation was thus at an MAP 20 mmHg less than in control rats, this probably reflects suppression of cerebral metabolism, rather than an effect of ethanol on CBF autoregulation per se.

Alcoholic Intoxication↗
PubMed1984

The intracarotid 133xenon injection method for measurement of cerebral blood flow (CBF) in rats: evaluation of the effect of bolus volume.

It is assumed that the cerebral microcirculation is not perturbed by the intraarterial injection used in determination of cerebral blood flow (CBF) with the intraarterial 133Xenon technique (and in various assessments of blood brain barrier (BBB) permeability). The application of these techniques to the rat, where the injectate is large compared to normal blood flow, places this problem is focus and it has been claimed that since large intracarotid injections increased cerebral venous outflow, the CBF must also increase. We investigated this problem in the rat by means of the intraarterial 133Xenon injection technique, using a saline bolus injected in less than 1 sec and found that CBF was unaltered at bolus volumes between 10 and 100 microliters. Furthermore, injection of 100-200 microliters saline during washout detection did not change the slope of the semilogarithmic wash-put curves. It is concluded that in spite of large intracarotid injections the CBF remained constant and that the hemodilution produced by the saline bolus is not sufficient to influence CBF. Consequently, estimations of CBF yield valid results in the present rat preparation.

Animals↗
PubMed1984

Blind study of the effect of the alpha-adrenergic agonists clonidine and lofexidine on alcohol withdrawal in the rat.

Alpha-adrenergic agonists have been reported to block the opiate withdrawal reaction in animals and humans, probably by interference with the catecholaminergic hyperactivity that prevails during opiate withdrawal. Since catecholaminergic hyperactivity also occurs during alcohol withdrawal, the present study investigated whether the central alpha-adrenergic agonists clonidine and lofexidine could interfere with this type of withdrawal reaction. During withdrawal from a 4-day intoxication period, male Wistar rats were assigned to one of three groups: clonidine treatment (0.15 mg/kg, N = 11), lofexidine treatment (0.50 mg/kg, N = 11) and control (N = 11). The study was performed blind, the code for the saline control and two drug treatment groups being broken only after the last rating of withdrawal symptoms. Since neither clonidine nor lofexidine modified the development or degree of the alcohol withdrawal reaction, there was no support for the assumption of a common mechanism involving the alpha-adrenergic system during opiate and alcohol dependence.

Alcohol Drinking↗
PubMed1984

Converting enzyme inhibition and autoregulation of cerebral blood flow in spontaneously hypertensive and normotensive rats.

The cerebrovascular effects of the converting enzyme inhibitor captopril were examined after intravenous or intracerebroventricular administration in normotensive and hypertensive rats. Cerebral blood flow (CBF) was measured using the intracarotid 133xenom method in halothane/nitrous oxide anaesthetised animals. Captopril given either way did not influence the absolute value of CBF. The main finding, however, was that following intravenous administration of captopril at a dose of 10 mg/kg, both the lower pressure limit of CBF autoregulation were shifted to lower pressure and the autoregulatory plateau shortened. The lower limit was shifted 20-30 mm Hg, the upper limit 50-60 mm Hg, and the autoregulatory plateau consequently shortened by 20-30 mm Hg. In contrast to the marked effects of intravenous captopril, intracerebroventricular captopril was without effect on CBF autoregulation. The effect of intravenous captopril was thus probably mediated by converting enzyme in the cerebrovascular endothelium.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Cerebral blood flow autoregulation in hypertension and effects of antihypertensive drugs.

If antihypertensive treatment, especially emergency blood pressure lowering, is always to be safe, more thought should be given to autoregulation of cerebral blood in the hypertensive patient. This topic is reviewed in the present article, in the hypertensive patient. This topic is reviewed in the present article, particular emphasis being placed on the resetting of the lower limit of autoregulation to higher pressure in hypertension and the effects of acute administration of anti-hypertensive drugs on CBF and CBF-autoregulation.

Animals↗
PubMed1983

Effect of diazoxide-induced hypotension on cerebral blood flow in hypertensive rats.

The effect on cerebral blood flow of acute diazoxide-induced hypotension was studied in rats with renal and spontaneous hypertension. Diazoxide (5 mg/kg, i.v. bolus), caused arterial pressure to fall rapidly to that of normotensive rats, i.e. c. 75 mmHg. There was a concomitant fall in cerebral blood flow of about 35% (P less than 0.01) in renal hypertensive rats and 25% (P less than 0.05) in spontaneously hypertensive rats; the greater fall in flow in the former corresponded to a greater drop in pressure. Flow remained at these reduced levels during a 2 h observation period. Histological examination revealed small areas of ischaemic damage in the brains of five of the twelve animals. In control hypertensive rats not given diazoxide, cerebral blood flow and blood pressure were stable during a 2 1/2 h period and there was no evidence of ischaemic damage to the brains. The diazoxide-induced reduction in cerebral blood flow was interpreted as being secondary to a blood pressure fall to below the lower limit of cerebral blood flow autoregulation. No evidence was found of direct effects on the cerebral circulation such as seen with ganglionic blockers, alpha-blockers and cerebral vasodilators.

Animals↗
PubMed1983

Cerebro-circulatory effects of so-called 'vasodilators' in the anaesthetised rat.

The cerebro-vascular effects of various agents used in the treatment of cerebral disorders (dihydroergotoxine, ifenprodil, naftidrofuryl, nicardipine, nicergoline, papaverine and vincamine) were studied in the anaesthetised rat. The agents effected an increase in global cerebral blood flow, each to a different magnitude, in a dose-related manner. The changes in flow induced in the normal brain are unlikely to be of much relevance to the use of these compounds in the treatment of focal cerebral ischaemia.

Anesthetics↗
PubMed1983

Cerebrovascular effects of the converting enzyme inhibitor captopril.

The effect of captopril on cerebral blood flow (CBF) and its autoregulation was studied in spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Wistar rats. CBF was measured by the intracarotid 133Xe injection method. In one study 1 and 10 mg/kg captopril respectively were given intravenously to SHR and WKY. This caused the blood pressure to fall transiently below the lower blood pressure limit of CBF autoregulation; nonetheless CBF remained normal during captopril induced hypotension. In a second study it was shown with an integral uptake method that captopril is a very poor penetrator of the blood-brain barrier. In a third study captopril was instilled intracerebroventricularly in Wistar rats without any effect on CBF or its autoregulation. Thus when given intravenously, but not intracerebroventricularly captopril caused cerebral vasodilatation during acute hypotension.

Animals↗
PubMed1983

Cerebral blood-flow tomography: xenon-133 compared with isopropyl-amphetamine-iodine-123: concise communication.

Tomographic maps of local cerebral blood flow (CBF) were obtained with xenon-133 and with isopropyl-amphetamine-iodine-123 (IMP) in 11 subjects: one normal, two tumor cases, and eight cerebrovascular cases. A highly sensitive four-face, rapidly rotating, single-photon emission tomograph was used. The Xe-133 flow maps are essentially based on the average Xe-133 concentration over the initial 2 min during and after an inhalation of the inert gas lasting 1 min. These maps agreed very well with the early IMP maps obtained over the initial 10 min following an i.v. bolus injection. The subsequent IMP tomograms showed a slight decrease in contrast amounting to appr. five percentage points in the CBF ratio between diseased and contralateral areas. It is concluded that Xe-133 is more practical: low cost, available on a 7-day basis, easily repeatable, quantifiable without the need for arterial sampling, and with low radiation exposure to patient and personnel. On the other hand, IMP gives an image of slightly higher resolution. It also introduces a new class of iodinated brain-seeking compounds allowing, perhaps, imaging of other functions more important than mere blood flow.

Amphetamines↗
PubMed1982

Cerebral blood flow in rats with renal and spontaneous hypertension: resetting of the lower limit of autoregulation.

The effect of chronic hypertension on cerebral blood flow (CBF) was studied in anaesthetised rats. CBF was measured with the intracarotid 133Xe injection method. Rats with spontaneous and renal hypertension were compared with normotensive controls. The lower limit of autoregulation was determined during controlled haemorrhage. In the normotensive rats, CBF remained constant until mean arterial pressure (MAP) had decreased to the range of 50-69 mm Hg. Thereafter, CBF decreased with each further decrease in MAP. In both types of hypertensive rats, CBF remained constant until MAP had decreased to the range of 70-89 mm Hg. Thus, a 20-mm Hg shift of the lower limit of CBF autoregulation was found in both spontaneous and renal hypertensive rats. A neuropathological study revealed ischaemic brains lesions in half of the hypertensive rats following hypotension, whereas only a single lesion was found in one of six normotensive rats. No ischaemic brain lesions were found in a control study in which CBF was shown to be stable over a 21/2-h period. In conclusion, hypertensive rats showed a shift of the lower limit of CBF autoregulation as well as an increased susceptibility to ischaemic brain damage during hypotension. These findings presumably reflect hypertensive structural changes in the cerebral circulation.

Animals↗