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D Heistad

Publications and source records attributed to D Heistad.

7 recordsLinked to original sources
PubMed1991

Effects of sympathetic nerves on collateral vessels in the limb of atherosclerotic primates.

This study was performed to examine effects of sympathetic nerves on collateral vessels in the limb. We studied normal (N) and atherosclerotic (AS) cynomolgus monkeys that were fed atherogenic diet for 21 months. A common iliac artery was ligated 13 months before hemodynamic measurements. Using histofluorescence microscopy, a plexus of noradrenergic nerves was identified in the adventitia of collateral vessels. We measured blood flow to the limb with microspheres, and the pressure gradient from aorta to the iliac artery beyond the occlusion. The lumbar sympathetic chain was stimulated electrically at 3 Hz (SNS-3) and 15 Hz (SNS-15). In normal monkeys, conductance of collateral vessels (in ml/min per 100 g per 100 mm Hg) was 19 +/- 3.6 (mean +/- SE) during control, 14 +/- 1.6 during SNS-3, and 9.8 +/- 0.9 during SNS-15 (P less than 0.05 vs control). In AS monkeys, collateral conductance was 12 +/- 2.9 during control, 7.5 +/- 1.7 during SNS-3 and 3.9 +/- 1.8 during SNS-15 (P less than 0.05). In summary, collateral vessels in the limb are innervated and sympathetic stimulation produces pronounced constriction of collateral vessels in both normal and atherosclerotic monkeys. Thus, the effectiveness of collateral vessels in maintaining blood flow to the limb may be compromised by increased activity of sympathetic nerves.

Animals↗
PubMed1988

Validation studies for brain blood flow assessment by radioxenon tomography.

A tomographic technique has been used recently for cerebral blood flow measurements with inhaled radioxenon. Based on experiments in a specially developed dynamic phantom and on studies in primates in vivo, we have analyzed the validity of this method for measurements of both regional and total blood flow in the brain. We have also examined the errors introduced into flow computations as a function of changes in such parameters as: rate of xenon input, size of region of interest, magnitude of regional flow rates, and inter-regional flow differences. Our findings indicate a reasonable degree of accuracy for flow measurements in gray matter regions that are 3 cm in diameter or larger, while white matter blood flow is generally overestimated. The accuracy for regional flow assessments degrades as a function of: diminishing region size, increasing inter-regional flow differences, and flow rates in excess of 100 ml/100 g/min. Measurements for brain regions 2 cm or smaller in diameter can be in error by 25-50% as a result of partial volume averaging. Although the technique is not ideal for accurate flow measurements in small regions of the brain, it nevertheless provides a convenient means of assessing perfusion in major vascular territories of the brain in routine clinical applications.

Animals↗
PubMed1986

Effects of vasodilator stimuli on resistance of large and small cerebral vessels.

We have examined effects of vasodilator stimuli on segmental resistance in the cerebral circulation. Our hypothesis was that resistance of large arteries, as well as small vessels, contributes to cerebral vascular responses to vasodilator stimuli. We measured cerebral blood flow with microspheres in anesthetized rabbits and measured pressure in pial arteries approximately 100 microns diameter using a servo-null method. These values were used to calculate resistance of large arteries (greater than 100 microns diameter) and small vessels (less than 100 microns diameter). Under control conditions, resistance of large arteries accounted for one-third to one-half of total cerebral vascular resistance. Intracarotid infusion of acetylcholine (1 microgram/min) reduced large arterial resistance by 69% and small vessel resistance by 58%. Adenosine also produced marked reductions in resistance of both large and small cerebral vessels. In contrast, seizures reduced large arterial resistance by 50% and small vessel resistance by 85%. Pial arterial pressure, which depends on the ratio of large and small vessel resistance, increased during infusion of acetylcholine and adenosine, but decreased during seizures. We conclude that both large and small cerebral vessels are responsive to acetylcholine and adenosine, and seizures produce preferential reduction in resistance of small vessels.

Acetylcholine↗
PubMed1975

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation.

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Animals↗
PubMedDate not supplied

Sympathetic nerves protect the blood-brain barrier in stroke-prone spontaneously hypertensive rats.

Disruption of the blood-brain barrier may play a major role in the pathogenesis of hypertensive encephalopathy. In this study we determined whether sympathetic nerves to cerebral vessels protect the blood-brain barrier during chronic hypertension. We removed the cervical sympathetic ganglion on one side in 24 stroke-prone hypertensive rats when they were 1 month old. After signs of cerebral dysfunction developed at the mean age of 160 +/- 5 days (SE), we injected 125I-albumin and Evans blue dye intravenously to evaluate the permeability of the 125I-albumin was 3.53 +/- 0.83 (brain albumin x 100/blood albumin) in areas of the cerebrum stained with blue dye and 0.24 +/- 0.02 in unstained areas (p less than 0.05). We conclude that sympathetic nerves protect the blood-brain barrier against disruption during chronic hypertension and thereby may protect against hypertensive encephalopathy.

Albumins↗
PubMedDate not supplied

Effects of atherosclerosis on cerebral vessels: hemodynamic and morphometric studies.

In this study hemodynamic and morphometric consequences of atherosclerosis were examined in cynomolgus monkeys. We tested the hypothesis that atherosclerosis augments cerebral vasoconstrictor responses to serotonin. We studied 8 normal and 8 atherosclerotic monkeys, which were fed an atherogenic diet for 17 months. Morphometric studies indicated marked intimal proliferation of extracranial carotid arteries, with only modest reduction in the vascular lumen, as atherosclerotic lesions were displaced outward. Cerebral blood flow was measured with microspheres and microvascular pressure was measured with a micropipette in pial arteries approximately 350 microns diameter. Intracarotid infusion of serotonin reduced microvascular pressure, which indicates constriction of large arteries upstream, but cerebral blood flow did not decrease. Serotonin produced a 2-fold greater reduction in cerebral microvascular pressure in atherosclerotic monkeys than in normal monkeys. Intracarotid histamine increased flow and hypocapnia reduced flow in both normal and atherosclerotic monkeys, without altering cerebral microvascular pressure. We conclude: First, atherosclerosis potentiates constrictor responses to serotonin in large cerebral arteries. Because platelets release serotonin when they aggregate, augmentation of responses by atherosclerosis may have implications for cerebral vascular responses during aggregation of platelets at carotid lesions. Second, despite marked proliferation of intima, atherosclerotic lesions are displaced outward during a prestenotic phase of the disease, so that the lumen is relatively well preserved.

Animals↗