Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concept that reflex control of cerebral vessels is unimportant has been challenged by recent studies which suggest that carotid baroreceptors have an important role in regulation of cerebral blood flow (CBF). In this study we have tested the hypothesis that arterial baroreceptors contribute to regulation of total or regional CBF. CBF was measured in anesthetized dogs with 15 mu microspheres. Stimulation of carotid baroreceptors, by raising carotid sinus pressure, did not alter or redistribute cerebral flow. Responses to baroreceptor stimulation were intact, as manifested by vasodilation in skeletal muscle. CBF decreased during systemic hypocapnia and increased during hypercapnia, which indicates that failure of cerebral flow to change during baroreceptor stimulation was not due to unresponsiveness of cerebral vessels. During hypercapnia, baroreceptor stimulation also failed to alter CBF. In other studies CBF was measured during increases in systemic arterial pressure, before and after denervation of arterial baroreceptors. Increases in arterial pressure did not increase CBF either before or after denervation of baroreceptors. We conclude that baroreceptor stimulation does not alter total or regional CBF and that baroreceptors do not regulate cerebral flow during systemic hypertension.
Stroke
PMID:Total and regional cerebral blood flow during stimulation of carotid baroreceptors. 94 13

To investigate the influence of the carotid arterial baroreceptors on right atrial mechanics, the carotid sinus region was isolated surgically in eight dogs prepared acutely under pentobarbital. Right atrial pressure and conductance volume were measured with a strain-gauge tip catheter and a conductance catheter, respectively. Reduction of carotid sinus pressure from 225 to 50 mmHg elicited significant increases in the a wave in right atrial pressure, in atrial stroke volume, in atrial stroke work (2.5-fold), and in atrial stroke power (4-fold). Mean central venous pressure and atrial volume at the onset of each beat did not change. These responses were unchanged after bilateral cervical vagotomy. Head-up tilt was applied at carotid sinus pressures less than or equal to 150 mmHg in four dogs to oppose any contribution of decreased systemic venous capacity to the responses through increased atrial filling. Tilt did not change atrial stroke work or atrial filling during late ventricular systole before vagotomy but inhibited these variables significantly after vagotomy. The slope of the relationship between right atrial stroke work and atrial volume at the onset of contraction increased significantly with reduction of carotid sinus pressure. This response was unaffected by either vagotomy or tilt. Carotid arterial hypotension appears to augment right atrial stroke work and stroke volume through an increase in atrial contractility. A decrease in venous capacity may contribute to this response especially after vagotomy.
 ...
PMID:Carotid baroreceptor control of right atrial mechanics in dogs. 175 May 43

We studied brain retroperfusion in nine adult baboons. Experiments in four baboons determined techniques and the safety of retroperfusion, and experiments in three baboons determined the ability of retroperfusion to reverse cerebral ischemia. Two baboons died before retroperfusion. Arterial blood was continuously circulated by an external pumping system from one femoral artery into the intracranial sinuses through specially designed balloon-tipped catheters placed percutaneously into the sigmoid sinuses bilaterally. The balloons intermittently occluded the sinuses. Ischemia was produced by occluding the left middle cerebral artery. Standard and computed electroencephalography with topographic mapping monitored the onset and reversal of ischemia. Retroperfusion rate exceeded 50 ml/min with a mean intrasinus pressure increase of 27 (0-149) mm Hg in all seven experiments. Venograms demonstrated complete or partial filling of the superior sagittal sinus in each experiment. Four experiments without ischemia established maximal balloon occlusion cycles, retroperfusion rates, and sinus pressure changes. These four baboons were neurologically normal after retroperfusion; two had normal magnetic resonance imaging scans. Ischemic changes, detected by electroencephalography following middle cerebral artery occlusion, were reversed with retroperfusion in all three ischemia experiments. Autopsies in the seven baboons demonstrated no parenchymal hemorrhage or edema. Our results suggest that further investigation of retroperfusion, and possibly retroinfusion of agents for cerebral protection, is warranted.
Stroke 1990 Jan
PMID:Ischemic brain rescue by transvenous perfusion in baboons with venous sinus occlusion. 230 Sep 96

The contributions of the carotid sinus and cardiopulmonary baroreflexes to the interindividual variation in sympathetic nervous system activation caused by postural adaptation were indirectly assessed in 68 mild hypertensive subjects. Supine and upright plasma norepinephrine (NE), blood pressure (cuff) and cardiac output (acetylene rebreathing) were measured. Mean arterial pressure (MAP), carotid sinus pressure, stroke volume and systemic vascular resistance were calculated. Stroke volume was assumed to be proportional to the degree of stretch of cardiac mechanoreceptors, carotid sinus MAP was assumed to be proportional to carotid sinus stretch and plasma NE to reflect sympathetic nervous activity. Plasma NE correlated inversely with stroke volume (r = -0.62, p less than 10(-14] and estimated carotid sinus MAP (r = -0.33, p less than 0.0002) and positively with systemic vascular resistance (r = 0.59, p less than 10(-10]. Holding systemic vascular resistance constant by partial regression, the inverse relation between plasma NE and stroke volume remained (partial r = -0.36, p less than 0.02). Multiple linear regression yielded the equation: plasma NE (pg/ml) = 720 + 4.3 age - 5.1 stroke volume (ml) - 1.0 carotid sinus MAP (mm Hg). Substituting mean supine and upright values for stroke volume and carotid sinus MAP in this equation, it can be roughly estimated that changes in stroke volume account for as much as 60% of the postural variation in plasma NE in hypertensives, whereas only 15% of this variation is caused by changes in carotid sinus pressure. These findings suggest that cardiopulmonary baroreflexes are primary activators of the sympathetic nervous system during postural adaptation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of postural stimulation on systemic hemodynamics and sympathetic nervous activity in systemic hypertension. 230 Dec 62

Blood-brain barrier integrity during cardiopulmonary resuscitation may be important because of the potential effects of adrenergic agonists administered during arrest on cerebral metabolism and the cerebral vasculature. As an index of blood-brain barrier permeability to small molecules, we measured the brain uptake of [14C]alpha-aminoisobutyric acid during a 10-minute period in 25 anesthetized dogs. To correct for the amount of carbon-14 label in the plasma space, we administered [3H] inulin 2 minutes before death. The mean transfer coefficient in 14 brain regions of five control dogs ranged from 0.002 to 0.007 ml/g/min. After 8 (n = 15) or 15 (n = 5) minutes of cardiac arrest, external chest compression was instituted to maintain aortic blood pressure above 60 mm Hg. The transfer coefficient was not elevated during chest compression (n = 10), immediately following defibrillation (n = 5), or 4 hours after resuscitation (n = 5); in some brain regions the transfer coefficient decreased. However, the decrease in the transfer coefficient was proportional to the decrease in the cerebral plasma volume as measured by the ratio of the [3H]inulin concentration in the tissue to that in the plasma. Thus, it is unlikely that a decrease in capillary surface area masked an increase in blood-brain barrier permeability. Therefore, we found no evidence of blood-brain barrier disruption during or after cardiopulmonary resuscitation in dogs. Despite the large phasic increases in sagittal sinus pressure associated with external chest compression, concurrent increases in cerebrospinal fluid pressure apparently protect the microcirculation from increased transmural pressure.
Stroke 1990 Aug
PMID:Blood-brain barrier integrity during cardiopulmonary resuscitation in dogs. 238 99

An experimental model was designed to study circulatory drug effects with or without barostatic reflex influences. In dogs anaesthetized with chloralose, both carotid sinuses were perfused from a femoral by-pass either with systemic arterial pressure or with a pump in order to control the sinus pressure. Cardiac and aortic baroreceptors were denervated. I.v. metoprolol (240 micrograms X kg-1 + 102 micrograms X kg-1 X h-1) with constant carotid sinus pressure and thereby constant baroreceptor activation reduced cardiac output, heart rate, cardiac contractility and left ventricular stroke work index. Systemic vascular resistance increased. This response was independent of the degree of baroreflex activation. During the combined administration of enflurane (1.6% end-tidal concentration) and metoprolol, cardiac performance (cardiac output, stroke volume, heart rate, cardiac contractility and left ventricular stroke work index) was depressed independent of the degree of baroreflex activation. Barostatic reflexes, however, counteracted an observed decrease in systemic vascular resistance. This reflex vascular response was, during metoprolol-enflurane administration, associated with an increased left ventricular end-diastolic pressure.
 ...
PMID:Cardiovascular studies during controlled baroreflex activation in the dog: II. Effects of metoprolol and enflurane. 298 11

Whether cardiac tamponade causes myocardial ischemia and whether volume resuscitation can improve coronary perfusion pressure and myocardial blood flow were studied by hemodynamic responses to three blood infusions of 15 ml/kg in dogs with left ventricular hypovolemia produced by cardiac tamponade (N = 10) or hemorrhage (N = 10). Coronary perfusion pressure decreased to 37 +/- 2 mm Hg with tamponade and 39 +/- 1 mm Hg with hemorrhage, causing significant blood flow decreases in both ventricles. Myocardial oxygen extraction increased significantly in both groups without affecting lactate extraction. Volume resuscitation after hemorrhage progressively restored hemodynamic variables to baseline values. Volume resuscitation after tamponade did not increase stroke volume, whereas it increased coronary sinus pressure to 19.2 +/- 1.0 mm Hg (p less than 0.05). Coronary perfusion pressure increased to 53 +/- 5 mm Hg following the first infusion (p less than 0.05), but exhibited no further improvement. Tamponade did not produce myocardial ischemia. Coronary perfusion pressure and blood flow were not restored to baseline values with volume resuscitation since coronary sinus pressure rose incrementally with each volume infusion.
 ...
PMID:Efficacy of intravascular volume resuscitation in dogs with acute cardiac tamponade. 337 80

In chloralose-anaesthetized dogs the carotid sinuses were bilaterally perfused with blood from a femoral artery, either at systemic arterial pressure through a direct by-pass or with a pump in order to control the sinus pressure. Influences from cardiac receptors and aortic baroreceptors were eliminated by denervation. Administration of enflurane (1.6% end-tidal concentration) with the presence of barostatic modulation, i.e. the carotid sinuses were perfused at prevailing systemic arterial pressure, reduced cardiac performance (cardiac output, cardiac contractility, heart rate and left ventricular stroke work) and mean arterial pressure. When barostatic compensation of enflurane-induced circulatory changes was prevented by maintaining sinus perfusion pressure constant at the pre-enflurane level, these haemodynamic alterations, with the exception of cardiac output, were significantly more pronounced. Furthermore, systemic vascular resistance decreased. We conclude that barostatic reflexes significantly modify cardiovascular depressive effects of enflurane.
 ...
PMID:Cardiovascular studies during controlled baroreflex activation in the dog: I. Effects of enflurane. 397 27

Complications of carotid sinus pressure, which are rare, include cardiac arrhythmias and cerebrovascular accidents. A 79-year-old man experienced a flaccid right hemiplegia one minute after left carotid sinus pressure. At necropsy, an atheromatous embolus occluded the left middle cerebral artery, resulting in hemorrhagic infarction in its vascular territory. Atheromatous embolism following carotid sinus pressure has not been previously documented. Most sudden stroke deficits following carotid sinus pressure are probably caused by this mechanism.
 ...
PMID:Cerebral atheromatous embolism following carotid sinus pressure. 722 20

Superior sagittal sinus pressure, intracranial pressure and arterial pressure were recorded in an experimental series on 10 cats. During drug-induced, severe, acute arterial hypertension and parallel hypercapnia, venous pressure could exceed intracranial pressure in both the supra- and infratentorial compartment. From these data it is concluded that cerebral venous pressure during acute arterial hypertension may contribute to protein extravasation at the postcapillary-venular level.
Stroke
PMID:Cerebral venous pressure during actively induced hypertension and hypercapnia in cats. 736 47


1 2 Next >>