Changes In Cerebral Microcirculation Research Articles

Impact of cerebral microcirculatory changes on cerebral blood flow during cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Impact of cerebral microcirculatory changes on cerebral blood flow during cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Room 220-222, 10/17/2000 3: 30 PM - 5: 00 PM (PD) Changes in Cerebral Microcirculation after the Release of Aortic Clamp in Rabbits

<b>Room 220-222, 10/17/2000 3: 30 PM - 5: 00 PM (PD) Changes in Cerebral Microcirculation after the Release of Aortic Clamp in Rabbits</b>

Impact of cerebral microcirculatory changes on cerebral blood flow during cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) are still controversial and uncertain. The aim of this study was to investigate the changes of cerebral microcirculation during cerebral vasospasm and to clarify the roles of microcirculatory disturbances in cerebral ischemia by measuring cerebral circulation time (CCT) and regional cerebral blood flow (rCBF). In 24 cases with aneurysmal SAH, rCBF studies by single-photon emission CT and digital subtraction angiography (DSA) were performed on the same day between 5 and 7 days after SAH and/or within 4 hours after the onset of delayed ischemic neurological deficits. CCT was obtained by analyzing the time-density curve of the contrast media on DSA images and was divided into proximal CCT, which was the circulation time through the extraparenchymal large arteries, and peripheral CCT, which was the circulation time through the intraparenchymal small vessels. They were analyzed in association with rCBF and angiographic vasospasm. Severe angiographic vasospasm statistically decreased rCBF, and correlation between the degree of angiographic vasospasm and rCBF was seen (r=0.429, P=0.0006). Peripheral CCT showed strong inverse correlation with rCBF (r=-0.767, P<0.0001). Even in none/mild or moderate angiographic vasospasm, prolonged peripheral CCT was clearly associated with decreased rCBF. In addition to the marked luminal narrowing of large arteries detected as severe angiographic vasospasm, microcirculatory changes detected as prolonged peripheral CCT affected cerebral ischemia during cerebral vasospasm. These results suggested that impaired autoregulatory vasodilation or decreased luminal caliber in intraparenchymal vessels may take part in cerebral ischemia during cerebral vasospasm.

Effect of cerebral ischaemia on the cerebrovascular and cardiovascular response to haemorrhage.

Reports studying the combination of low blood pressure and cerebral ischaemia are few, and it remains to be determined how cerebral circulatory insufficiency modifies the cerebral perfusion and the central haemodynamic response to blood loss. We hypothesised that occlusion of arteries to the brain modifies the cerebrovascular and cardiovascular responses to blood loss. Continuous measurements of the cerebral microcirculation with laser Doppler microprobes in the cerebral cortex were performed in anaesthetised pigs during cerebral ischaemia and haemorrhagic hypotension. The response to rapid bleeding (25% of the blood volume) was recorded during normal conditions and during cerebral ischaemia induced by bilateral occlusion of the common carotid arteries. During normal conditions haemorrhage caused insignificant decreases in cerebral microcirculation. Haemorrhage during bilateral carotid artery occlusion, however, caused significantly greater changes in cerebral microcirculation and a greater posthaemorrhagic increase in cerebrovascular resistance shortly after the blood loss. Haemorrhage during bilateral carotid artery occlusion also caused greater reductions in cardiac output and arterial pressure than similar blood loss caused during normal conditions. This study showed a disproportionate decrease in cerebral blood flow with haemorrhage during bilateral carotid occlusion, caused by an immediate increase in cerebrovascular resistance. The results suggest that even a moderate blood loss in patients with impaired cerebral circulation could be dangerous, because normal compensatory mechanisms to haemorrhage are impaired.

Cerebral microcirculatory changes during and following transient ventricular tachycardia in cats

Although reduced cerebral perfusion is believed to be the cause of syncope due to cardiac arrhythmias, investigations on the cerebral microcirculation during cardiac arrhythmias have been rare. We therefore studied the effects of transient ventricular tachycardia on the local cerebral blood volume and blood flow. Experimental ventricular tachycardia was induced in cats by electrically stimulating the ventricle of the heart at a rate of 300/min for 1 min. Using our photoelectric method, the local cerebral blood volume, mean transit time of blood, and cerebral blood flow in the parieto-temporal region were measured during and for 3 h after ventricular tachycardia. Transient ventricular tachycardia of as short as 1 min caused cerebral ischemia with a blood flow reduction of approximately 30%. This was considered to be due to reduced blood pressure plus transient autonomic dysfunction, or dysautoregulation, during the ventricular tachycardia. Mild and transient reactive hyperemia occurred immediately after termination of the dysrhythmia, but continuous reductions of cerebral blood flow were observed thereafter for 3 h. This delayed hypoperfusion is attributable to either vasoconstriction of the large resistance vessels or changes in the hemorheological properties of the blood caused by cerebral ischemia. Ventricular tachycardia of the type reported has significant and long-lasting effects on the cerebral microcirculation.

Cerebral microcirculatory changes after cerebral embolization induced by glass bead injection in rabbits.

The authors investigated microcirculatory changes in cerebral embolization induced by an injection of glass beads (mesh size 20/400, 15 mg/body) using intravital microscopy and reflectance spectrophotometry in normal rabbits. Cerebral embolization with the glass bead injection reduced the inner diameter of cerebral arterioles, the index of cerebral hemoglobin concentration (IHb), and the index of oxygen saturation (ISO2). Moreover, platelet aggregation rates and plasma levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) appreciably increased. During observation of the pial vasculature, "white bodies" became visible at the entrance of arteriolar branchings two to three minutes after the glass bead injection. After indomethacin administration (3 mg/kg, IV), they could not observe white bodies, and platelet aggregation rates were significantly reduced. The plasma levels of TXB2 and 6-keto-PGF1 alpha were also significantly reduced. These findings suggest that glass beads do injury to the microvascular endothelial cells leading to development of white bodies, ie, "flying thrombi." Therefore, the cerebral microvascular embolization induced by the glass bead injection appears to be an experimental model for evaluating efficacy of remedies for the cerebral microcirculatory disorders.

Brattleboro rats exhibit normal Pa co 2-induced changes in cerebral microcirculation

Prominent biochemical theories of psychiatry are based on proposed catecholaminergic mechanisms. Furthermore, the central adrenergic system (CAS) has been implicated in various central phenomena (e.g., sleep, memory, motivation) and psychiatric disorders (e.g., affective disorders, schizophrenia). Yet the knowledge of cellular mechanisms involved in mediating these actions remains beyond our understanding. A synthesis of anatomical and physiological research has led to the development of a neurohumoral hypothesis proposing that one function of the CAS is the regulation of the blood-brain barrier as part of an intraaxial autonomic system anatomically distinct from, but having central functions analogous to, those of the peripheral sympathetic system (Hartman et al. 1980). One specific function predicted by this concept is modulation of cerebral microvascular flow and permeability. By regulating cerebral capillary permeability, the CAS-and drugs that act on it-could have profound effects on cerebral fluid dynamics, metabolism, and ultimately, brain function. Moreover, the relationship between the CAS and the cerebral microvasculature can serve as a model in which the effects of a defined neural system on an end-organ within the brain can be quantified in vivo. This relationship represents one of the few examples of a central neuron terminating directly on an end-organ (i.e., the cerebral capillary) instead of on another neuron. Such a model system is of relevance to understanding neuron-end-organ mechanisms and, ultimately, their relationship to psychiatric disorders. We have explored the relationship between the CAS and cerebromicrocirculatory regulation using pharmacological (Preskom et al. 1980, 1982a,b; Kent et al. 1986) and physiological (Raichle et al. 1975; Elam et al. 1981) paradigms, An example of the latter is the inhalation of co*, which induces changes in the cerebromicrocirculation and increases the firing rate of the locus coeruleus (LC) (Kent et al. 1986). A remaining question is whether the CO*-induced release of norepinephrine (NE) from the LC affects the microvasculature directly or not.

Amitriptyline normalizes tetrabenazine-induced changes in cerebral microcirculation

The cerebromicrocirculation in the tetrabenzaine (TBZ) model of depression has been found to be abnormal with respect to (1) responsiveness of cerebral blood flow to increases in arterial CO 2 content and (2) the effective permeability of the blood-brain barrier to water. Development of these abnormalities temporally paralleled the behavioral disturbances and catecholamine depletion induced by TBZ. These TBZ-induced changes occurred globally throughout the brain, being apparent in the forebrain, cerebellum, and medulla-pons. Pretreatment with the antidepressant amitriptyline prevented both behavioral and physiological effects of TBZ, whereas amitriptyline administered after TBZ was less effective. The results suggest that an important action of tricyclic antidepressants may be cerebromicrocirculatory effects.