Reduction In Cortical Perfusion Research Articles

Role of Pial Microvasospasms and Leukocyte Plugging for Parenchymal Perfusion after Subarachnoid Hemorrhage Assessed by In Vivo Multi-Photon Microscopy.

Subarachnoid hemorrhage (SAH) is associated with acute and delayed cerebral ischemia. We suggested spasms of pial arterioles as a possible mechanism; however, it remained unclear whether and how pial microvasospasms (MVSs) induce cerebral ischemia. Therefore, we used in vivo deep tissue imaging by two-photon microscopy to investigate MVSs together with the intraparenchymal microcirculation in a clinically relevant murine SAH model. Male C57BL/6 mice received a cranial window. Cerebral vessels and leukocytes were labelled with fluorescent dyes and imaged by in vivo two-photon microscopy before and three hours after SAH induced by filament perforation. After SAH, a large clot formed around the perforation site at the skull base, and blood distributed along the perivascular space of the middle cerebral artery up to the cerebral cortex. Comparing the cerebral microvasculature before and after SAH, we identified three different patterns of constrictions: pearl string, global, and bottleneck. At the same time, the volume of perfused intraparenchymal vessels and blood flow velocity in individual arterioles were significantly reduced by more than 60%. Plugging of capillaries by leukocytes was observed but infrequent. The current study demonstrates that perivascular blood is associated with spasms of pial arterioles and that these spasms result in a significant reduction in cortical perfusion after SAH. Thus, the pial microvasospasm seems to be an important mechanism by which blood in the subarachnoid space triggers cerebral ischemia after SAH. Identifying the mechanisms of pial vasospasm may therefore result in novel therapeutic options for SAH patients.

Age-associated reductions in cerebral blood flow are independent from regional atrophy

Prior studies have demonstrated decreasing cerebral blood flow (CBF) in normal aging, but the full spatial pattern and potential mechanism of changes in CBF remain to be elucidated. Specifically, existing data have not been entirely consistent regarding the spatial distribution of such changes, potentially a result of neglecting the effect of age-related tissue atrophy in CBF measurements. In this work, we use pulsed arterial-spin labelling to quantify regional CBF in 86 cognitively and physically healthy adults, aged 23 to 88years. Surface-based analyses were utilized to map regional decline in CBF and cortical thickness with advancing age, and to examine the spatial associations and dissociations between these metrics. Our results demonstrate regionally selective age-related reductions in cortical perfusion, involving the superior-frontal, orbito-frontal, superior-parietal, middle-inferior temporal, insular, precuneus, supramarginal, lateral-occipital and cingulate regions, while subcortical CBF was relatively preserved in aging. Regional effects of age on CBF differed from that of grey-matter atrophy. In addition, the pattern of CBF associations with age displays an interesting similarity with the default-mode network. These findings demonstrate the dissociation between regional CBF and structural alterations specific to normal aging, and augment our understanding of mechanisms of pathology in older adults.

Quantification of renal allograft perfusion using arterial spin labeling MRI: initial results

To quantify renal allograft perfusion in recipients with stable allograft function and acute decrease in allograft function using nonenhanced flow-sensitive alternating inversion recovery (FAIR)-TrueFISP arterial spin labeling (ASL) MR imaging. Following approval of the local ethics committee, 20 renal allograft recipients were included in this study. ASL perfusion measurement and an anatomical T2-weighted single-shot fast spin-echo (HASTE) sequence were performed on a 1.5-T scanner (Magnetom Avanto, Siemens, Erlangen, Germany). T2-weighted MR urography was performed in patients with suspected ureteral obstruction. Patients were assigned to three groups: group a, 6 patients with stable allograft function over the previous 4 months; group b, 7 patients with good allograft function who underwent transplantation during the previous 3 weeks; group c, 7 allograft recipients with an acute deterioration of renal function. Mean cortical perfusion values were 304.8 +/- 34.4, 296.5 +/- 44.1, and 181.9 +/- 53.4 mg/100 ml/min for groups a, b and c, respectively. Reduction in cortical perfusion in group c was statistically significant. Our results indicate that ASL is a promising technique for nonenhanced quantification of cortical perfusion of renal allografts. Further studies are required to determine the clinical value of ASL for monitoring renal allograft recipients.

Reduction of infarct size by the NO donors sodium nitroprusside and spermine/NO after transient focal cerebral ischemia in rats

Nitric oxide (NO) plays a dual role (neuroprotection and neurotoxicity) in cerebral ischemia. NO promoting strategies may be beneficial shortly after ischemia. Therefore, we have studied the hemodynamic and possible neuroprotective effects of two NO donors, the classical nitrovasodilator sodium nitroprusside (SNP) and the NONOate spermine/NO, after transient focal cerebral ischemia in rats. Parietal cortical perfusion was measured by laser-Doppler flowmetry. The effects of increasing intravenous doses (10–300 μg) of sodium nitroprusside and spermine/NO on cortical perfusion and arterial blood pressure were assessed. Transient (2 h) focal cerebral ischemia was carried out by the intraluminal thread method. The effects of intraischemic intravenous infusion of SNP (0.11, 1.1 mg/kg) and spermine/NO (0.36, 3.6 mg/kg) on hemodynamic parameters and infarct size developed after 1 week reperfusion were assessed. In control conditions, SNP and, to a lesser extent, spermine/NO induced dose-dependent hypotension and concomitant reduction in cortical perfusion. In focal cerebral ischemia, infusion of SNP (0.11 mg/kg) and spermine/NO (0.36, 3.6 mg/kg) reduced the infarct size. In the case of spermine/NO, cortical perfusion was maintained above the control levels during the ischemic insult. No significant hypotension was elicited by NO donors at the dose-ratios infused. In conclusion, brain damage induced by transient focal ischemia is reduced by intravenous NO donors. Neuroprotective effects of spermine/NO are due at least in part to improvement of brain perfusion, while sodium nitroprusside must provide direct cytoprotection. These results give further support to the protective effect of NO in the early stages of cerebral ischemia and point to the therapeutic potential of NONOates in the management of brain ischemic damage.

Crossed cerebellar diaschisis associated with balloon test occlusion of the carotid artery.

99Tcm-hexamethylpropyleneamine oxime (99Tcm-HMPAO) single photon emission computed tomographic (SPECT) brain imaging performed in conjunction with balloon test occlusion of the carotid artery has been used to assess risk of neurologic sequelae that might follow permanent surgical ligation of the artery. The predictive value of cortical hypoperfusion during temporary carotid occlusion for adverse neurologic events has been debated in previous publications. We believe that the risk of an adverse event is greater when a reduction in cortical perfusion during balloon test occlusion is associated with crossed cerebellar diaschisis (CCD). To test our hypothesis we evaluated the results of 27 99Tcm-HMPAO SPECT brain studies obtained in association with balloon test occlusions of the carotid artery. In each case we correlated clinical outcome with the presence or absence of regional decreases in cerebral perfusion and CCD. All of the 27 patients were free of neurologic symptoms during the balloon test occlusion. Seventeen of the 27 scintigraphic studies were felt to be abnormal, showing cortical perfusion defects all on the side of the occlusion. Among these 17 patients, five demonstrated CCD. Four of these five CCD patients showed evidence for cerebral cortical ischaemia on the side of the temporary carotid occlusion either shortly after the procedure or following carotid artery sacrifice. Of the remaining 12 patients with regionally reduced cerebral perfusion and no CCD, none showed evidence for cortical ischaemia in association with balloon test occlusion, and five of these 12 patients had carotid ligation without subsequent neurologic sequelae.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal injury in complete ureteric obstruction

This preliminary study examined reno-vascular injury sustained by the multipapillary porcine kidney in acute and chronic complete ureteric obstruction. In combination with measurement of upper tract pressure, regional function was assessed by [99mTc]-dimercaptosuccinic acid (DMSA) uptake and qualitative renal perfusion, by resin casting of the arterial tree prior to scanning electron microscopy (SEM). In acute obstruction, segmental defects were noted in the renal poles on both [99mTc]-DMSA scanning and casting. On SEM there was a polar afferent arteriolar vasodilatation after 30 min of obstruction and, subsequently, a segmental reduction in cortical perfusion. In kidneys that had been obstructed for 20 days, we observed a marked reduction in outer cortical perfusion coincident with afferent arteriolar vasoconstriction. The pathogenesis and significance of segmental injury to the multipapillary kidney in obstructive uropathy is discussed.

The effect of angiotensin II and vasopressinonrenal haemodynamics

A comparison was made of the vascular actions of two hormones having a renal site of action, angiotensin II and vasopressin, using laser Doppler flowmetry to measure perfusion of the cortical and papillary regions of the kidney. Angiotensin II infusion caused dose-related increases in blood pressure and reductions in cortical perfusion, the latter responses being potentiated in the presence of the converting enzyme inhibitor, cilazapril. However, angiotensin II had no effect on papillary perfusion either before or following cilazapril. The reasons for this differing vasoconstrictor ability of angiotensin II at the cortex and papilla are unclear, but it could be due to medullary generation of prostaglandin or bradykinin. Administration of equipressor doses of vasopressin caused graded reductions in both cortical and papillary perfusions, and subsequent cilazapril significantly enhanced the papillary responses. This study demonstrates that the regulation of blood flow through the different regions of the kidney can be differentially regulated by the peptide hormones angiotensin II and vasopressin.

Acute Renal Failure in McArdle's Disease and Myoglobinuric States

Reversible acute oliguric renal failure associated with skeletal muscle abnormalities due to either McArdle's disease or myoglobinuria developed in two patients. Renal angiographic and hemodynamic data revealed a preferential diffuse reduction in cortical perfusion. Arteriography showed absence of a cortical nephrogram and attenuation of the distal interlobar and arcuate arteries. Contrast medium was delayed in passage through the edematous kidney. These changes are distinct from those of chronic renal failure due to parenchymal disease. The renal arteriogram can be a useful adjunct in the differential diagnosis of acute renal failure of obscure origin.

Renal failure in the patient with cirrhosis: The role of active vasoconstriction

Renal hemodynamics were studied with the ¹³³Xe washout technic and renal arteriography in fifteen patients with cirrhosis and varying degrees of renal functional impairment. In cirrhotic patients with renal failure extreme hemodynamic instability was encountered, characterized by variability and irregularity of xenon washout, in contrast to patients with renal failure of other etiology. Marked instability was more frequent in cirrhotic patients with azotemia, and was so severe in three instances that the curves were unanalyzable. The remaining curves revealed a decrease in both mean renal blood flow and the percentage of flow in the rapid flow component in approximate proportion to the decrease in creatinine clearance, suggesting a reduction in cortical perfusion. The arteriographic findings, including the absence of a cortical nephrogram and unrecognizable renal cortical vasculature in the patients with the most severe degree of renal failure, support the concept of a reduction in renal cortical perfusion. The finding of marked hemodynamic instability strongly suggests that the renal ischemia is secondary to active vasoconstriction. Consistent reversal of all the vascular abnormalities in the kidneys of five cirrhotic patients at postmortem angiography provides further evidence for the functional basis of the renal failure, operating through active renal vasoconstriction. Phentolamine infusion into the renal artery in four patients did not significantly alter renal hemodynamics indicating that increased sympathetic nervous system activity was not responsible for the active vasoconstriction and cortical ischemia.