scholarly journals Metabolic and Hemodynamic Activation of Postischemic Rat Brain by Cortical Spreading Depression

1990 ◽  
Vol 10 (4) ◽  
pp. 564-571 ◽  
Author(s):  
M. Kocher

Following transient ischemia of the brain, the coupling between somatosensory activation and the hemodynamic-metabolic response is abolished for a certain period despite the partial recovery of somatosensory evoked responses. To determine whether this disturbance is due to alterations of the stimulus-induced neuronal excitation or to a breakdown of the coupling mechanisms, cortical spreading depression was used as a metabolic stimulus in rats before and after ischemia. Adult rats were subjected to 30 min of global forebrain ischemia and 3–6 h of recirculation. EEG, cortical direct current (DC) potential, and laser-Doppler flow were continuously recorded. Local CBF (LCBF), local CMRglc (LCMRglc), regional tissue contents of ATP, glucose, and lactate, and regional pH were determined by quantitative autoradiography, substrate-induced bioluminescence, and fluorometry. Amplitude and frequency of the DC shifts did not differ between groups. In control animals, spreading depression induced a 77% rise in cortical glucose consumption, a 66% rise in lactate content, and a drop in tissue pH of 0.3 unit. ATP and glucose contents were not depleted. During the passage of DC shifts, transient increases (<2 min) in laser-Doppler flow were observed, followed by a post-spreading depression hypoperfusion. A comparable although less expressed pattern of hemodynamic and metabolic changes was observed in the postischemic rats. Although baseline LCMRglc was depressed after ischemia, it was activated 47% during spreading depression. Lactate increased by 26%, pH decreased by 0.3 unit, and ATP and glucose remained unchanged. The extent of the transient increase in laser-Doppler flow did not differ from that of the control group, and a post–spreading depression hypoperfusion was also found. The results demonstrate that the postischemic brain may, although to a lesser degree, cover additional energy demands. The previously observed suppression of functional activation after ischemia is probably caused by both alterations in afferent synaptic transmission and subsequent neuronal excitation and the diminution of the metabolic response to a local stimulus as observed during spreading depression.

1986 ◽  
Vol 251 (1) ◽  
pp. F115-F124 ◽  
Author(s):  
R. J. Roman ◽  
C. Smits

Renal hemodynamics and renal blood flow autoregulatory ability differ in young (body wt 100 g) and adult (body wt 300 g) rats. Possible age-dependent changes in inner medullary hemodynamics have not been examined because it has not been possible to expose the papilla of adult rats for direct study of the vasa recta circulation. This study presents a technique for exposure of the papilla in any size rat. Seven days before an acute experiment, a small amount of cortical tissue overlying the papilla on the dorsal surface of the kidney was removed. The creation of this papillary window allowed for exposure of the papilla in adult rats after removal of the ureter. Using this preparation, we compared papillary blood flow in young and adult rats using a Periflux differential laser-Doppler flowmeter (Perimed, Stockholm, Sweden). The meter was calibrated by comparing the signal obtained from the papilla of 28 rats with papillary flow measured from the accumulation of 51Cr-labeled erythrocytes in the papilla. The laser-Doppler flow signal was linearly related and highly correlated (r = 0.92) to the red cell flow into the papilla. Comparisons of laser-Doppler flow signals obtained from the papilla of young and adult animals indicated that papillary blood flow was approximately 2-fold greater in the adult rats than in the young animals. This finding was associated with an enhanced maximal urine concentrating ability found in the younger rats. These studies demonstrate the utility of the laser-Doppler flowmeter for the assessment of papillary blood flow and suggest that inner medullary hemodynamics differ in young and adult rats.


2021 ◽  
Vol 79 (1) ◽  
pp. 121-128
Author(s):  
Lars Saemann ◽  
Anne Großkopf ◽  
Fabio Hoorn ◽  
Gábor Veres ◽  
Yuxing Guo ◽  
...  

BACKGROUND: Machine perfusion (MP) is a novel method for donor heart preservation. The coronary microvascular function is important for the transplantation outcome. However, current research on MP in heart transplantation focuses mainly on contractile function. OBJECTIVE: We aim to present the application of Laser-Doppler-Flowmetry to investigate coronary microvascular function during MP. Furthermore, we will discuss the importance of microcirculation monitoring for perfusion-associated studies in HTx research. METHODS: Porcine hearts were cardioplegically arrested and harvested (Control group, N = 4). In an ischemia group (N = 5), we induced global ischemia of the animal by the termination of mechanical ventilation before harvesting. All hearts were mounted on an MP system for blood perfusion. After 90 minutes, we evaluated the effect of coronary perfusion pressures from 20 to 100 mmHg while coronary laser-doppler-flow (LDF) was measured. RESULTS: Ischemic hearts showed a significantly decreased relative LDF compared to control hearts (1.07±0.06 vs. 1.47±0.15; p = 0.034). In the control group, the coronary flow was significantly lower at 100 mmHg of perfusion pressure than in the ischemia group (895±66 ml vs. 1112±32 ml; p = 0.016). CONCLUSIONS: Laser-Doppler-Flowmetry is able to reveal coronary microvascular dysfunction during machine perfusion of hearts and is therefore of substantial interest for perfusion-associated research in heart transplantation.


1986 ◽  
Vol 87 (5) ◽  
pp. 634-636 ◽  
Author(s):  
Lars Erik Lindblad ◽  
Lena Ekenvall ◽  
Klas Ancker ◽  
Håkan Rohman ◽  
P Åke Öberg

1997 ◽  
Vol 17 (5) ◽  
pp. 586-590 ◽  
Author(s):  
Sachiko Osuga ◽  
Antoine M. Hakim ◽  
Hitoshi Osuga ◽  
Matthew J. Hogan

We report autoradiographic measurements of the in vivo uptake of [3H]nimodipine during the nonischemic depolarization of cortical spreading depression (CSD) in rat brain. [3H]Nimodipine uptake in brain was determined regionally in rats undergoing CSD (n = 8) and was significantly increased in cortex (14 ± 7%) and hippocampus (10 ± 6%) on the stimulated side relative to the contralateral hemisphere when compared with the same measurements in a control group (n = 8). A similar measurement using the physiologically inert radiotracer [14C]iodoantipyrine to control for potential effects of CSD on radioligand distribution showed a minimal increase (2.4 ± 0.7%) of radiotracer uptake in cortex after CSD. This increase was significantly less than that observed in the [3H]nimodipine uptake studies. We hypothesize that increased in vivo [3H]nimodipine uptake in CSD identifies regions of depolarization and thus infers activation of the L-type voltage sensitive calcium channels.


2009 ◽  
Vol 2 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Euclides Mauricio Trindade-Filho ◽  
Carlos Augusto Carvalho de Vasconcelos ◽  
Rubem Carlos Araújo Guedes

1998 ◽  
Vol 274 (4) ◽  
pp. R1158-R1161
Author(s):  
Evvi-Lynn M. Rollins ◽  
James E. Fewell

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.


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