Non‐Uniform Blood Flow in the Left Ventricular Wall of Dogs Measured by the Xe‐133 Wash‐out Technique

Andersen, Henning; Bagger, Henning; Gøtzsche, H

doi:10.1111/j.1748-1716.1969.tb04481.x

Cited by 34 publications

(7 citation statements)

References 16 publications

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“…However, studies on myocardial flow distribution using washout of locally injected depots of a radioactive tracer have consistently shown a smaller flow rate in deep regions, averaging 70% of flow to superficial regions in the unstressed heart (3,4). This observation is at variance with the present and previous findings (7)(8)(9)(10).…”

Section: Control Preloadcontrasting

confidence: 73%

“…This observation is at variance with the present and previous findings (7)(8)(9)(10). In addition, myocardial flow determined from locally injected depots has shown a smaller flow rate compared with flow rates determined from intracoronary injections (4). It is conceivable that the volume of the intramyocardial injectate increases local tissue pressure in excess of that effectively counteracted by the autoregulatory mechanism.…”

Section: Control Preloadcontrasting

confidence: 70%

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Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Kjekshus

1973

Circulation Research

123

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The effects of increased ventricular preload on the distribution of regional blood flow in normal and ischemic myocardium were determined in deep and superficial regions of the left ventricle by using labeled microspheres. The ratio of flow in deep regions to flow in superficial regions in nonischemic tissue was 1.06 ± 0.06 and increased to 1.14 ± 0.06 when left ventricular end-diastolie pressure was raised from 4.8 ± 1 mm Hg to 18 ± 2 mm Hg by intravenous infusion of blood. In ischemic areas the ratio of flow in deep regions to flow in superficial regions fell simultaneously from 0.71 ±0.12 to 0.45 ±0.07 ( P < 0.001). Control of coronary flow during increased preload was studied in a separate preparation in which coronary flow was decreased in steps by reducing coronary perfusion pressure during periods of constant cardiac performance. The increased preload was associated with loss of autoregulation of coronary flow. It is suggested that, in myocardium with unrestricted coronary supply, regional distribution of flow is independent of gradients in tissue pressure during the described changes in preload due to an autoregulatory mechanism. However, when autoregulation of coronary flow is abolished by coronary artery occlusion, the coronary bed is fully dilated, and distribution of flow is directly dependent on gradients in myocardial tissue pressure. Increased ventricular preload consequently augments the underperfusion of the subendocardial regions of an ischemic area.

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Section: Control Preloadcontrasting

confidence: 73%

Section: Control Preloadcontrasting

confidence: 70%

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Kjekshus

1973

Circulation Research

123

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“…The lamellar hypothesis of hippocampal function in its simplest original form posited that excitatory activity travels from the entorhinal cortex and through the hippocampus via a “trisynaptic circuit” lying within a series of parallel hippocampal “slices” or “lamellae” (Andersen et al, 1969, 1971). In this way, it was envisaged that temporal lobe interactions between the entorhinal cortex and the hippocampus were organized topographically, and that “lamellae” might operate independently, permitting a relatively simple structure to mediate complex behaviors.…”

Section: Origins Of the Lamellar Hypothesismentioning

confidence: 99%

“…The lamellar hypothesis as originally conceived (Andersen et al, 1969) was greatly influenced by the still unpublished anatomical findings of Blackstad and his colleagues in Århus, Denmark, who had made two observations based on the distribution of degenerating fibers after focal injury in the dentate gyrus or entorhinal cortex. First, Blackstad et al (1970) reported that after small lesions of the dentate gyrus, degenerating mossy fibers exhibited a “lamellar” pattern in the transverse plane, and they also noted that “very narrow bands were seen in a few animals with particularly small lesions.” Second, Andersen and colleagues cited as a personal communication from Jeune the subsequently published finding that, “each specific level of the entorhinal area distributes fibers to a restricted segment of the hippocampus” (Hjorth-Simonsen and Jeune, 1972).…”

Section: Origins Of the Lamellar Hypothesismentioning

confidence: 99%

Updating the Lamellar Hypothesis of Hippocampal Organization

Sloviter¹,

Lømo²

2012

Front. Neural Circuits

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Andersen et al. (1971) proposed that excitatory activity in the entorhinal cortex propagates topographically to the dentate gyrus, and on through a “trisynaptic circuit” lying within transverse hippocampal “slices” or “lamellae.” In this way, a relatively simple structure might mediate complex functions in a manner analogous to the way independent piano keys can produce a nearly infinite variety of unique outputs. The lamellar hypothesis derives primary support from the “lamellar” distribution of dentate granule cell axons (the mossy fibers), which innervate dentate hilar neurons and area CA3 pyramidal cells and interneurons within the confines of a thin transverse hippocampal segment. Following the initial formulation of the lamellar hypothesis, anatomical studies revealed that unlike granule cells, hilar mossy cells, CA3 pyramidal cells, and Layer II entorhinal cells all form axonal projections that are more divergent along the longitudinal axis than the clearly “lamellar” mossy fiber pathway. The existence of pathways with “translamellar” distribution patterns has been interpreted, incorrectly in our view, as justifying outright rejection of the lamellar hypothesis (Amaral and Witter, 1989). We suggest that the functional implications of longitudinally projecting axons depend not on whether they exist, but on what they do. The observation that focal granule cell layer discharges normally inhibit, rather than excite, distant granule cells suggests that longitudinal axons in the dentate gyrus may mediate “lateral” inhibition and define lamellar function, rather than undermine it. In this review, we attempt a reconsideration of the evidence that most directly impacts the physiological concept of hippocampal lamellar organization.

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“…The hippocampus consists of three main fields, dentate gyrus (DG), areas CA3 and CA1, and each field displays unique anatomical, molecular, and connectivity patterns [11, 12]. The tri-synaptic circuit conducts synaptic transmission in the hippocampus, and consists of three major excitatory synaptic pathways: perforant path (PP) → DG, mossy fiber (MF) → CA3, and Schaffer collateral (SC) → CA1 [13]. All three hippocampal pathways have been associated with learning and memory [14–16], and disruption of the hippocampal network has been implicated in AD.…”

Section: Introductionmentioning

confidence: 99%

Presenilins regulate synaptic plasticity and mitochondrial calcium homeostasis in the hippocampal mossy fiber pathway

Lee

Lutz

Mossalam

et al. 2017

Mol Neurodegeneration

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BackgroundPresenilins play a major role in the pathogenesis of Alzheimer’s disease, in which the hippocampus is particularly vulnerable. Previous studies of Presenilin function in the synapse, however, focused exclusively on the hippocampal Schaffer collateral (SC) pathway. Whether Presenilins play similar or distinct roles in other hippocampal synapses is unknown.MethodsTo investigate the role of Presenilins at mossy fiber (MF) synapses we performed field and whole-cell electrophysiological recordings and Ca2+ imaging using acute hippocampal slices of postnatal forebrain-restricted Presenilin conditional double knockout (PS cDKO) and control mice at 2 months of age. We also performed quantitative electron microscopy (EM) analysis to determine whether mitochondrial content is affected at presynaptic MF boutons of PS cDKO mice. We further conducted behavioral analysis to assess spatial learning and memory of PS cDKO and control mice at 2 months in the Morris water maze.ResultsWe found that long-term potentiation and short-term plasticity, such as paired-pulse and frequency facilitation, are impaired at MF synapses of PS cDKO mice. Moreover, post-tetanic potentiation (PTP), another form of short-term plasticity, is also impaired at MF synapses of PS cDKO mice. Furthermore, blockade of mitochondrial Ca2+ efflux mimics and occludes the PTP deficits at MF synapses of PS cDKO mice, suggesting that mitochondrial Ca2+ homeostasis is impaired in the absence of PS. Quantitative EM analysis showed normal number and area of mitochondria at presynaptic MF boutons of PS cDKO mice, indicating unchanged mitochondrial content. Ca2+ imaging of dentate gyrus granule neurons further revealed that cytosolic Ca2+ increases induced by tetanic stimulation are reduced in PS cDKO granule neurons in acute hippocampal slices, and that inhibition of mitochondrial Ca2+ release during high frequency stimulation mimics and occludes the Ca2+ defects observed in PS cDKO neurons. Consistent with synaptic plasticity impairment observed at MF and SC synapses in acute PS cDKO hippocampal slices, PS cDKO mice exhibit profound spatial learning and memory deficits in the Morris water maze.ConclusionsOur findings demonstrate the importance of PS in the regulation of synaptic plasticity and mitochondrial Ca2+ homeostasis in the hippocampal MF pathway.

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Non‐Uniform Blood Flow in the Left Ventricular Wall of Dogs Measured by the Xe‐133 Wash‐out Technique

Cited by 34 publications

References 16 publications

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Updating the Lamellar Hypothesis of Hippocampal Organization

Presenilins regulate synaptic plasticity and mitochondrial calcium homeostasis in the hippocampal mossy fiber pathway

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