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Biomedical subjects

M L Rennels

Publications and source records attributed to M L Rennels.

15 recordsLinked to original sources
PubMed1990

Focal cerebral edema impedes convective fluid/tracer movement through paravascular pathways in cat brain.

Cerebral blood vessels are accompanied by longitudinal paravascular fluid pathways that communicate with the subarachnoid space. After infusion into the subarachnoid space, the tracer protein, HRP, distributes throughout the brain with such rapidity as to suggest that the paravascular fluid transport system serves to flush the entire brain parenchyma. However, it was found that the tracer is largely excluded from regions of experimental vasogenic brain edema as well as from remotely situated white matter in the cold-lesioned hemisphere. The results suggest that the persistence and spread of vasogenic edema may be related to an impairment or disruption of the normal paravascular fluid transport system of the brain.

Animals↗
PubMed1990

Rapid solute transport throughout the brain via paravascular fluid pathways.

Solutes in CSF have rapid access to ECS throughout the CNS (within 5-10 min). This occurs by solute/fluid influx through PVS around penetrating arteries, followed by longitudinal spread along the BL of capillaries to reach venules and veins. These paravascular pathways can be demonstrated light-microscopically by infusion of the tracer protein, HRP, into SAS and the subsequent localization of this probe molecule in brain sections using the sensitive histochemical method based on TMB. This unidirectional tracer/fluid movement along the intraparenchymal vascular network, with accompanying spread into the cerebral interstitium, appears to be facilitated by the pulsation of penetrating arterioles within their PVS with each cardiac contraction.

Animals↗
PubMed1977

Spinal cord injury. The role of vascular damage in the pathogenesis of central hemorrhagic necrosis.

We postulated that damage to the endothelial lining of the spinal cord vasculature is a major factor in the pathogenesis of the characteristic lesion of the spinal cord (progressive, central, hemorrhage necrosis) that occurs after acute trauma. Endothelial damage may occur as a result of primary injury to the vessels or after arterial spasm. This damageresults in deposition of platelets and formation of thrombi on the exposed subendothelial tissues and embolization of such thrombi to smaller vessels of the spinal cord parenchyma.

Animals↗
PubMed1977

Ultrastructure of pericytes in mouse heart.

The pericytes of mouse myocardium are extensively branched cells that form an incomplete layer around the endothelium of capillaries and postcapillary venules. The membranes of pericytes and endothelial cells are connected by specialized junctions. Microtubules, intermediate (10-nm) filaments and microfilaments are oriented within circumferentially-arranged cytoplasmic processes of pericytes so as partially to encircle the endothelial cylinder. The intracellular organization of these myocardial pericytes suggests that they are smooth muscle-like cells which may be capable of influencing microvascular dynamics in the heart.

Animals↗
PubMed1977

Innervation of myocardial microcirculation; terminal autonomic axons associated with capillaries and postcapillary venules in mouse heart.

Efferent terminal axons are associated with numerous capillaries and postcapillary venules in both the atria and ventricles of mouse heart. These axons possess ultrastructural characteristics which are typical of peripheral autonomic fibers in other tissues. Many are found near pericytes, in a relationship closely resembling that between terminal axons and smooth muscle cells of larger vessels. To demonstrate adrenergic terminals, mice were pretreated with 5- or 6-hydroxydopamine; examination of these animals' hearts revealed that both adrenergic and cholinergic axons terminate near pericytes and endothelial cells. The results of this study are consistent with the view that there may be a functional innervation of capillaries and postcapillary venules of the mouse heart.

Adrenergic Fibers↗
PubMed1976

Endothelial cell damage by temporary arterial occlusion with surgical clips. Study of the clip site by scanning and transmission electron microscopy.

The effects of temporary vascular occlusion with surgical clips on the underlying endothelial lining were studied with scanning (SEM) and transmission (TEM) electron microscopy. Twenty-five rabbits were anesthetized and both common carotid arteries exposed. A Heifetz clip was used to occlude the right carotid artery for 5, 15, and 30 minutes, and 2 hours in five animals each. The clips were removed and the vessels immediately perfused with glutaraldehyde. In five remaining animals, the right carotid arteries were occluded for 30 minutes followed by removal of the clip and resumption of blood flow for 30 minutes prior to fixation. Combined SEM and TEM examination of the endothelium of compressed segments revealed "craters" and "balloons", blebs and vacuoles, swollen mitochondria, dilated granular endoplasmic reticulum, and subendothelial edema. There were also areas of endothelial cell flattening, discontinuity, and desquamation exposing the subendothelial tissues. Following restoration of flow, platelets and fibrin were found adherent to altered endothelial cells and to exposed subendothelial tissues. Endothelial craters and balloons were also found distal and, significantly less frequently, proximal to the site of occlusion. It is suggested that antiplatelet aggregating agents may prove beneficial for the prevention of thrombus formation at the site of the clip as well as craters and balloons distal to the clip following procedures requiring temporary vascular occlusion.

Animals↗
PubMed1976

Ischemic carotid endothelium. Transmission electron microscopic studies.

The endothelium of monkey and rabbit common carotid arteries subjected to ischemia was examined by transmission electron microscopy (TEM). The right carotid artery of 24 rhesus monkeys was occluded by proximal and distal placement of removable surgical clips for periods ranging from five minutes to four hours. A single clip was used to occlude the right carotid artery of 15 rabbits for periods ranging from 5 to 30 minutes. With TEM, numerous blebs, intracytoplasmic vacuoles, membranous whorls, and pseudopodia were found in the endothelium of arterial segments subjected to ischemia by double or single clipping for as little as five minutes. Following occlusion of one hour or longer, disruption of interendothelial junctions was also noted. These TEM findings were compared with earlier TEM studies of the response of endothelium to other injurious stimuli and with previous scanning electron microscopic studies in which the same ischemic models were utilized.

Animals↗
PubMed1975

Ischemic carotid endothelium. Scanning electron microscopical studies.

The normal luminal surface and the effect of ischemia on the endothelium of the common carotid arteries of rhesus monkeys were examined by scanning electron microscopy. Clamps were placed proximally and distally on the right common carotid arteries, totally occluding the vessels for periods ranging from five minutes to four hours. The clamps were then removed and fixation carried out by intravascular perfusion. The contralateral sham-operated carotids, as well as those from unoperated animals were used as control specimens. The most obvious effect of ischemia was the appearance of conical, crater-like defects in the cytoplasm of endothelial cells. Such "craters" were observed following as little as 15 minutes of ischemia, were much less frequent in sham-operated vessels, and were not seen in the unoperated control specimens.

Animals↗
PubMedDate not supplied

Endothelial cell ischemic injury: protective effect of heparin or aspirin assessed by scanning electron microscopy.

Scanning electron microscopic observations of the luminal surface of the rabbit common carotid artery subjected to occlusion for 30 minutes or two hours revealed crater-like and balloon-like defects in the endothelial surface. The frequency of occurrence of these abnormalities was significantly decreased by pretreatment with heparin or aspirin in doses considered to have antiplatelet aggregating activity.

Animals↗