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Biomedical subjects

E B Griepp

Publications and source records attributed to E B Griepp.

10 recordsLinked to original sources
PubMed1998

Minimizing spinal cord injury during repair of descending thoracic and thoracoabdominal aneurysms: the Mount Sinai approach.

In an effort to reduce the incidence of spinal cord injury following resection of descending thoracic and thoracoabdominal aneurysms, we have developed a multifaceted approach to maximize spinal cord perfusion which involves monitoring spinal cord function using somatosensory evoked potentials (SSEPs) intraoperatively and postoperatively. Intercostal and lumbar intersegmental vessels are sacrificed in a gradual stepwise fashion before the aneurysm is incised: none of these vessels is reattached unless SSEPs are abnormal following temporary occlusion, and this has not yet been observed. Postoperative spinal cord perfusion is maximized by keeping arterial pressure high and by draining cerebrospinal fluid if intrathecal pressure is elevated. Only two cases of permanent paraplegia have developed in 95 patients. Multivariate analysis showed extensive aneurysms (spanning 10 or more intersegmental arteries) and a history of smoking as the only significant risk factors for development of spinal cord injury.

Aortic Aneurysm, Abdominal↗
PubMed1994

Computer-generated 3D representations of the aorta: a new tool in the management of aortic aneurysm patients.

In order to facilitate care of patients with thoracic aortic aneurysms, we have developed a computer program which allows three dimensional (3D) reconstructions of the aorta from serial sections of CT scans. Each completed study, which can be displayed on a single data sheet, provides a 3D drawing of the aorta, the diameter of each aortic slice, the volume of each aortic segment, the total volume and surface area of the aorta, and a quantity we have called the tortuosity index. The method enables appreciation of transverse as well as longitudinal increases in aneurysm size, and eccentricities in aortic pathology can easily be recognized. The data are stored on floppy discs: this allows a second program to provide comparisons of the important findings from multiple and long-term serial CT studies.

Aorta↗
PubMed1994

Hypothermic circulatory arrest and other methods of cerebral protection during operations on the thoracic aorta.

Current surgical techniques in operations on the thoracic aorta frequently require exclusion of the cerebral circulation for varying periods. During these periods, hypothermic circulatory arrest (HCA), selective cerebral perfusion (SCP), and retrograde cerebral perfusion (RCP) can be used for cerebral protection. Hypothermia is the principle component of these methods of protection. The main protective effect of hypothermia is based on reduction of cerebral energy expenditures and largely depends on adequate suppression of cerebral function. It is most effective at deep hypothermic levels (13 degrees C to 15 degrees C). Measures that preserve autoregulation of cerebral blood flow help increase the margin of safety with all methods of protection. There is solid experimental and clinical data indicating the safe limits and outcome following HCA. Current applications of SCP and RCP are fairly recent developments and do not have comparable supporting data. SCP can be used without deep hypothermia and allows prolonged periods of cerebral protection, but is complex in application. RCP is simpler, but always requires deep hypothermia. Present clinical data do not allow separation of its protective effect from that of HCA alone. Recent modifications in the application of HCA include monitoring of cerebral O2 extraction, and selective use of supplemental SCP to limit arrest times to less than 50 minutes, or RCP to prevent embolic strokes, as indicated. These changes appear to have reduced the overall mortality, the severity of embolic strokes, and stroke-related mortality.

Adult↗
PubMed1992

Cerebral consequences of hypothermic circulatory arrest in adults.

Despite widespread use of hypothermic circulatory arrest (HCA) in aneurysm surgery and for repair of congenital heart defects, there is continued concern about possible adverse cerebral sequelae. The search for ways to improve implementation of HCA has inspired retrospective clinical studies to try to identify risk factors for cerebral injury, and clinical and laboratory investigations to explore the physiology of HCA. At present, risk factors associated with less favorable cerebral outcome after HCA include: prolonged duration of HCA (usually greater than 60 min); advanced patient age; rapid cooling (less than 20 min); hyperglycemia either before HCA or during reperfusion; preoperative cyanosis or lack of adequate hemodilution; evidence of increased oxygen extraction before HCA or during reperfusion; and delayed reappearance of electroencephalogram (EEG) or marked EEG abnormality. Strategies advocated to increase safety of HCA include: pretreatment with barbiturates and steroids; use of alpha-stat pH regulation during cooling and rewarming; intraoperative monitoring of EEG; slow and adequate cooling, including packing of the head in ice; monitoring of jugular venous oxygen content; hemodilution; and avoidance of hyperglycemia. Current investigation focuses on delineating the relationship of cerebral blood flow (CBF) to cerebral oxygen consumption and glucose metabolism during cooling, HCA, rewarming, and later recovery, and identifying changes in acute intraoperative parameters, including the presence of intracerebral enzymes in cerebral spinal fluid, with cerebral outcome as assessed by neurological evaluation, quantitative EEG, and postmortem histology. Clinically, intraoperative monitoring of EEG and measurement of CBF by tracer washout or Doppler flows are contributing to better understanding of the physiology of HCA, and in the laboratory, nuclear magnetic resonance (NMR) spectroscopy has provided valuable insights into the kinetics of intracerebral energy metabolism. Promising strategies for the future include investigation of other pharmacological agents to increase cerebral protection, and use of "cerebroplegia" or intermittent perfusion between intervals of HCA to improve cerebral tolerance for longer durations of HCA.

Animals↗
PubMed1983

Participation of plasma membrane proteins in the formation of tight junctions by cultured epithelial cells.

Measurements of the transepithelial electrical resistance correlated with freeze-fracture observations have been used to study the process of tight junction formation under various experimental conditions in monolayers of the canine kidney epithelial cell line MDCK. Cells derived from previously confluent cultures and plated immediately after trypsin- EDTA dissociation develop a resistance that reaches its maximum value of several hundred ohms-cm(2) after approximately 24 h and falls to a steady-state value of 80-150 ohms- cm(2) by 48 h. The rise in resistance and the development of tight junctions can be completely and reversibly prevented by the addition of 10 mug/ml cycloheximide at the time of plating, but not when this inhibitor is added more than 10 h after planting. Thus tight junction formation consists of separable synthetic and assembly phases. These two phases can also be dissociated and the requirement for protein synthesis after plating eliminated if, following trypsinization, the cells are maintained in spinner culture for 24 h before plating. The requirement for protein synthesis is restored, however, if cells maintained in spinner culture are treated with trypsin before plating. Actinomycin D prevents development of resistance only in monolayers formed from cells derived from sparse rather than confluent cultures, but new mRNA synthesis is not required if cells obtained from sparse cultures are maintained for 24 h in spinner culture before plating. Once a steady-state resistance has been reached, its maintenance does not require either mRNA or protein synthesis; in fact, inhibition of protein synthesis causes a rise in the resistance over a 30-h period. Following treatments that disrupt the junctions in steady- state monolayers recovery of resistance also does not require protein synthesis. These observations suggest that proteins are involved in tight junction formation. Such proteins, which do not turn over rapidly under steady-state conditions, are destroyed by trypsinization and can be resynthesized in the absence of stable cell-cell or cell-substratum contact. Messenger RNA coding for proteins involved in tight junction formation is stable except when cells are sparsely plated, and can also be synthesized without intercellular contacts or cell-substratum attachment.

Animals↗
PubMed1978

Acquisition of synchronous beating between embryonic heart cell aggregates and layers.

Synchronous beating between chick embryonic heart cell aggregates and heart cell layers was used to study the relationship between intercellular adhesion and ionic coupling. Adhesion was measured by counting the proportion of aggregates which were not to be removed from cell layers by gentle washing after a 30 min incubation. Synchrony between bound aggregates and contiguous layers was assessed by phase microscopy. The first evidence of synchrony was seen 1.5 h after addition of aggregates to layers, following which there was an increase in the percentage of aggregates beating synchronously, reaching over 50% at 7 h and slowly increasing to a maximum of 65% by 24 h. Scanning electron microscopy and autoradiography of thymidine-labeled cells suggest that synchrony does not depend on cell movement at the interface between aggregate and layer. Acquisition of synchrony can be prevented completely by inhibiting protein synthesis, although pulsation of aggregates and layers continues in proportions unchanged from controls. After reversal of protein synthesis inhibition, synchrony is acquired at a rate and to an extent closely resembling that of newly adherent controls. These data indicate that ionic coupling is neither an inevitable nor an immediate consequence of adhesion. Since ionic coupling has been shown to correlate with the presence of gap junctions, the findings suggest that gap junctions are not involved in the initial events responsible for intercellular adhesion in vitro and that their formation following adhesion in this system may depend upon protein synthesis.

Animals↗
PubMed1978

Morphological and functional correlates of synchronous beating between embryonic heart cell aggregates and layers.

We have examined correlations between morphological and functional evidence of cell coupling between aggregates of beating embryonic heart cells and underlying layers. Synchronously beating aggregate-layer pairs were compared with asynchronous pairs. Intracellular microelectrode studies demonstrated that asynchronously beating aggregate-layers could not be induced to beat synchronously by electrical stimulation of the aggregate, whereas 86% of synchronous instances showed propagation of stimulating current pulses from aggregate to layer. By freeze fracture we have found significant differences both in the number and in the total area of gap junctions between the aggregate-layer interfaces of synchronous and asynchronous preparations. The data suggest that synchronous beating is a reliable functional indication of effective ionic coupling, and requires a certain area and number of gap junction/cell.

Action Potentials↗
PubMedDate not supplied

Use of hypothermic circulatory arrest for cerebral protection during aortic surgery.

Optimal use of hypothermic circulatory arrest during aortic surgery requires understanding of its physiology. Research in laboratory animals and clinical observations have now documented that considerable residual cerebral metabolism remains with cooling to levels of 15-18 degrees C, especially if cooling intervals are short, reflected by persistent jugular venous desaturation. Cooling should be continued to below 15 degrees C if the duration of HCA is expected to exceed 20 minutes, and continued until jugular venous saturations exceed 95%. There is considerable laboratory evidence that even short durations of HCA are followed by a prolonged interval of increased cerebral vascular resistance during which cerebral metabolism is maintained at normal levels by markedly increased oxygen extraction. Clinical observations have now confirmed that considerable jugular venous desaturation is present in patients following HCA: it is more pronounced with prolonged HCA, and is still present as late as six hours after the start of rewarming. This reinforces the concept of a prolonged postoperative vulnerable interval following HCA, during which any compromise in oxygen delivery has the potential for producing cerebral injury. Several adjunctive measures have been shown to improve outcome following HCA. The simplest and most important is topical hypothermia: packing the head in ice during the interval of HCA. Retrograde cerebral perfusion (RCP) has also been shown to improve EEG recovery as well as histological and behavioral outcome in laboratory animals following prolonged HCA, but some of its effect may be secondary to its efficacy in keeping the brain cold, since RCP provides very low rates of flow and supports metabolism at a much lower level than antegrade perfusion at the same temperature. But despite the clear superiority of antegrade perfusion, and the documentation of some benefits of RCP in laboratory measures of cerebral protection, clinical results using RCP and ACP have not yet demonstrated the superiority of these methods over use of HCA alone, perhaps because these modalities are usually employed in patients with unusually high risk of neurological injury: those with dissection or with clot or atheroma in the aorta. Nevertheless, recent years have seen considerable reduction in mortality following aortic surgery, especially in older patients, and a trend toward a lower incidence of permanent neurologic dysfunction. The presence of preoperative rupture or hemodynamic compromise, and of clot or atheroma in the aorta, remain the most significant risk factors both for death and occurrence of stroke.

Animals↗