Glenn T. Suehiro

Intestinal blood flow at various intraluminal pressures in the piglet with closed abdomen.

The influence of intraluminal pressure on intestinal blood flow was studied in two segments of the small intestine and two of large intestine ligated after insertion of intraluminal catheters in ten piglets. Intestinal segments were inflated in stepwise increments in intraluminal pressures of 15, 30, 45 and 60 mmHg and blood flow was measured with radioactive micro-spheres using four isotopes (Ce, Cr, Sr, Sc). Other segments were inflated to a pressure of 60 mmHg and then pressure decreased in a stepwise fashion to 30, then 0 mmHg for the last two injections. Small and large intestinal blood flow fell progressively with increasing intraluminal pressure. At 60 mmHg a forward flow of 25% of normal was still present. Furthermore, not only was there an absolute decrease in blood flow with increasing intraluminal pressure but this decrease was disproportionately large in the intestinal mucosa. A hyperemic response lasting approximately 15 minutes was observed after complete decompression. The intestinal blood flow distal to the ligated segments was always moderately increased as compared to intestinal blood flow proximal to the segments. The results reported herein are at some variance from other reported studies performed with the abdomen open and on isolated segment preparations. The reasons for these variations are discussed.

Platelet trapping in myocardial infarct in baboons: Therapeutic effect of aspirin

Abstract Blood platelet trapping has been demonstrated in the area of evolving myocardial infarction in baboons. Sixteen baboons were subjected to ligation of the diagonal branch of the left anterior descending coronary artery, and the extent of myocardial ischemia was monitored with a 64 to 72 electrode epicardial electrocardiographic grid. Eight animals received no treatment and eight were pretreated twice (at 12 hours and at 2 hours before ligation) with aspirin, 600 mg orally. Measurement of infarct extent included all electrode points with S-T segment elevation of 2 mV or greater. Chromium-51-tagged autologous platelets were injected 15 minutes before ligation. In all animals an area of ischemia developed in which typical changes evolved in S-T segments. In three of the eight aspirin-treated animals, double ligation was carried out. Aspirin was administered after release of the first ligature but before religation, and the area of S-T segment elevation was reduced by as much as 23 percent after aspirin treatment. Platelet trapping outside the area of S-T elevation was seen in 25± 3 percent of the total wall samples in aspirin-treated animals compared with 44 ± 7 percent of those in control animals (p

Failure of nifedipine therapy to reduce myocardial infarct size in the baboon.

The value of nifedipine in reducing the ultimate size of an infarct associated with a period of coronary occlusion followed by reperfusion was assessed. Eight baboons were administered a bolus dose of nifedipine, 5 micrograms/kg intravenously, and then a maintenance dose of 30 micrograms/kg per hour was begun 1 hour before occlusion. This regimen resulted in an 8.5 +/- 1.2 percent (mean +/- standard error) decrease in mean arterial pressure. The left anterior descending coronary artery was occluded for 2 hours and then perfusion restored. At 2 hours after reperfusion the nifedipine infusion was discontinued. Eight control baboons underwent an identical protocol without nifedipine therapy. At 24 hours after occlusion, microvascular dyes were injected into the left anterior descending coronary artery and adjacent arteries to delineate the perfusion bed of the previously occluded artery. The volume of infarction was determined with planimetry and compared with the volume of the perfusion bed of the occluded artery. The area of infarction was always contained within the perfusion bed of the occluded artery. The mean percent of the perfusion bed with infarction was 50.1 +/- 5.8 in the control group and 41.7 +/- 9.5 in the treated group (difference not significant; p greater than 0.05). In both control and treated groups of baboons hemorrhage occurred only within the region of infarction. In both groups electron microscopy revealed large electron-dense granules within the mitochondria. In conclusion nifedipine therapy during a 2 hour period of coronary occlusion followed by reperfusion did not result in any significant reduction in ultimate infarct size in the baboon.

The effects of thoracic aortic cross-clamping and declamping on visceral organ blood flow.

Blood flow was measured using radioactive microspheres in 11 macaque monkeys 1) before hemorrhage shock, 2) after onset of shock, 3) after aortic cross-clamping and resuscitation, and 4) after release of the cross-clamp and stabilization. Hemodynamic parameters (cardiac output, arterial, right atrial and left atrial pressure) and blood gases were also monitored. Total abdominal organ flow fell with hemorrhage and fell further with aortic clamping. Reinfusion of shed volume did not restore abdominal organ flow (4.7% baselines) but increased LAP and cardiac output to the upper body. Release of the cross-clamp produced profound acidosis that was treated effectively with NcHCO3. After stabilization of blood, flow to kidney remained low (49% baseline) although intestinal flow was increased threefold (320% of baseline). It is clear that thoracic aortic cross-clamping in shock further compromises already reduced visceral blood flow and may contribute to the problem of ischemic multiple organ failure after resuscitation from hemorrhagic shock.

Myocardial platelet trapping after coronary ligation in primates (Papio anubis) Platelet trapping in infarct marginal zone

51Cr-Labeled platelets were injected into baboons prior to coronary ligation. Area of ischemia and infarction was determined with an epicardial ECG grid. ST elevation of more than 4 mV was considered as the center of the region of ischemia. Platelets were found to accumulate in significantly higher concentrations at the margins of the infarct in the three animals sacrificed 6 hr after permanent ligation and in the center of the infarct in animals reperfused 3 hr after ligation and 3 hr prior to sacrifice. The data are interpreted as demonstrating platelet trapping in the margins of an evolving infarct which may play a role in infarct evolution. High concentration in the center of infarct in reperfused animals is consistent with the nonreflow phenomenon into the infarcted area.

Comparison of filtering efficiency of four new in-line blood transfusion filters.

Efficient removal of debris from stored human blood prior to transfusion has become increasingly important. The debris, consisting largely of microaggregates of platelets and fibrin, is not effectively removed by passage through a standard transfusion filter. This study evaluated the performance of four of the currently available small pore in-line blood transfusion filters. Filters tested included the Bentley PF-127, the Pall Ultipor SQ-40, the Swank In-Line IL-200 and the Fenwal Microaggregate Blood Filter. A standard blood administration filter was also tested, the McGraw V-2950. The rate of blood flow through the filters was recorded using single and multiple units of blood. The screen filtration pressure and debris weight of the filtered blood were studied to compare effectiveness of filtration. The Swank filter was effective in debris removal and maintained good flow rates. The Bentley and Fenwall filters removed debris nearly as well, but had reduction of flow rates after smaller infusions. The Pall filter maintained high flow rates but did not remove debris as effectively, particularly with pressure infusion. The standard 170 mu pore blood transfusion filter does not remove microaggregates.

Detection of Hydroxyl free Radicals in the Reperfused Primate Heart

Early reperfusion of an ischemic region can result in significant salvage of the area at risk. We show the presence of hydroxyl free radicals at the time of post ischemia reperfusion using electron paramagnetic resonance (EPR) spectroscopy in a macaque model. These free radicals may be formed as a result of reperfusion or may be an un-involved bystander. It is possible that they may be involved in reperfusion injury.

Regional myocardial blood flow in experimental myocardial infarction after pretreatment with aspirin

The effects of aspirin on myocardial blood flow in an area of ischemia were studied in 12 baboons. In each, a diagonal branch of the left anterior descending coronary artery was ligated. Six of the baboons received aspirin (2 X 600 mg orally, 12 hours and 1 hour before ligation); the other six did not receive aspirin and served as a control group. The extent of myocardial ischemia was delineated with an electrode wire grid on the surface of the anterior left ventricular wall. The maximal area circumscribed by electrodes with 2 mV or more ST segment elevation was compared with the area of reduced myocardial blood flow. Myocardial blood flow was measured with the radioactive microspheres method using strontium-85-labeled carbonized spheres. Two areas of reduced myocardial blood flow were noted, one with severely reduced flow in the center of the myocardial infarct (0 to 49% of noninfarcted myocardium) and another with mild to moderately reduced myocardial blood flow at the border of the myocardial infarct (50 to 90% of noninfarcted myocardium). Myocardial blood flow in the border area (margins of ST elevation area) for the total wall was 85 +/- 8% of normal in the aspirin-treated animals and 40 +/- 4% in the control group (p less than 0.01); for the epicardium it was 67 +/- 10% of normal in noninfarcted myocardium after aspirin and 37 +/- 5% for the control group (p less than 0.05); and for the endocardium it was 78 +/- 8% of normal in noninfarcted myocardium after aspirin and 39 +/- 6% in the control group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Maintenance of Viable Segments of Human Artery in Vitro

A system for maintaining viable segments of atherosclerotic human artery in vitro for periods of up to 32 days is described. Viability of the segment has been confirmed from study of lactate metabolism and vessel wall histology. Preliminary lipid studies using TLC on plasma perfusate indicate lipid may be removed from the vessel wall during perfusion.

Oxygen consumption changes with stored blood infusions.

Stored blood contains microaggregates, often implicated in the pathogenesis of post-traumatic pulmonary insufficiency. This study was an attempt to further elucidate the effect of autologous stored, filtered and non-filtered blood infusions and homologous stored and fresh blood infusions on pulmonary function and hemodynamics. Inconsistent changes in pulmonary hemodynamics and blood oxygenation were noted. The one significant finding was an increase in oxygen consumption, which occurred with unfiltered autologous or homologous blood but not with fresh or filtered blood. Since an increased oxygen consumption results in an oxygen demand which is difficult to meet in the face of multiple other injuries, it is conceivable that this observation implicates massive stored blood transfusion as a major contributing factor in the development of so-called irreversible shock.