Anthony 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

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.

Effects of perfluorocarbon exchange transfusion on reducing myocardial infarct size in a primate model of ischemia-reperfusion injury: a prospective, randomized study.

BACKGROUND This study was undertaken to test the hypothesis that perfluorocarbons were able to reduce myocardial infarct size in a baboon model of ischemia-reperfusion injury. Exchange transfusion of perfluorocarbons has been shown to reduce myocardial infarct size in the dog, who, unlike the baboon, has an extensive collateral circulation. METHODS After 15 minutes of occlusion of the left anterior descending coronary artery, 14 baboons were bled to attain a hematocrit of 24% to 26% and were simultaneously transfused, six with Fluosol-DA 20% emulsion and eight with FC-43 emulsion. After 2 hours of ligation, the coronary arteries were reperfused. Baboons were killed 24 hours after ligation, and the hearts were excised. Microvascular dye was infused into the coronary artery to delineate its perfusion bed. Ratios of the mean volume of infarct to the mean volume of perfusion bed were calculated and compared by use of planimetry. A similar protocol was followed in two other groups of baboons except that lactated Ringers solution was infused into six of them, whereas eight had no exchange transfusions. RESULTS The ratios of the mean volume of infarct to the mean volume of perfusion bed of the four groups were as follows: Fluosol-DA, 38.1% +/- 7.5%; FC-43, 37.7% +/- 8.3%; lactated Ringers, 46.9% +/- 10.5%; controls, 65.6% +/- 6.9%. Statistical significance was reached when comparing both perfluorocarbon-treated groups with the controls (p < 0.05 for both groups) but not significant when comparing them with the Ringers lactate-treated group. CONCLUSIONS Results suggest that the beneficial effects of exchange transfusion with the perfluorocarbons may be primarily due to hemodilution.

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)

Does intravenous glutamine prevent bacterial translocation in hemorrhagic shock

Bacterial translocation across the gut wall may be associated with insult to the latter. In this situation, intestinal flora can enter the blood stream and lymph nodes and be transported to other organs. Glutamine is a nonessential amino acid not presently included in total parenteral nutrition (TPN) preparations. The use of glutamine-enriched TPN in the rat has resulted in a significant reduction in bacterial translocation. This study attempted to evaluate the role of glutamine in preventing bacterial translocation following hemorrhagic shock in a rat model. Forty Sprague-Dawley rats were equally divided into two groups. The controls were given TPN solution, while the treated group had glutamine instead of the standard alanine present in TPN. Hemorrhagic shock was induced in both groups and blood cultures were performed. Glutamine-treated rats did not show a significant difference in survival suggesting that it is of no particular value in severe hemorrhagic shock in rats.

Mechanisms of shock blood induced tissue anoxia

An isolated limb perfusion system in pigs was used to assess and relate hemodynamic variables to oxygen consumption in shock. Perfusion with shock blood results in a significantly increased peripheral vascular resistance, which can be blocked by phentolamine. However, a significantly reduced oxygen consumption seen during perfuslion with shock blood is not eliminated with phentolamine despite normal peripheral vascular resistance. The cause of the reduced oxygen consumption is not known, but the results suggest that other factors apart from a decreased blood flow due to catecholamine release are important in contributing to end organ anoxia and failure in shock.

230 MEASUREMENT OF OXYGEN FREE RADICALS (OFR) IN A RABBIT SHOCK LUNG INJURY MODEL: EFFECT OF SUPEROXIDE DISMUTASE (SOD) AND VITAMIN A

Lung injury by oleic acid (OA) or phorbol myristate acetate (20ng/ml) plus polymorphonuclear cells (PMA-PMN) in an ex vivo rabbit shock lung model has been suggested to be caused by OFR production. Using a standard heart/lung preparation with New Zealand rabbits (2.4-4.5 Kg), baseline mean pulmonary artery pressure (PAP) was maintained at 15mmHg and mean airway pressure (MAP) at 10mmHg. Experimental perfusates were infused over 30 minutes followed by Krebs solution. Dimethyl pyroline oxide (DMPO, infused over 30 min) captured OFR which were measured by electron spin resonance. Lung injury was assessed by light and scanning electron microscopy, and lung weight.A five-fold increase in MAP and PAP occurred with both OA and PMA-PMN (p less than 0.003). SOD (20,000 U/kg), but not Vit.A (2,000 IU), prevented lung injury and the increase in OFR with PMA-PMN.We conclude that 1) the mechanism of PMA-PMN lung injury is via OFR because SOD prevents both the rise in OFR and lung injury; 2) Vit.A does not prevent lung injury; 3) OA does not produce injury by increase in OFR but by other unknown mechanisms. We speculate that lung damage by OA and PMA-PMN models have different mechanisms.