Complement-unlike hemolytic activity in lobster hemolymph.
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Biomedical subjects
Publications and source records attributed to J L Hall.
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The histology of the specialized region of the carotid bifurcation in man was studied with Orcein stain for elastic tissue, Masson's trichrome for muscle and connective tissue, and Bodian's silver method for neural elements. Four distinct regions exist: the common carotid, which appears to be solely a conduit; the carotid sinus, which is thin and very elastic with its baroreceptors in the medial wall; the external carotid, which is highly muscular and presumably active; and the internal carotid, also highly muscular and presumably active. The transition between zones is abrupt. Prominent clusters of up to 30 or 40 multipolar nerve cells, 15 to 25 microns in diameter, were found in the subintimal region of the internal carotid artery, some in the common, and a few in the external carotid. Occasional rounder cells of similar size with only one process were seen, possibly of sensory type. No cell bodies were seen in the adventitia of any vessel. No relation to the perivascular plexus was established. It is speculated that the neurons may be related to the reported local differential response to environment by the internal and external carotid systems.
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The purpose of this investigation was to assess the effects of ischemia and reperfusion on the transmural levels of glucose and lactate in the interstitium in 11 open-chest swine. Microdialysis probes were used to estimate changes in interstitial metabolities across the ventricular wall. Probes were placed in the subepicardium and the subendocardium of the left anterior descending (LAD) coronary artery perfusion bed and in the midmyocardium of the circumflex (CFX) perfusion bed. The LAD coronary artery was cannulated and perfused with blood from the femoral artery through an extracorporal perfusion circuit. Ischemia was induced in the LAD perfusion bed by reducing the flow of the LAD perfusion pump by 60% for 50 min, and was followed by 30 min of reperfusion. Regional myocardial blood flow was assessed with fluorescent microspheres. Ischemia resulted in a transmural gradient in blood flow, with the most severe reduction in flow occurring in the subendocardium (p < 0.05). We found a significant reduction in interstitial glucose in both the LAD subepicardium (1.26 +/- 0.24 mM) (p = 0.0009) and subendocardium (0.89 +/- 0.21 mM) (p = 0.0001) during ischemia compared to the aerobic (non-ischemic) period (1.97 +/- 0.25 mM, 2.03 +/- 0.29 mM for the subepicardium and subendocardium, respectively). This coincided with a significant reduction in glucose delivery (LAD pump flow * arterial glucose) to the LAD perfusion bed during ischemia (54.5 +/- 8.5 mumol/min) compared to aerobic values (182.1 +/- 25.3 mumol/min) (p < 0.05). Interstitial lactate levels were significantly increased during ischemia in the LAD subendocardium (3.39 +/- 0.46 mM) compared to the aerobic values (1.73 +/- 0.46 mM) (p < 0.0029). A transmural gradient in interstitial lactate levels was observed during ischemia: this gradient was not seen during the aerobic period and was negated upon reperfusion. In conclusion, ischemia resulted in a decrease in interstitial glucose in both the LAD subepicardium and subendocardium, and an increase in interstitial lactate in the LAD subendocardium. Further, a transmural gradient in interstitial lactate levels was observed during ischemia, with the highest lactate values appearing in the subendocardium.
Coronary artery disease causes an increase in glutamate uptake and alanine output by the heart. We assessed the effects of acute myocardial ischemia on alanine and glutamate exchange and ammonia production in 10 anesthetized open-chest domestic swine (46.9 +/- 0.7 kg). Coronary blood flow was controlled through an extracorporal perfusion circuit. After a nonischemic control period (aerobic) the blood flow in the left anterior descending coronary artery was reduced by 60%. Arterial and anterior interventricular venous samples where drawn before and during 35 min of ischemia. Subendocardial blood flow, measured using radiolabeled microspheres, decreased from 1.27 +/- 0.16 to 0.25 +/- 0.09 (ml/g)/min, and left-ventricular wall-thickening fell to 47% of aerobic values. Ischemia resulted in a significant increase in the rate of glucose uptake (p less than 0.05) and a switch to net lactate production (p less than 0.01). Ischemia did not affect the rates of alanine output (-0.9 +/- 1.0 vs. -0.3 +/- 0.3 mumol/min) or glutamate uptake (-0.4 +/- 1.1 vs. 0.3 +/- 0.6 mumol/min), but did increase the venous-arterial difference for ammonia (-4.1 +/- 4.1 to 52.7 +/- 5.5 microM, p less than 0.0001) and the ammonia output (-0.33 +/- 0.24 to 1.34 +/- 0.14 mumol/min, p less than 0.0001). In conclusion, acute ischemia did not stimulate greater alanine output or glutamate uptake. However, acute ischemia did cause an increase in anaerobic glycolysis rate and ammonia output, which reflects a profound disruption in myocardial energy metabolism.
Many of the wound infections that occur after arterial surgery require prolonged attention with frequent changes of dressings. However, the traditional way of reporting wound infections is to only declare the overall incidence of this adverse event. In this study, we have evaluated 302 patients undergoing arterial surgery to determine the relationship between the incidence of wound infection, the length of time that wounds were dressed, and the results of a modified ASEPSIS wound scoring system. The overall incidence of wound infection was 14% (43/302). It was noted that patients with high wound scores had a correspondingly high incidence of conventionally defined wound infections; and, in addition, such patients required dressing changes over prolonged periods. It is concluded that the documentation of both the duration of wound dressings and a wound scoring system are useful tools when evaluating the outcome of patients after arterial surgery.