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Biomedical subjects

G T Shires

Publications and source records attributed to G T Shires.

At least 73 records · Page 4Linked to original sources

Hepatocellular membrane function during chronic burn injury.

Hepatocellular membrane dysfunction, as indicated by depolarization of the membrane potential, occurs after acute injury and early bacteremia. To determine whether hepatocellular membrane dysfunction occurs in the setting of ongoing thermal injury and infection, Wistar rats were divided into four groups: (1) sham-burned, freely fed controls (FF); (2) rats sustaining approximately 30% total body surface area dorsal full-thickness scald burn (Burn); (3) rats sustaining burns as in group 2 followed by immediate inoculation of 1 x 10(8) CFU Pseudomonas aeruginosa (Burn/Inf); and (4) sham-burned rats pair-fed to the food intake of the Burn/Inf group (PF). On the third and seventh days postburn, body and liver weights were determined. In vivo hepatocellular transmembrane potentials were measured and hepatic ATP, RNA, DNA, and protein contents were assayed. By Day 7, despite greater weight loss in the Burn/Inf group than due to starvation alone (P less than 0.01 Burn/Inf vs FF and PF), hepatic mass was conserved. This was associated with hyperpolarization of the hepatic transmembrane potential (-46.6 +/- 1.5 vs -32.1 +/- 0.6 mV, Burn/Inf vs FF, P less than 0.01) and increases in RNA (141 +/- 9 vs 91 +/- 4 mg/liver, Burn/Inf vs FF, P less than 0.01) and DNA (37 +/- 5 vs 22 +/- 2 mg/liver, Burn/Inf vs FF, P less than 0.05) contents, with no change in ATP or hepatic protein contents. There was a significant hypercorticosteronemia observed in the Burn/Inf group (43 +/- 9 vs 2.8 +/- 0.7 micrograms/dl, Burn/Inf vs FF, P less than 0.01). This hepatic membrane hyperpolarization and augmented RNA content were not secondary to burn or starvation alone as the response in these groups was significantly less than that of the Burn/Inf group. It is suggested that this hepatic membrane hyperpolarization is one mechanism by which hepatic function is maintained during ongoing burn infection in the rat.

Adenosine Triphosphate↗

The post-operative electrocardiogram and creatine kinase: implications for diagnosis of myocardial infarction after non-cardiac surgery.

The objective of this study was to evaluate different approaches to the diagnosis of post-operative myocardial infarction. A total of 232 patients, mostly hypertensive and/or diabetic patients, who were undergoing elective non-cardiac surgery were evaluated pre-operatively. They were followed serially from the day of operation to discharge or the sixth post-operative day with daily clinical evaluations, electrocardiograms, creatine kinase and creatine kinase isoenzymes. In total 22% (51/232) of the patients had post-operative ECG changes in two or more leads. Only 1% developed new Q waves; most of the changes involved changes in the T or ST segments. Seventy percent of patients who had changes in their electrocardiogram were completely asymptomatic. The highest risk of ECG changes or symptoms occurred on the day of operation and the first post-operative day; evidence of post-operative infarction was infrequent after the second post-operative day. Creatine kinase levels rose an average of 250-300 IU on the first and second post-operative day (also the peak time for post-operative ECG changes), reducing its utility as an adjunct to the diagnosis of post-operative infarctions. Importantly, 52% (12/23) of the patients who had greater than or equal to 5% MB isoenzyme had neither ECG changes nor symptoms; the diagnosis of a myocardial infarction should not be made in these patients. In summary, most patients who experience ischemia or infarction post-operatively are asymptomatic. Symptoms should not be required for the diagnosis of post-operative infarction. Seemingly minor differences in criteria can produce major discrepancies in post-operative myocardial infarction rates (from 1 to 9%). The development of a final set of criteria will require further study but the diagnosis of post-operative infarction should probably be based on ECG changes, their duration and consistency, and the association of a positive MB fraction.

Aged↗

Evaluation and management of massive lower gastrointestinal hemorrhage.

Sixty-eight patients with massive lower gastrointestinal (G.I.) hemorrhage underwent emergency arteriography. Patients were transfused an average of six units of packed red blood cells within 24 hours of admission. The bleeding source was localized arteriographically in 27 (40%), with a sensitivity of 65% among patients requiring emergency resection. However, twelve of the 41 patients with a negative arteriogram still required emergency intestinal resection for continued hemorrhage. Radionuclide bleeding scans had a sensitivity of 86%. The right colon was the most common site of bleeding (35%). Diverticulosis and arteriovenous malformation were the most common etiologies. Selective intra-arterial infusion of vasopressin and embolization were successful in 36% of cases in which they were employed and contributed to fatality in two patients. Twenty-three patients underwent segmental resection, whereas seven patients required subtotal colectomy for multiple bleeding sites or negative studies in the face continued hemorrhage. Intraoperative infusion of methylene blue via angiographic catheters allowed successful localization and resection of bleeding small bowel segments in three patients. Overall mortality was 21%. The mortality for patients without a malignancy, with a positive preoperative arteriogram, and emergency segmental resection was 13%.

Aged↗

Postoperative changes in serum creatinine. When do they occur and how much is important?

The objective of this study was to evaluate the use of the serum creatinine in following postoperative renal function. In this prospective study of 278 patients (mainly hypertensives and diabetics) undergoing noncardiac surgery, the serum creatinines were followed from the first through the sixth postoperative day. Creatinine clearances were evaluated before operation and on the fourth to fifth postoperative day. During the first six days after the operation, 23% (65 of 278 patients) had an increase of serum creatinine greater than or equal to 20%. Such increases were sustained for greater than or equal to 48 hours in 12% of the patients (32 of 278), and half of these patients had not returned to their initial level of renal function by the time of discharge. Patients who sustained such a deterioration were at risk for nonoliguric renal failure if they had a subsequent insult (i.e., hypotension, reoperation, angiography, aminoglycosides). Such increases occurred early in the postoperative period--on the first or second postoperative day. As judged by the creatinine clearances, postoperative increases of greater than or equal to 20% in the serum creatinine identified most patients whose clearance fell more than 50%, although the serum creatinine did not accurately reflect changes in creatinine clearance among those patients who had undergone an amputation. It is concluded that the serum creatinine is useful in monitoring postoperative renal function. Of those patients who had postoperative increases in serum creatinine sustained for greater than or equal to 48 hours, as many as one third had evidence of impairment in renal function at the time of discharge.

Acute Kidney Injury↗

Total parenteral nutrition and bowel rest modify the metabolic response to endotoxin in humans.

Intestinal mucosal atrophy, as induced by total parenteral nutrition (TPN) and/or prolonged bowel rest, is hypothesized to enhance bowel endotoxin (LPS) translocation and may alter host responses to infection. To examine the effect of TPN-induced bowel atrophy on the response to LPS, 12 healthy volunteers were randomized to receive either enteral feedings (ENT, n = 6) or seven days of TPN without oral intake (TPN, n = 6). Enteral or TPN feedings were terminated 12 hours before the study period when a constant dextrose infusion (50 mg/kg/hour) was initiated and continued throughout the subsequent study period. After placement of arterial, hepatic vein, and femoral vein catheters, metabolic parameters were determined before and for six hours after an intravenous E. coli LPS challenge (20 U/kg). Subsequent peak levels of arterial glucagon (ENT, 189 +/- 39 pg/mL; TPN, 428 +/- 48; p less than 0.01), arterial epinephrine (ENT, 236 +/- 52 pg/mL; TPN, 379 +/- 49; p less than 0.05) and hepatic venous cachectin/tumor necrosis factor (cachectin/TNF) (ENT, 250 +/- 56 pg/mL; TPN, 479 +/- 136; p less than 0.05) were significantly higher in the TPN group than in the ENT group. The extremity efflux of lactate (ENT, -16 +/- 4 micrograms/min-100cc tissue; TPN, -52 +/- 13; t = 2 hours; p less than 0.05) and of amino acids (ENT, -334 +/- 77 nmol/min-100cc tissue; TPN, -884 +/- 58; t = 4 hours; p less than 0.05) were higher in the TPN subjects after the endotoxin challenge. Circulating C-reactive Protein (CRP) levels measured 24 hours postendotoxin were also significantly higher in the TPN subjects (ENT, 1.7 +/- 0.2 mg/dL; TPN, 3.2 +/- 0.3; p less than 0.01). Hence the counter-regulatory hormone and splanchnic cytokine responses to LPS were enhanced after TPN and bowel rest. This is associated with a magnified acute-phase response, peripheral amino acid mobilization, and peripheral lactate production. Thus antecedent TPN may influence the metabolic alterations seen in infection and sepsis via both an exaggerated counter-regulatory hormone response as well as an enhanced systemic and splanchnic production of cytokines.

Adult↗

The preoperative and intraoperative hemodynamic predictors of postoperative myocardial infarction or ischemia in patients undergoing noncardiac surgery.

Among hypertensive and diabetic patients undergoing elective noncardiac surgery, preoperative status and intraoperative changes in mean arterial pressure (MAP) were evaluated as predictors of postoperative ischemic complications. Of 254 patients evaluated before operation and monitored during operation, 30 (12%) had postoperative cardiac death, ischemia, or infarction. Twenty-four per cent of patients with a previous myocardial infarction or cardiomegaly had an ischemic postoperative cardiac complication. Only 7% of those without either of these conditions sustained an ischemic complication. No other preoperative characteristics, including the presence of angina, predicted ischemic cardiac risk. Nineteen per cent of patients who had 20 mm Hg or more intraoperative decreases in MAP lasting 60 minutes or more had ischemic cardiac complications. Patients who had more than 20 mm Hg decreases in MAP lasting 5 to 59 minutes and more than 20 mm Hg increases lasting 15 minutes or more also had increased complications (p less than 0.03). Changes in pulse were not independent predictors of complications and the use of the rate-pressure product did not improve prediction based on MAP alone. In conclusion patients with a previous infarction or radiographic cardiomegaly are at high risk for postoperative ischemic complications. Prolonged intraoperative increases or decreases of 20 mm or more in MAP also resulted in a significant increase in these potentially life-threatening surgical complications.

Adult↗

Occult diaphragmatic injury from stab wounds to the lower chest and abdomen.

Ninety-five patients with stab wounds to the lower chest and abdomen underwent routine abdominal exploration. Eighteen of these patients had diaphragmatic injury and in five patients it was the only injury found. Isolated diaphragmatic injury in asymptomatic patients cannot be reliably delineated by either serial physical examination or peritoneal lavage. Delayed recognition of incarcerated diaphragmatic hernia after stab wounds to the lower left chest and upper abdomen has an associated mortality rate of 36%. The anatomic area of concern can be defined as stab wounds that penetrate the left side of the chest below the fourth intercostal space anteriorly, the sixth intercostal space laterally, and the tip of the scapula posteriorly. Exploratory laparotomy is necessary in these patients until a reliable nonoperative method is established that can exclude injuries to the diaphragm.

Abdominal Injuries↗

Smoke inhalation injury: evaluation of radiographic manifestations and pulmonary dysfunction.

Inhalation injury is a frequent complication in burned patients. Upper airway injury is reliably diagnosed endoscopically, but early diagnosis of pulmonary parenchymal injury is less reliable. Radiographic diagnosis in such cases is inconsistent. This study correlated degree of chest X-ray (CXR) change with pulmonary function in 29 adult patients during the first 5 days after inhalation injury. Daily CXRs were graded: 0 (normal), 1+ (peribronchial cuffing or perivascular edema), 2+ (edema involving one third of the lung field), 3+ (edema involving two thirds of the lung field), and 4+ (edema involving the entire lung field). Extravascular lung water volume (EVLW) was measured in vivo with the thermal/green dye double indicator technique. Twenty-five of the 29 patients were intubated on admission. Of these patients with serious inhalation injury, 84% showed some abnormality on CXR within 48 hours after injury. When abnormalities were present on CXR, pulmonary dysfunction (increases EVLW, increases Qs/Qt, decreases compliance) was clinically important. These data suggest that this grading scale may have utility in reports of CXR findings in inhalation injury.

Adult↗

Adrenergic mechanisms contribute to alterations in regional perfusion during normotensive E. coli bacteremia.

The complex role of adrenergic mechanisms in the pathogenesis of sepsis and shock remains incompletely understood. Recent reports have suggested that adrenergic mechanisms may play an important modulatory role in arachidonate metabolism during early sepsis, specifically in the synthesis of the vasoactive metabolites thromboxane A2 and prostacyclin. The purpose of the present set of experiments was to evaluate the extent to which adrenergic mechanisms contribute to early alterations in regional perfusion during Gram-negative bacteremia, using the mixed alpha adrenergic receptor antagonist phenoxybenzamine hydrochloride. Male Sprague-Dawley rats received a 3-hour continuous intraarterial infusion of either saline (n = 7) or 6.6 +/- 0.4 x 10(8) live E. coli colony forming units (n = 7), after which regional perfusion was determined using 51Cr-labelled microspheres (16.5 +/- 0.1 micron). Significant reductions (p less than 0.05) in blood flows to the renal, gastric, cecal, pancreatic, and splenic beds, as well as a reduction (p less than 0.05) in the calculated portal venous flow, were observed in the bacteremic group while mean arterial blood pressure remained unchanged. Further experiments conducted in 14 rats with preexisting alpha adrenergic receptor blockade revealed relative preservation of renal, gastric, cecal, and portal venous blood flows during bacteremia. These data identify alterations in regional perfusion during early E. coli bacteremia occurring before changes in systemic arterial blood pressure, and indicate that adrenergic mechanisms participate in the modulation of such.

Animals↗

Burn unit treatment of acute, severe exfoliating disorders.

In this chapter, we review the experience gained in the burn unit treatment of two of the severe exfoliating disorders, toxic epidermal necrolysis (TEN) and the Stevens-Johnson syndrome (SJS). Septic mortality was higher if high doses of corticosteroids were given versus the current protocol, which avoids these drugs. Current controversies include the role of topical therapy, leukopenia, and invasive catheters in septic complications as well as nutritional requirements. Concomitant viral infection and the macrophage may each play a role in the etiology of TEN and SJS.

Acute Disease↗

An in vivo examination of rat brain during sepsis with 31P-NMR spectroscopy.

Neurological symptoms including lethargy, obtundation, and confusion are early and common findings in patients with sepsis. The etiology of the mental status changes that occur during severe infection is not known. We investigated the effects of sepsis on the levels of high-energy phosphates to determine whether decreased energy metabolism was a factor in the depressed neurological state. The time course of changes in brain pH and brain high-energy phosphate metabolites during an Escherichia coli infusion was determined from sequential phosphorus-31 nuclear magnetic resonance (31P-NMR) spectra of ketamine-xylazine-anesthetized rats. A second group of rats received 0.9% saline infusion and served as a control group. Despite severe obtundation and near loss of righting reflex, the rats in the septic group had no significant differences in the brain pH, the ratio of phosphocreatine (PCr) to beta-adenosine 5'-triphosphate (beta-ATP), or in the ratio of PCr to Pi. The only significant decrease in brain high-energy phosphates or pH occurred terminally in the septic rat group and corresponded with a rapidly falling arterial blood pressure. We conclude that the severe neurological depression that is characteristic of sepsis is not due to decreased levels of brain high-energy phosphates or brain acidosis.

Adenosine Triphosphate↗

Role of leukocytes in reperfusion injury of skeletal muscle after partial ischemia.

These experiments evaluated the leukocyte as a potential source of oxygen free radical (OFR) generation during reperfusion injury in post-ischemic skeletal muscle. The infrarenal aorta of heparinized Sprague-Dawley rats was clamped for 90 min, declamped, and reperfused for 60 min. Hindlimb muscle resting transmembrane potential difference (Em) and high-energy phosphate content were determined at base line, during ischemia, and on reperfusion. Four groups were studied: a control group, a second group receiving superoxide dismutase and catalase (SOD + CAT) on declamping, a third group receiving dimethylmyleran (DMM) 7 days before the experiment to obtain a selective leukopenia (white blood cells = 1,210 +/- 144/mm3, neutrophils = 1.2%), and a fourth group pretreated with allopurinol (ALLO). During the ischemic period, resting Em was significantly depolarized (-78.6 +/- 0.5 mV from -90.3 +/- 0.3; P less than 0.05) in the control group, whereas creatine phosphate (CP) was depleted and ATP maintained. Data collected during the ischemic phase of the three other groups were similar to the control group (P = NS). On reperfusion, persistent depolarization of resting Em was observed despite restoration of muscle CP content in the control and ALLO groups (-75.4 and -77.0 mV, respectively). In contrast, significant repolarization of resting Em was noted after reperfusion in the SOD + CAT and DMM groups (-86.5 and -88.6 mV, respectively). These data implicate leukocyte-generated OFR as mediators of reperfusion-associated cellular membrane injury in postischemic skeletal muscle.

Adenosine Triphosphate↗

Important factors in the maintenance of homeostasis in the surgical patient.

Three factors that influence homeostasis are discussed: fluids and electrolytes, energy and nutrition, and immune response mediators. Cell injury induces changes in the sodium-potassium pump that disrupt fluid and electrolyte homeostasis, and surgery causes changes in functional extracellular fluid. Caloric requirements increase in proportion to the severity of the injury, and are generally greater than expected. Both parenteral and enteric feeding restore alanine and glutamine levels toward normal. Studies suggest that some of the adverse effects of surgery on homeostasis may be alleviated by specific treatments. A major key in modulating the stress response to surgery may lie in controlling immune response mediators, in particular cachectin, which has been shown to cause effects identical to those of septic shock. Recent studies have indicated that injections of small doses of specific monoclonal antibody to cachectin can avert all of the mediator's adverse effects.

Energy Intake↗

Postoperative renal dysfunction can be predicted.

The two prior hypotheses of the study were that, among a high risk population of patients who were hypertensive, who had diabetes and who underwent elective general surgical treatment, the duration of intraoperative hypotension and hypertension (greater than 20 millimeters of mercury above or below the preoperative base line) and intraoperative administration of less than 300 milliliters per hour of saline solution containing fluids would identify patients at higher risk for postoperative renal dysfunction. Among those who had an intraoperative mean arterial pressure (MAP) that fell more than 20 millimeters of mercury below the base line, 15 per cent of those with fall of MAP lasting for greater than or equal to 60 minutes had postoperative renal dysfunction, whereas those with drops in pressure lasting for less than 60 minutes did not sustain increased postoperative renal dysfunction. Patients who had intraoperative MAP rise to greater than 20 millimeters of mercury above the preoperative base line value for greater than 30 minutes also had twice the rate of postoperative renal dysfunction. Fifteen per cent of the patients who received less than 300 milliliters per hour of isotonic saline-like fluids had postoperative renal dysfunction, significantly more than the 8 per cent of those who received greater than or equal to 300 milliliters per hour. Two intraoperative events also significantly increased postoperative renal dysfunction rates: cardiac arrest and the drainage of massive ascites. Patients with decompensated congestive heart failure at admission to the hospital had significantly increased postoperative renal dysfunction; these patients and probably should not undergo an operation unless it is an emergency. All of the patients, regardless of the magnitude of the operation and of its projected length or type of anesthesia, should be given greater than 300 milliliters per hour of isotonic saline-like solutions.

Aged↗

Tumor necrosis factor-enhanced leukotriene B4 generation and chemotaxis in human neutrophils.

In an in vivo study of five normal volunteers infused with endotoxin (20 U/kg of US reference endotoxin lot EC-5), increased neutrophil (PMN) generation of leukotriene B4 and chemotaxis to leukotriene B4 were found concomitantly with elevated plasma tumor necrosis factor (TNF) levels. To clarify the role of TNF in PMN activation, neutrophil responsiveness after in vitro treatment with TNF was examined. Neutrophils from seven normal subjects were incubated with TNF for 30 minutes and tested for chemotaxis to leukotriene B4, formyl-methionyl-leucyl-phenylalanine and zymosan-activated serum, or the calcium ionophore A23187 to assess leukotriene B4 generation. A range of 10(-13) to 10(-9) mol/L of TNF was used for these assays. When 10(-9) mol/L of TNF was used, the amount of leukotriene B4 that was produced was significantly greater than in control cells. The effect of TNF on PMN chemotaxis was uniformly inhibitory for the three stimuli at 10(-10) mol/L compared with untreated cells. At a picomolar range, PMN migration to leukotriene B4, but not to zymosan-activated serum or formyl-methionyl-leucyl-phenylalanine, was significantly increased over that of PMNs not exposed to TNF. This suggests that TNF has a specific facilitatory effect on PMN responsiveness for both leukotriene B4 production and chemotaxis to leukotriene B4 and may be the same signal for this phenomenon in endotoxemic patients.

Calcimycin↗

Granulocyte contamination of Ficoll-Hypaque preparations of mononuclear cells following thermal injury may lead to substantial overestimation of lymphocyte recovery.

During ongoing flow cytometric studies of burned patient blood leukocytes, it was noted frequently that large numbers of granulocytes were present along with the mononuclear cells at the plasma/Ficoll-Hypaque (F-H) interface following centrifugation over F-H. Since differential WBC counts are not routinely performed on F-H interface cells, it is possible that many previous immunologic studies of burned patients have greatly overestimated numbers of lymphocytes recovered. The present study sought to quantify the extent to which granulocyte contamination of F-H separated cells occurs following burn injury. Blood from 15 thermally injured patients (7-55% total body surface area burn) was studied serially at 24 hr, 48 hr, and weekly thereafter through 6 weeks postburn (PB). Controls were age-matched normals (No. of control bloods = 59). Three-part differential cell counts (lymphocytes, monocytes, and granulocytes) were performed on both F-H interface cells and RBC-lysed whole blood. Counts were performed by light scatter analysis on a flow cytometer. Except at 48 hr, at every time studied through 4 weeks PB, there was significant contamination of F-H interface cells with granulocytes. At 24 hr PB, 41 +/- 9% of the interface cells were granulocytes while at 4 weeks, PB 24 +/- 8% of the interface cells were granulocytes. The data did not support the interpretation that this increase in F-H interface granulocytes was simply reflective of the granulocytosis commonly observed after burn. Thus artificial generation of granulocytosis by addition of extra normal leukocytes to normal blood resulted in complete separation of granulocytes from mononuclear cells following centrifugation over F-H.(ABSTRACT TRUNCATED AT 250 WORDS)

Burns↗

Differential neutrophil activation before and after endotoxin infusion in enterally versus parenterally fed volunteers.

This study was done to determine whether or not increased susceptibility to infection seen in enterally versus parenterally fed patients was caused by altered neutrophil (PMN) responsiveness. To determine the differential effects of route of feeding on human PMN activation, plasma C3a levels, circulating PMN counts, PMN migration to leukotriene B4 (LTB4), the peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and zymosan activated serum (ZAS) and generation of LTB4 were assayed before and after and infusion of endotoxin. Nine normal volunteers were enterally (n=4) or parenterally (n=5) fed a diet sufficient to maintain body weight for seven days prior to a standard challenge of endotoxin. Samples were taken prior to the infusion and hourly thereafter for six hours. Prior to the injection of endotoxin, significant differences were seen in the two feeding groups. Plasma C3a levels, absolute circulating PMN counts and chemotaxis to LTB4 were all significantly (p less than 0.02) elevated in the enterally fed group. Generation of LTB4 was higher in the intravenously fed group at base line than the orally fed group (p less than 0.05). Plasma C3a levels rose in the enterally fed group, but not in the intravenously fed group, at two hours after infusion. Neutrophil counts rose in both feeding groups after endotoxin infusion; but the change in percentage was greater in the enterally fed group than in the intravenously fed group. Chemotaxis to FMLP and ZAS was not different during the study and did not differ between the two feeding can have significant impact on neutrophil function and that parenteral nutrition may impair host responsiveness.

Chemotaxis↗

Laser-induced fluorescence detection of atherosclerotic plaque with hematoporphyrin derivative used as an exogenous probe.

Clinical use of laser angioplasty is limited by the lack of an adequate guidance system. As a first step toward developing a reliable guidance system, laser-induced surface fluorescence and a fluorescent probe were used to differentiate plaque from normal arterial wall. The aortas from four normal New Zealand white rabbits and six atherosclerotic rabbits were studied in vitro. Rabbits from each group received 2.5 mg/kg of hematoporphyrin derivative intravenously 24 hours before death. Segments of the aortas were irradiated with a helium-cadmium laser, and the tissue surface fluorescence spectra were recorded with an optical multichannel analyzer. A plaque index, based on the resulting spectra, was calculated for each specimen of aorta. The spectra from normal aorta without hematoporphyrin derivative, normal aorta with hematoporphyrin derivative, and from plaque of atherosclerotic rabbits without hematoporphyrin derivative showed the same wavelength dependence. The plaque index values were not significantly different from one another. However, in plaque from atherosclerotic rabbits given hematoporphyrin derivative, the spectrum was markedly different, showing a broad spectral peak at 632 nm. This spectral peak corresponds to the spectral peak of hematoporphyrin derivative and was only seen in the plaque of atherosclerotic rabbits given hematoporphyrin derivative. The plaque index for these specimens was significantly different from all other specimens (p less than 0.001). This difference in fluorescence spectra and plaque index could be incorporated into a guidance system for laser angioplasty.

Angioplasty, Balloon↗