Maximal utilization of the left internal mammary artery for coronary bypass grafting.

A technique is described for using the internal mammary artery to bypass the left anterior descending coronary artery and another adjacent coronary artery even when the alignment of the two vessels is not favorable for a conventional sequential graft. The distal end of the mammary artery is amputated and used to construct a Y graft to the anterior descending artery and to the secondary target vessel.

Cox/maze procedure for atrial septal defect with atrial fibrillation: management strategies.

Atrial fibrillation is found at late follow-up in approximately half of all adults who have had correction of atrial septal defect, even if it was not present preoperatively. These patients are thus exposed to the risks of stroke and chronic drug therapy even after a successful operation. Simultaneous surgical correction of atrial septal defect and atrial fibrillation was accomplished in a 52-year-old man by means of the Cox/maze procedure. The small added risk and the substantial benefit of eliminating atrial fibrillation suggest that this approach is warranted in selected adults with atrial septal defect.

A simple and safe technique of left ventricular venting.

Left ventricular venting has many physiologic and practical benefits. A venting technique is described that employs a simple, closed system which allows the perfusionist to monitor left ventricular distention. By monitoring the left ventricular volume the perfusionist can regulate the degree of negative pressure on the vent and thus reduce the chance of air entering the heart.

Applicability of noncardioplegic coronary bypass to high-risk patients. Selection of patients, technique, and clinical experience in 3000 patients.

Although some surgeons still prefer noncardioplegic coronary bypass, most surgeons are skeptical of its suitability for high-risk patients. We analyzed the first 3000 patients who had primary coronary bypass without cardioplegia since our program's inception. Patients with reoperations, valve operations, or carotid endarterectomies were excluded. Multivariate predictors of operative death included age, sex, left ventricular dysfunction, preoperative intraaortic balloon pumping, and urgency of operation. Eight hundred seventy-nine patients (29%) were more than 70 years of age; 795 (27%) were female; 290 (9.7%) had an ejection fraction less than 0.30, and another 77 (2.6%) had left ventricular aneurysms; 196 (6.5%) had an acute myocardial infarction, and another 397 (13%) had a myocardial infarction less than 1 week preoperatively; 917 (31%) had rest pain in the hospital (preinfarction angina). Only 790 (26%) had elective operations. The overall operative mortality rate was 1.47% (44/3000): The mortality rate for elective operations was 0.5% (4/790); urgent 1.7% (28/1687); emergency 2.3% (12/523). In patients with an ejection fraction less than 0.30 the mortality rate was 6.2% (18/290); with age more than 70 years, it was 3.9% (34 of 879); with acute myocardial infarction it was 3.1% (6/196); and with left ventricular aneurysmectomy it was 1.3% (1/77). Inotropic support after leaving the operating room was needed in 6.6% (199 patients), and 1% (30 patients) required new intraaortic balloon pumping postoperatively (two of these 30 patients died). These results provide reassurance that noncardioplegic coronary artery bypass grafting provides excellent myocardial protection and operating conditions for primary coronary bypass and is particularly suitable for high-risk patients.

Beta-hydroxybutyrate and response to hypoxia in the ground squirrel, Spermophilus tridecimlineatus.

1. Previous studies have suggested that elevated ketone levels are associated with increased survival time in rodents exposed to hypoxia. In this study the association between whole blood BHB (beta-hydroxybutyrate) and hypoxic survival time was investigated in hibernating and non-hibernating ground squirrels and in rats. 2. Non-hibernating ground squirrels and rats were exposed to hypoxia (4.5% O2). One hundred per cent of ground squirrels survived 1 hr of hypoxia vs 20% of rats. 3. Ketone levels were significantly higher in ground squirrels than rats during hypoxia, and rats surviving the longest had the highest ketone levels. 4. When hibernation was induced in ground squirrels there was a significant increase in beta-hydroxy-butyrate from 0.45 to 1.6 mM (P = 0.0005). 5. Ground squirrel heart mitochondrial respiratory control ratios and ATP synthesis rates indicated no preferential ketone utilization which might suggest a possible extramitochondrial role of BHB during hypoxia. 6. We conclude that elevated blood BHB levels are associated with increased hypoxic survival and they may have evolved in response to life-threatening hypoxia as experienced during hibernation.

Effects of lodoxamide tromethamine on paraplegia that occurs after infrarenal aortic occlusion in the rabbit.

The antioxidant lodoxamide tromethamine was assessed for effects on experimental spinal cord ischemia in the rabbit. Lodoxamide (20 mg/kg/hr) or 0.9% sodium chloride was infused beginning 15 minutes before infrarenal aortic occlusion and continuing for 105 minutes. With an occlusion time of 20 minutes, eight of eight lodoxamide-treated animals and five of eight saline-treated animals regained function after reperfusion. However, by 48 hours after occlusion, seven of eight saline-treated animals were completely paralyzed, whereas only two of eight lodoxamide-treated animals were paralyzed. An ischemia time of 30 minutes exceeded the protective capacity of this treatment. These results suggest lodoxamide may be useful in alleviating ischemic damage to the spinal cord.

Dextrose administration increases sensory/motor impairment and paraplegia after infrarenal aortic occlusion in the rabbit.

Spinal ischemia with resultant cord infarction is a catastrophic complication of surgical procedures involving the thoracoabdominal aorta. A rabbit spinal ischemia model was used to test if glucose administration would increase neurologic deficit of the lower extremity. Rabbits (2 to 3 kg), anesthesized with halothane, had a snare occluder placed around the aorta just below the left renal artery. After a 2-hour recovery, the aorta was occluded for 15 minutes. Before occlusion animals received an intraperitoneal injection of isotonic glucose (2 gm/kg; n = 11), isotonic mannitol (2 gm/kg; n = 3), or an equal volume of saline solution (n = 11). Four sham-operated animals received glucose and an identical surgical procedure, but the aorta was not occluded. Average blood glucose level at the time of occlusion for the glucose group was 249 +/- 15 versus 156 +/- 6 for the control group (p less than 0.01). At 1, 4, 18, and 24 hours, a neurologic impairment score (1 = normal, 2 = partial impairment, 3 = complete impairment) was assigned. At 4, 18, and 24 hours, the glucose group had significantly greater neurologic impairment than did control groups (p less than 0.02). Glucose administration had an adverse effect in a controlled and highly reproducible model of spinal cord ischemia. Exogenous glucose administration should potentially be avoided during complex aortic reconstruction.

Elevated blood ketone and glucagon levels cannot account for 1,3-butanediol induced cerebral protection in the Levine rat.

1,3-Butanediol is an ethanol dimer that induces systemic ketosis. It has previously been shown to increase hypoxic survival time and reduce neurologic deficit in several experimental preparations. The aim of this study was to determine if the mechanism of 1,3-butanediol-induced cerebral protection was elevation of blood ketone levels, blood glucagon levels, or both. Blood beta-hydroxybutyrate levels, glucagon levels, or both produced by a previously reported protective dose of 1,3-butanediol (47 mmol/kg) were simulated by direct i.v. infusion of the ketone beta-hydroxybutyrate and glucagon separately and in combination, and the effect on hypoxic survival time in instrumented Levine rats (unilateral carotid ligation and hypoxic exposure) was determined. To test if the mechanism was a direct or osmotic effect of the alcohol, an equimolar dose of ethanol (47 mmol/kg) was administered and the effect on hypoxic survival time was compared with that produced by 1,3-butanediol. As in previous studies, 1,3-butanediol significantly increased hypoxic survival time (241% of control, Scheffe p less than 0.05). Various doses of beta-hydroxybutyrate and glucagon were infused to approximate the blood levels of beta-hydroxybutyrate and glucagon produced by a protective dose of 1,3-butanediol. Although beta-hydroxybutyrate or glucagon infusions produced blood levels of these substances that were comparable with those produced by administering butanediol, they failed to prolong hypoxic survival time as long as 1,3-butanediol. No correlation was detected between hypoxic survival time and blood levels of beta-hydroxybutyrate, glucagon, insulin, or glucose. An equimolar dose of ethanol did not significantly increase hypoxic survival time.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphometric evaluation of brain infarcts in rats and gerbils.

The Levine rat preparation, the gerbil stroke model, and appropriate control animals were used to determine if the 2,3,5-triphenyltetrazolium chloride (TTC) would selectively identify noninfarcted versus infarcted cerebral tissue. The TTC is frequently used to quantify infarcted myocardial tissue and has been shown to have great specificity, reproducibility, and efficacy. The TTC produces a red product upon reaction with the respiratory enzymes (dehydrogenases) present in non-infarcted tissues. Irreversibly damaged tissues, lacking dehydrogenases, do not form red reaction products. Six gerbil brains and seven rat brains were incubated with the TTC, and the unreacted areas were macroscopically identified. The brains were fixed and sectioned for routine hematoxylin and eosin staining to determine the specificity of the TTC. The TTC was found to react selectively only with non-infarcted cerebral tissue. The gross brain sections were evaluated by macroscopic morphometric analysis, and the unreacted area was always ipsilateral to ligation and correlated with histologic identification of infarct. The brains from neurologically intact animals demonstrated neither macroscopic nor histological evidence of infarction. This technique allows macroscopic quantification of infarct size by planimetry. The average area of infarct for the neurologically impaired rats was 34.7% and it was 31.4% for the impaired gerbils. The percentage of surface area of each infarcted slice was found to correlate with the severity of the neurologic deficit. We conclude that TTC staining is effective for macroscopically delineating cerebral infarcts in rats and gerbils, thus permitting quantification of infarct size.

Dextrose containing intravenous fluid impairs outcome and increases death after eight minutes of cardiac arrest and resuscitation in dogs.

Use of dextrose in intravenous resuscitation fluids is common practice; however, this study indicates that 5% dextrose solutions, even if administered in physiologic quantities, greatly worsens the outcome of survivable cardiac arrest. Twelve adult male mongrel dogs were premedicated with morphine, anesthetized with halothane, instrumented, intubated, and ventilated. Each dog was first given 500 ml of either lactated Ringer's (LR) (n = 6) or 5% dextrose in LR (D5LR) (n = 6). Halothane was stopped and fibrillation was induced (60 Hz). Blood glucose just before cardiac arrest was 129 mg/dl in the LR dogs and was increased to 335 mg/dl in the D5LR dogs. After eight minutes of arrest, resuscitation, including internal cardiac massage and standard advanced cardiac life support drug protocols (modified for dogs), was begun. When stable cardiac rhythm was obtained, the chest was closed, and LR or D5LR continued until a total of 1L was given. A neurologic score (0 = normal to 100 = dead) was assigned at 1, 2, 6, and 24 hours. The LR group did not differ statistically from the D5LR group in operative time, number of defibrillatory shocks, time to spontaneous ventilation, time to extubation, or drugs required. Resuscitation was successful in all six LR and five of six D5LR group; however, by 2 hours after resuscitation and thereafter, D5LR group had a significantly greater neurologic deficit (p less than 0.05) than did the LR group. By 9 hours, four of six D5LR dogs displayed convulsive activity and died. At 24 hours the D5LR group had a greater (p less than 0.008) neurologic deficit (82 +/- 11) than did the LR group (21 +/- 7), which walked and ate. We conclude that the addition of 5% dextrose to standard intravenous fluids greatly increases the morbidity and mortality associated with cardiac resuscitation.

Reduction of neurologic deficit by 1,3-butanediol induced ketosis in levine rats.

The objective of this study was to determine if 1,3-butanediol would reduce a neurologic deficit in rats exposed to ischemic-hypoxia (Levine rats). Age and weight matched male Sprague-Dawley rats were anesthetized with 2% halothane. The right common carotid and external jugular vein were ligated and cannulated and EEG screws were implanted followed by a 2 hour recovery period. Thirty minutes prior to exposure the rats received either 1,3-butanediol (47 mmole/kg i.v.; n = 11) or an equal volume of saline (n = 10). The rats were then exposed to 4.5% O2 until mean arterial blood pressure fell to 70 mm Hg. The oxygen level was then increased to 8% for 30 minutes, after which the rats were returned to room air. Posture, hemiparesis, circling, shuffling, activity, and ability to hang on to a vertical screen were scored 1 (normal) to 5 (severe deficit) at 2 and 20 hours after insult. The time to 70 mm Hg was extended from 7.9 +/- 0.9 min for saline treated rats to 19.0 +/- 2.3 min for the 1,3-butanediol treated rats (p less than 0.001). All eleven 1,3-butanediol treated rats survived the hypoxic insult; 90% (9/10) saline treated rats died. In an attempt to reduce the insult, six additional saline treated rats were switched to 8% O2 at 75 mm Hg and still 4/6 died. The mean score at 20 hours for three surviving saline treated rats was 3.4. A significantly better (p less than 0.002) mean 20 hour score for the surviving 8/11 1,3-butanediol treated rats was 1.2. 1,3-butanediol increases survival and decreases the neurologic deficits associated with this ischemic-hypoxic insult.

Butanediol induced cerebral protection from ischemic-hypoxia in the instrumented Levine rat.

To determine if 1,3-Butanediol (BD), which protects mice from hypoxia, would extend the tolerance of rats to ischemic-hypoxia, the Levine rat (unilateral carotid ligation and conscious hypoxic exposure) was modified to record mean arterial pressure (BP), heart rate (HR), central venous pressure (CVP), spontaneous respiration and EEG. Age and weight matched, male, Sprague-Dawley rats were anesthetized under halothane (1-2%), ligated, instrumented, and recovered 2 hrs before hypoxia (4.5% oxygen). Thirty minutes prior to hypoxia, groups of rats received, BD (47 mmoles/kg i.v.; n = 7), equal volumes of saline (S) (n = 6) or no-infusion (NI) (n = 7). Since no significant difference was observed between S and NI they were combined into a single control group (C). In a parallel group administered BD, resultant beta- hydroxybutarate ( BHB ) levels increased from 0.13 +/- 0.02 to 0.84 +/- 0.03 mM and temperature declined only 1.5 degrees C. The EEG of all ischemic-hypoxic rats invariably became isoelectric before cessation of spontaneous respiration and eventual loss of BP. BD significantly (p less than 0.01, Student's t) increased ischemic-hypoxic tolerance (time to isoelectric EEG) from 875 +/- 56 for the control group to 1338 +/- 67 seconds for the BD group, without changing the interval from isoelectric EEG to loss of BP. Further, EEG activity persisted at a lower mean BP (p less than 0.01) in the BD group (44 +/- 5 mm Hg) than in the control group (66 +/- 4 mm Hg). In summary, isoelectric EEG invariably precedes ventilatory failure and cardiovascular collapse. BD increases ischemic-hypoxic tolerance in the conscious rat by extending, at a lower mean BP, the time to isoelectric EEG.