Baroreceptor sensitivity in two-week-old rat pups: effects of nutrient deprivation and sino-aortic denervation.

Resting cardiac rates are reduced 40% by nutrient deprivation in two-week-old rats while arterial pressure is maintained at stable levels. Previous evidence implicated arterial baroreceptors and suggested the hypothesis that the cardiac rate changes result from increased baroreceptor sensitivity following nutrient deprivation. In order to test this hypothesis, cardiac reflex responses were elicited by graded doses of phenylephrine and sodium nitroprusside before and after nutrient deprivation. Although cardiac rate decelerations in response to phenylephrine were greater in fed pups (p less than 0.05) and acceleration in response to nitroprusside were greater in the deprived condition (p less than 0.01), these could be attributed to 'ceiling' and 'floor' effects of the resting cardiac rates characteristic of the two nutrient conditions. Sino-aortic denervation eliminated cardiac reflex responses, substantiating their dependence on baroreceptor afferents. Regression analysis of cardiac reflex responses to arterial pressure changes failed to show changes in baroreceptor sensitivity that would support the hypothesis. Alternate mechanisms mediating the nutrient effect on cardiac rate (e.g., involving neural and peptide hormonal pathways) should be pursued.

Reperfusion conditions: critical importance of total ventricular decompression during regional reperfusion.

This study tests the hypothesis that failure to minimize left ventricular oxygen demands by venting during reperfusion diminishes recovery after controlled blood cardioplegic reperfusion. Of 25 dogs undergoing 2 hours of left anterior descending coronary occlusion, nine were reperfused with normal blood without bypass and five were reperfused with normal blood during total vented bypass. Eleven other dogs were reperfused with aspartate-glutamate-enriched, diltiazem-supplemented blood cardioplegic solution for 20 minutes during cardiopulmonary bypass; the left ventricle was decompressed by venting in only five of them. Regional systolic shortening was measured by ultrasonic crystals and myocardial damage estimated from triphenyltetrazolium chloride staining. All segments developed systolic bulging during ischemia (-23% systolic shortening, p less than 0.05), with no segmental recovery after reperfusion with normal blood without bypass (-27% systolic shortening, p less than 0.05) and negligible recovery following reperfusion with normal blood during total vented bypass (6 +/- 2%, p less than 0.05). In contrast, there was immediate recovery of regional contractility (+ 53% systolic shortening, p less than 0.05) in bypassed hearts reperfused with aspartate-glutamate-enriched, diltiazem-supplemented blood cardioplegic solution when venting was used and triphenyltetrazolium chloride nonstaining fell from 43% to 12% (p less than 0.05). Conversely, there was no postischemic recovery (-8% systolic shortening, p less than 0.05) when the same blood cardioplegic reperfusate was given over a comparable time without venting; triphenyltetrazolium chloride damage increased to 25% (p less than 0.05). Minimizing O2 demands by left ventricular decompression with venting during blood cardioplegic reperfusion is essential to ensure immediate functional recovery and limit histochemical damage.

Immediate functional recovery after six hours of regional ischemia by careful control of conditions of reperfusion and composition of reperfusate.

This study tests the hypothesis that irreversible muscle damage does not occur after as long as 6 hours of ischemia before reperfusion, immediate functional recovery is possible by controlling the conditions of reperfusion during total vented bypass and the composition of the reperfusate with substrate-enriched blood cardioplegic solution, and such control can be accomplished without thoracotomy. Of 43 dogs undergoing 2 to 6 hours of left anterior descending coronary occlusion, seven were studied by ultrastructural and mitochondrial analyses after 6 hours of regional coronary occlusion without reperfusion. Sixteen other dogs were reperfused with normal blood, with the heart in the beating state after 2 to 4 hours of ischemia, and 20 dogs received regional substrate-enriched blood cardioplegic reperfusion after 2 to 6 hours of ischemia for 20 minutes during total vented bypass accomplished through the femoral artery, femoral vein, and transaortic left ventricular venting. Six hours of ischemia without reperfusion caused minimal changes in mitochondrial structure and retained mitochondrial adenosine triphosphate production capacity at 64% of control values despite complete depletion of tissue adenosine triphosphate. Reperfusion with normal blood in the beating, working hearts caused extensive structural damage, reduced reflow, and failed to restore contractility in any instance (-27% systolic shortening, p less than 0.05). In contrast, regional cardioplegic reperfusion during total vented bypass at 2, 4, and 6 hours caused 52 +/- 3%, 41 +/- 7%, and 21 +/- 6% immediate recovery of regional contractile function. The seven hearts reperfused at 6 hours of ischemia had more segmental shortening (21% versus -27%, p less than 0.05), less edema (81% versus 83% water content, p less than 0.05), and more postischemic flow (57 versus 18 ml/100 gm/min in subendocardial muscle, p less than 0.05) than did 2-hour controls, and postischemic ultrastructure was not altered by reperfusion. Six hours of ischemia does not produce irreversible damage, and immediate recovery of contractile function is possible if the conditions of reperfusion are controlled with total vented bypass and a regional substrate-enriched blood cardioplegic solution is administered. Such control can be obtained by the peripheral cannulation technique.

Biochemical studies: failure of tissue adenosine triphosphate levels to predict recovery of contractile function after controlled reperfusion.

This study tests the hypotheses that postischemic adenosine triphosphate levels are unreliable predictors of functional recovery, myocardial adenosine triphosphate concentration of less than 2 mumol/gm does not indicate irreversible damage, mitochondrial adenosine triphosphate generating capacity can be nearly normal despite low levels of tissue adenosine triphosphate and the failure to replenish adenosine triphosphate after ischemia is due to depletion of the adenosine nucleotide pool, which can be replenished partially by exogenous precursors (e.g., 5-amino-4-imidazolecarboxamide ribotide [AICAR]). Myocardial adenosine triphosphate was depleted to less than 2 mumol/gm by either global ischemia (37 degrees C aortic clamping) or regional ischemia (acute coronary occlusion). Reperfusion was either with normal blood or with substrate-enriched blood cardioplegic solution during total vented bypass. Tissue adenosine triphosphate content and mitochondrial adenosine triphosphate generating capacity were measured, and functional recovery was determined by right heart bypass function curves or regional segmental shortening (ultrasonic crystals). Hearts undergoing 15 minutes of global ischemia and normal blood reperfusion had impaired functional recovery (stroke work index = 58 +/- 5%; p less than 0.05 of control) despite adenosine triphosphate concentration greater than 2 mumol/gm. Transmural mitochondrial State 3 respiration averaged 83% of control values despite adenosine triphosphate levels of 1 mumol/gm in hearts undergoing 45 minutes of 37 degrees C global ischemia and 2 additional hours of aortic clamping with multidose glutamate-enriched blood cardioplegia. AICAR increased adenosine triphosphate to 2 mumol/gm (p less than 0.05), but functional recovery was nearly complete (stroke work index = 94 +/- 2% of control) and was comparable with and without AICAR. Hearts undergoing 4 hours of regional ischemia recovered 31 +/- 5% systolic shortening after controlled reperfusion despite tissue adenosine triphosphate less than 0.5 mmol/gm (15% of control), and they retained 63% adenosine triphosphate generating capacity. Postischemic adenosine triphosphate levels correlate poorly with functional recovery, and adenosine triphosphate levels less than 2 mumol/gm do not indicate irreversible ischemic injury. Low postischemic levels may be repleted partially by adenine nucleotide precursor supplementation (AICAR).(ABSTRACT TRUNCATED AT 400 WORDS)

Histochemical studies: inability of triphenyltetrazolium chloride nonstaining to define tissue necrosis.

Triphenyltetrazolium chloride has been used to detect irreversibly damaged tissue after regional ischemia and reperfusion. We used this staining technique in our studies of myocardial ischemia and reperfusion and found that a transmural triphenyltetrazolium chloride nonstaining pattern is not an accurate predictor of myocardial necrosis: functional recovery occurs despite nonstaining. Mongrel dogs (n = 91) were anesthetized and made ischemic by ligation of the left anterior descending coronary artery. Regional myocardial function was assessed by means of ultrasonic crystals. Following 2, 4, or 6 hours of ischemia, the ligature was removed, and each heart was reperfused either in the working state or during total bypass with either normal blood or substrate-enriched blood cardioplegic solution of differing composition. The hearts were then removed and incubated in triphenyltetrazolium chloride at 37 degrees C for 20 to 40 minutes. The pattern of nonstaining in the area at risk varied from patchy subendocardial, to confluent subendocardial, to transmural and did not correlate with the recovery of regional contraction following ischemia. Mitochondrial ultrastructure was altered minimally in nonstained muscle, which regained contractile function after 6 hours of ischemia. Fifty-two of sixty-five hearts (80%) showing a transmural nonstaining pattern in the area of ultrasonic crystal placement recovered the capacity to shorten systolically immediately after controlled reperfusion during total vented bypass. These results show that the triphenyltetrazolium chloride staining method does not predict myocardial necrosis and that appropriate reperfusion following 2 to 6 hours of ischemia will result in recovery of myocardial shortening despite transmural nonstaining.

Electron microscopic studies: importance of embedding techniques in quantitative evaluation of cardiac mitochondrial structure during regional ischemia and reperfusion.

This study applies the low protein-denaturation embedding technique for mitochondrial preparation to analyze control cardiac tissue, heart muscle subjected to 6 hours of regional ischemia without reperfusion, and myocardial tissue subjected to 4 to 6 hours of ischemia followed by reperfusion either with normal blood, with the heart in the beating, working state, or with substrate-enriched blood cardioplegia during total vented bypass. Parallel specimens of cardiac tissue were analyzed for ultrastructure by the conventional osmium tetroxide fixation method. Results following conventional tissue preparation with osmium tetroxide showed extensive ultrastructural damage in all hearts subjected to ischemia, with no correlation between ultrastructural findings and methods of reperfusion or functional recovery. In contrast, results following tissue preparation by the low protein-denaturation method showed reperfusion with normal blood in working hearts to cause severe mitochondrial damage, cardiac mitochondria that were intact structurally after 6 hours of ischemia and after controlled reperfusion, a logical sequence of mitochondrial structural changes that may lead to irreversibility, and a new method of quantification of such changes.

Superiority of surgical versus medical reperfusion after regional ischemia.

This study tests the hypothesis that surgical revascularization (i.e., simulating coronary artery bypass grafting) with control of reperfusion conditions (total vented bypass) and of reperfusate composition (substrate-enriched blood cardioplegic solution) produces better recovery than is possible in the non-surgical setting (i.e., normal blood in beating, working hearts to simulate streptokinase and angioplasty). Eighteen dogs underwent 2 hours of left anterior descending coronary artery ligation (35% of the left ventricle at risk) followed by 2 hours of reperfusion. In five dogs the ligature was released to simulate streptokinase thrombolysis and angioplasty in working hearts (medical). In 13 dogs, surgical reperfusion was accomplished during total vented bypass, where six dogs received normal blood and seven others received substrate-enriched blood cardioplegic solution with 1 additional hour of aortic clamping (i.e., a total of 3 hours of ischemia). Segmental shortening with ultrasonic crystals, tissue water content, and vital staining (triphenyltetrazolium chloride) were assessed. Ischemia produced severe systolic bulging (-42% of control systolic shortening, p less than 0.05). Medical reperfusion resulted in failure to restore regional contractility (-27% systolic shortening, p less than 0.05), severe edema (82.4% H2O content, p less than 0.05), and extensive transmural nonstaining (44%, p less than 0.05). In contrast, surgical reperfusion with substrate-enriched blood cardioplegic solution during total vented bypass restored regional contraction to 46% of control values (p less than 0.05) and resulted in less edema (80.6% H2O content, p less than 0.05), and only mild nonstaining (21%, p less than 0.05) restricted to the subendocardial region. Surgical revascularization with controlled reperfusion conditions and reperfusate composition produces better myocardial salvage than is possible in the medical setting, despite a longer period of ischemia.

Metabolic and histochemical benefits of regional blood cardioplegic reperfusion without cardiopulmonary bypass.

This study evaluates the capacity of regional substrate-enriched blood cardioplegic reperfusion (without bypass) to salvage cardiac muscle subjected to 40 minutes of regional ischemia. Results are compared with those obtained by normal blood reperfusion at either systemic or reduced perfusion pressure (i.e., simulating acute angioplasty or streptokinase thrombolysis). All studies were carried out in beating, working hearts when the conditions of reperfusion were not controlled. The results show that regional cardioplegic reperfusion without cardiopulmonary bypass reduces the incidence of perfusion ventricular fibrillation (15% versus 55%, p less than 0.05), increases recovery of subendocardial creatine phosphate (35.3 versus 14.0 mumol/gm, p less than 0.05) and adenosine triphosphate (6.0 versus 3.1 mumol/gm, p less than 0.05), reduces histochemical damage evaluated by triphenyltetrazolium chloride (0% versus 43% transmural nonstaining, p less than 0.05), and improves myocardial contractile reserve capacity (91% versus 41%, p less than 0.05). Normal blood reperfusion restored immediate systolic shortening in only 3 of 18 hearts (17%), and regional cardioplegic reperfusion without bypass produced early recovery of regional systolic shortening in only 10 of 16 hearts (63%, p greater than 0.05). Thus the value of controlling reperfusate composition without simultaneous control of reperfusion conditions is limited.

Regional blood cardioplegic reperfusion during total vented bypass without thoracotomy: a new concept.

This study tests the hypothesis that immediate functional recovery is possible after 2 to 3 hours of regional ischemia by control of the conditions of reperfusion (i.e., total vented bypass) and the composition of the reperfusate (substrate-enriched blood cardioplegic solution) by either central cannulation with thoracotomy or peripheral cannulation without thoracotomy. Total vented bypass could be established successfully in each of 14 experiments (100%) in which the peripheral cannulation method was tested. Regional function (evaluated by ultrasonic crystals in open-chest animals) recovered comparably when substrate-enriched blood cardioplegic solution was given either globally or regionally (46% versus 36%) and total vented bypass was accomplished by either central cannulation or peripheral cannulation technique (i.e., left ventricle decompressed through a transaortic vent catheter, right atrium cannulated through the femoral vein, femoral artery perfusion). In contrast, systolic bulging persisted (-23% control systolic shortening) following normal blood reperfusion in beating, working hearts. Controlled reperfusion (either global or regional) also minimized postischemic edema (81% versus 83% water content, p less than 0.05). The effectiveness of controlled reperfusion (substrate-enriched blood cardioplegic solution during total vented bypass) versus uncontrolled reperfusion (normal blood in beating, working hearts) was assessed also in closed-chest dogs with 3 hours of regional ischemia (i.e., balloon inflation in the left anterior descending coronary artery). Results after controlled reperfusion showed complete recovery of contractility (as shown by echocardiography) at 24 hours, in comparison with only minimal recovery in three of eight dogs receiving uncontrolled reperfusion, and minimal histochemical damage (less than 5% triphenyltetrazolium chloride nonstaining), in comparison with 34% necrosis after uncontrolled reperfusion. These studies suggest that control of the reperfusion conditions and reperfusate composition can be achieved comparably in either the catheterization laboratory or the operating room, and a proposed clinical model for the treatment of patients with acute myocardial infarction is presented for evaluation.

High oxygen requirements of dyskinetic cardiac muscle.

This study assesses the regional oxygen requirements of muscle segments that are beating and working, beating and empty, arrested and decompressed, and nonischemic that move dyskinetically. Regional oxygen demands were evaluated by producing a dyskinetic segment by infusing regional cardioplegic solution through a left anterior descending coronary artery catheter with and without extracorporeal circulation. The results show that the O2 demands of the perfused dyskinetic cardiac muscle segment (4 to 8 ml/100 gm/min) are approximately 55% of the contracting (beating, working) segment (7 to 12 ml/100 gm/min) and are fivefold more than when the same muscle segment is arrested and decompressed by total vented bypass (0.8 to 1.2 ml/100 gm/min). Additional studies showed that ischemia for 2 hours (left anterior descending coronary artery ligation) produced severe dyskinesia (-24% control systolic shortening), which failed to recover after reperfusion with the heart in the beating, working state. In contrast, lowering O2 demands by reperfusion during bypass restored occasional contractile function as a consequence of left ventricular decompression. Dyskinetic muscle segments have a high oxygen requirement that may affect their capacity to be salvaged if reperfusion is conducted without left ventricular decompression. These observations suggest that the value of revascularization in the working heart (i.e., streptokinase with or without angioplasty) may be limited unless the left ventricle is decompressed during reperfusion and provide an explanation for the delayed recovery of mechanical function in hearts reperfused surgically with normal blood during cardiopulmonary bypass.

Reperfusate composition: supplemental role of intravenous and intracoronary coenzyme Q10 in avoiding reperfusion damage.

This study tests the hypothesis that the oxygen radical scavenger coenzyme Q10 can be given both intravenously and in the cardioplegic solution and can improve muscle salvage following surgical revascularization. Pilot studies were carried out in dogs undergoing 40 minutes of coronary artery ligation with reperfusion with normal blood, with the heart in the beating, working state. Intravenous infusions of coenzyme Q10 (10 mg/kg) 5 minutes before reperfusion resulted in improved recovery of creatine phosphate, adenosine triphosphate, total adenine nucleotide, and myocardial function reverse estimated by postextrasystolic potentiation, in comparison with the degree of recovery in untreated dogs. Experimental studies were done on 27 dogs undergoing 2 hours of left anterior descending coronary artery occlusion and subsequent reperfusion with and without total vented bypass. Thirteen dogs received intravenous coenzyme Q10 10 minutes before extracorporeal circulation, six received substrate-enriched blood cardioplegic solution with added coenzyme Q10, and six received normal blood reperfusate. Six others had cardioplegic reperfusion without coenzyme Q10. The systolic bulging that occurred during ischemia (ultrasonic crystals) persisted after reperfusion with normal blood (-25% systolic shortening, p less than 0.05), and 44% transmural triphenyltetrazolium chloride nonstaining occurred in the area at risk. Conversely, hearts receiving substrate-enriched blood cardioplegic solution recovered 37% contractility (p less than 0.05), with the least, and only, subendocardial triphenyltetrazolium chloride nonstaining (25% of area at risk) occurring with intravenous coenzyme Q10 before bypass and coenzyme Q10 supplementation of the cardioplegic solution. Intravenous coenzyme Q10, given just before reperfusion (possibly in transit to the operating room), enhances the role of substrate-enriched blood cardioplegic solution (especially when added to the cardioplegic solution) in salvaging ischemic myocardium and allowing immediate functional recovery.

Reperfusate composition: benefits of marked hypocalcemia and diltiazem on regional recovery.

This study tests the hypothesis that improved muscle salvage is possible by markedly reducing the ionic calcium (Ca++) of the reperfusate (less than 250 mumol/L) and adding a calcium channel-blocking drug (diltiazem). Preliminary pilot studies showed that a 20-minute infusion of markedly hypocalcemic substrate-enriched blood cardioplegic solution (less than 250 mumol/L Ca++) did not affect left ventricular function adversely and that a 150 to 250 mumol/L substrate-enriched blood cardioplegic solution, delivered during total vented bypass with diltiazem, 300 micrograms/kg body weight, produced the most consistent functional recovery and the least histochemical evidence of damage (triphenyltetrazolium chloride nonstaining) after 2 hours of regional ischemia. Experimental studies of 2 hours of regional ischemia were followed by either regional normocalcemic (1000 to 1200 mumol/L) blood cardioplegic reperfusion in bypassed hearts, with or without diltiazem, or hypocalcemic (150 to 150 mumol/L) blood cardioplegic reperfusion with diltiazem for 20 minutes. Results showed that hypocalcemic blood cardioplegic solution with diltiazem produced superior recovery of systolic shortening (58% versus 11% systolic shortening, p less than 0.05) and limitation of histochemical damage (11% versus 54%, p less than 0.05), in comparison with normocalcemic blood cardioplegic solution without diltiazem. These studies suggest that modifying the regional reperfusate by markedly reducing ionic calcium levels and adding calcium channel-blocking drugs is safe and may improve myocardial salvage more than using substrate-enriched blood cardioplegic solution alone.

Reperfusate composition: interaction of marked hyperglycemia and marked hyperosmolarity in allowing immediate contractile recovery after four hours of regional ischemia.

This study tests the hypothesis that improved muscle salvage after prolonged ischemia (4 hours) occurs when the substrate-enriched blood cardioplegic solution is markedly hyperglycemic (greater than 400 mg/dl) and markedly hyperosmotic (greater than 400 mOsm). Thirty-five dogs underwent 4 hours of occlusion of the left anterior descending coronary artery and reperfusion during total vented bypass with substrate-enriched blood cardioplegic solution, in which the glucose concentration and osmolarity were varied in relation to one another. Spontaneous systolic shortening recovered consistently (31 +/- 6%) only when glucose was greater than 400 mg/dl and osmolarity was greater than 400 mOsm. The least recovery occurred (only one of six dogs recovering spontaneous shortening) when cardioplegic glucose was greater than 400 mg/dl and osmolarity was greater than 400 mOsm. Regional segments reperfused with our standard substrate-enriched blood cardioplegic solution had lower transmural flow rates following reperfusion (56 versus 87 ml/100 gm/min, p less than 0.05), markedly reduced mitochondrial State 3 and State 4 respiration in epicardial and endocardial muscle (p less than 0.05), and the most extensive histochemical evidence of damage (63% area of nonstaining versus area at risk, p less than 0.05). We conclude that markedly increased levels of osmolarity (greater than 400 mOsm) and glucose (greater than 400 mg/dl) improve the capacity of substrate-enriched blood cardioplegic solution to salvage myocardium after prolonged ischemia.

Effects of "duration" of reperfusate administration versus reperfusate "dose" on regional functional, biochemical, and histochemical recovery.

This study tests the hypothesis that improved myocardial salvage following regional ischemia occurs when attention is directed toward the duration of blood cardioplegic reperfusion rather than the reperfusate "dose". Pilot studies after global ischemia established the postischemic oxygen use pattern consistent with normal and impaired recovery; the best recovery occurred when postischemic muscle consumed oxygen in excess of basal demands. Experimental studies were then performed on 22 dogs undergoing 2 hours of left anterior descending coronary occlusion. Nine dogs received normal blood reperfusion, with the heart allowed to remain in the beating, working state. In 13 dogs, cardiac O2 demands were kept low during reperfusion by delivering a dose of 150 to 250 mumol/L Ca2++ aspartate-glutamate-enriched blood cardioplegic solution containing 250 to 350 micrograms/kg body weight diltiazem during total vented bypass. This same reperfusate dose with diltiazem was given over 10 minutes in five dogs and over 20 minutes in eight others. Persistent systolic bulging (ultrasonic crystals) of -27% (p less than 0.05) of systolic shortening followed normal blood reperfusion without bypass. During blood cardioplegic reperfusion, regional O2 uptake exceeded basal demands by 24 ml/100 gm/min at 10 minutes (p less than 0.05) and did not return to baseline until 20 minutes had elapsed. Hearts reperfused with blood cardioplegia for 20 minutes had better recovery of systolic shortening (58% versus 30%, p less than 0.05), less edema (79.8% versus 80.9% water content, p less than 0.05), and less triphenyltetrazolium chloride nonstaining (12% versus 21%, p less than 0.05) than those reperfused for 10 minutes with the same solution containing the same diltiazem dose. Continuing blood cardioplegic reperfusion until myocardial oxygen uptake reaches control levels enhances regional functional recovery after acute coronary occlusion. These results indicate that attention should be directed toward the duration of reperfusion, as well as the "dose" of cardioplegic reperfusate.

Reperfusion conditions: importance of ensuring gentle versus sudden reperfusion during relief of coronary occlusion.

This study tests the hypothesis that more muscle salvage after acute ischemia is possible by "gentle," temporary reperfusion than with sudden, complete revascularization. Ten dogs underwent 4 hours of left anterior descending coronary artery ligation with reperfusion during total vented bypass for 1 hour of the 2-hour reperfusion period. In five dogs, reperfusion was accomplished by release of the occlusion suddenly and completely. The five others received selective low-pressure (40 to 50 mm Hg) coronary reperfusion with normal blood for 20 minutes at 30 ml/min before the occlusion was relieved completely. Systolic shortening with ultrasonic crystals, triphenyltetrazolium chloride staining, and myocardial wet and dry weights were measured. Sudden relief of occlusion failed to restore contractility spontaneously (-7 +/- 1% systolic shortening, p less than 0.05) or with inotropic infusion (-2 +/- 4% systolic shortening, p less than 0.05) and caused the greatest amount of edema (82.2%, systolic shortening, p less than 0.05) and triphenyltetrazolium chloride nonstaining (76% area at risk, p less than 0.05). In contrast, temporary, gentle reperfusion allowed slight spontaneous recovery in four of five hearts (4 +/- 2% systolic shortening), increasing to 26 +/- 12% systolic shortening (p less than 0.05) with inotropic stimulation, limited edema (80.7%, p less than 0.05), and reduced triphenyltetrazolium chloride nonstaining to 55% (p less than 0.05). Early temporary, gentle reperfusion limits the postischemic damage that occurs with sudden, complete revascularization (aortic unclamping without control of reperfusion pressure or flow). These findings may have implications during revascularization for acute myocardial infarction when perfusion pressure and flow can be controlled.

A determination of the health-protective behaviors of female adolescents: a pilot study.

In this study, the unique needs and developmental stage of adolescent females were considered in the determination of health-protective behaviors and needs. Through the use of a questionnaire, 211 female freshman dormitory residents (17-22 years of age) attending a small, private, midwestern university, were surveyed to assess their knowledge, utilization, and perceived teaching needs regarding selected health-protective behaviors. Findings indicated that almost all of them identified basic forms of health-protective behaviors. However, a majority exhibited inadequate knowledge and use of basic health care practices. The health-teaching needs identified most frequently were in the areas of: stress control; rape/suicide prevention; safety; and prevention/care of minor illnesses. Suggestions for program design and implications for health promotion are presented.

Comparison of distribution beyond coronary stenoses of blood and asanguineous cardioplegic solutions.

In seven dogs on cardiopulmonary bypass, a critical stenosis (75% to 90%) of the left anterior descending coronary artery (LAD) was produced. Alternate 250 ml/min infusions of asanguineous and blood cardioplegic (4 degrees C) solutions were made for 3 to 5 minutes. Poststenotic flow (flowmeter), intramyocardial temperature, and aortic pressure were measured. During cardioplegic infusions of 250 ml/min, aortic pressure was 34 +/- 4 mm Hg higher with blood cardioplegia than with asanguineous cardioplegia (82 +/- 7 versus 48 +/- 8 mm Hg). Poststenotic cardioplegic flow was 39% +/- 9% higher (29 +/- 5 versus 18 +/- 5 ml/min) with blood cardioplegia. Consequently, blood cardioplegia resulted in more rapid arrest (20 +/- 2 versus 45 +/- 5 seconds) and lower myocardial temperature (6 degrees +/- 1 degree C) in the region of LAD blood supply; posterior ventricular myocardial cooling was similar (unobstructed vessels) with both solutions. These data show that the reduced viscosity of asanguineous cardioplegia compared to blood cardioplegia results in lower aortic pressure. Consequently, the higher aortic pressure with blood cardioplegia results in superior cardioplegic delivery beyond obstructed coronaries and better myocardial cooling. We conclude that the decreased viscosity of 4 degrees C asanguineous cardioplegia causes diversion of cardioplegic solution from the obstructed to the normal coronary bed.