Oral Coenzyme Q10 supplementation does not prevent cardiac alterations during a high altitude trek to everest base cAMP.

Exposure to high altitude is associated with sustained, but reversible, changes in cardiac mass, diastolic function, and high-energy phosphate metabolism. Whilst the underlying mechanisms remain elusive, tissue hypoxia increases generation of reactive oxygen species (ROS), which can stabilize hypoxia-inducible factor (HIF) transcription factors, bringing about transcriptional changes that suppress oxidative phosphorylation and activate autophagy. We therefore investigated whether oral supplementation with an antioxidant, Coenzyme Q10, prevented the cardiac perturbations associated with altitude exposure. Twenty-three volunteers (10 male, 13 female, 46±3 years) were recruited from the 2009 Caudwell Xtreme Everest Research Treks and studied before, and within 48 h of return from, a 17-day trek to Everest Base Camp, with subjects receiving either no intervention (controls) or 300 mg Coenzyme Q10 per day throughout altitude exposure. Cardiac magnetic resonance imaging and echocardiography were used to assess cardiac morphology and function. Following altitude exposure, body mass fell by 3 kg in all subjects (p<0.001), associated with a loss of body fat and a fall in BMI. Post-trek, left ventricular mass had decreased by 11% in controls (p<0.05) and by 16% in Coenzyme Q10-treated subjects (p<0.001), whereas mitral inflow E/A had decreased by 18% in controls (p<0.05) and by 21% in Coenzyme Q10-treated subjects (p<0.05). Coenzyme Q10 supplementation did not, therefore, prevent the loss of left ventricular mass or change in diastolic function that occurred following a trek to Everest Base Camp.

Effects of Tribuli saponins on ventricular remodeling after myocardial infarction in hyperlipidemic rats.

This experiment was designed to determine whether Tribuli saponins (TS) relieve left ventricular remodeling (VR) after myocardial infarction (MI) in a murine hyperlipemia (HL) model. MI and HL models were induced and high and low doses of TS and simvastatin were administrated to the rats. Four weeks later, echocardiographic observation was performed and the left and right ventricular weight index (LVWI, RVWI) was calculated. Echocardiographic results showed that both high dose of TS and simvastatin had a beneficial effect on increasing fractional shortening (FS) and ejection fraction (EF), reducing left ventricular end diastolic volume (LVEDV), systolic volume (LVESV), left ventricular dimension end diastole (LVDd) and systole (LVDs), and decreasing LVWI, as compared to those in the HL-MI model group (p < 0.05, 0.01). Both medicines had little impact on thickness of the anterior and posterior wall. No significant difference was observed between each treatment group (p > 0.05). In conclusion, TS not only lowered serum lipidemia, but also relieved left ventricular remodeling, and improved cardiac function in the early stage after MI.

The effect of combination therapy on regression of left ventricular hypertrophy in cases with hypertension.

OBJECTIVE: Up to this date, it is well shown that several antihypertensive drugs have different regressive effect on left ventricular hypertrophy (LVH). However, there are different studies regarding the effect of antihypertensive combination therapies on regression of LVH. In this study, 2 different combinations ACE-I plus calcium channel blocker and ACE-I plus diuretic were compared in cases with hypertension whose BPs were not controlled by ACE-I alone. METHODS: Forty patients with mild to moderate hypertension were included in this study. The treatment was continued for 6 months in the Faculty of Medicine at Ege University, Turkey, between January and December 2003. Adequate response with lisinopril 20 mg/daily failed to be achieved in all patients. Patients divided into 2 groups. There were no differences between the groups in patients' age, blood pressure (BP) and other clinical and laboratory range. First group patients received lisinopril 20 mg + nifedipine GITS 30 mg and second group patients received lisinopril 20 mg + hydrochlorothiazide 25 mg. The treatment was continued for 6 months. Blood pressure were measured every 2 weeks, echocardiographic findings, and blood and urinary analysis were performed before and at the end of treatment. RESULTS: Systolic and diastolic BP decreased significantly in both groups and no significant difference regarding BP was found between the 2 groups. Left ventricular mass index also decreased significantly in both groups. However, in the first group left ventricular mass index decreased more compared to the second group. CONCLUSION: The effect of combination therapies with angiotensin converting enzyme inhibitor (ACE-I) plus diuretic and ACE-I plus calcium channel blocker on systolic and diastolic BP are similar. However, when LVH is present, regressive effect of the combination of ACE-I plus calcium channel blocker is superior to the combination of ACE-I plus diuretic.

Validation of myocardial acceleration during isovolumic contraction as a novel noninvasive index of right ventricular contractility: comparison with ventricular pressure-volume relations in an animal model.

BACKGROUND: We have demonstrated that myocardial acceleration during isovolumic contraction (IVA) is a sensitive index of left ventricular contractile function. In this study, we assessed the utility of IVA to measure right ventricular (RV) contractile function. METHODS AND RESULTS: We examined 8 pigs by using tissue Doppler imaging of the RV free wall and simultaneous measurements of intraventricular pressure, volume, maximal elastance (e(max)), preload recruitable stroke work, and dP/dt(max) by conductance catheterization. Animals were paced in the right atrium at a rate of 130 beats per minute (bpm). IVA was compared with elastance during contractility modulation by esmolol and dobutamine and during preload reduction and afterload increase by transient balloon occlusion of the inferior vena cava and pulmonary artery, respectively. Data were also obtained during incremental atrial pacing from 110 to 210 bpm. Esmolol led to a decrease in IVA and dP/dt(max). During dobutamine infusion, IVA, dP/dt(max), preload recruitable stroke work, and e(max) all increased significantly. During preload reduction and afterload increase, IVA remained constant up to a reduction of RV volume by 54% and an RV systolic pressure increase of 58%. Pacing up to a rate of 190 bpm led to a stepwise increase in IVA and dP/dt(max), with a subsequent fall at a pacing rate of 210 bpm. CONCLUSIONS: IVA is a measurement of RV contractile function that is unaffected by preload and afterload changes in a physiological range and is able to measure the force-frequency relation. This novel index may be ideally suited to the assessment of acute changes of RV function in clinical studies.

[Correction of coronary insufficiency by dihydropiridine antagonists of calcium in patients with coronary artery bypass]. / Vozmozhnosti korrektsii koronarnoi nedostatochnosti digidropiridinovymi antagonistami kal'tsiia u bol'nykh, perenesshikh aortokoronarnoe shuntirovanie.

AIM: To study antiischemic and antianginal efficiency of adalat and its prolonged form adalat SL, dihydropiridin antagonists of calcium, in patients 1-3 years after surgical correction of stenosing coronary atherosclerosis. MATERIAL AND METHODS: The drugs were tried in 40 patients with angina of effort (functional class II-III) with a satisfactory inotropic function of the left ventricle 1 to 3 years after coronary artery bypass surgery (CABS). Myocardial circulation was measured with one-photon emission computed tomography using 99m-Tc-MIBI (CT). RESULTS: A 3-week therapy with adalat reduced the number of anginal attacks, nitroglycerin requirement, enhanced exercise tolerance. CT showed that myocardial blood flow significantly improved. CONCLUSION: Adalat proved to be effective in patients after CABS. Its prolonged form adalat SL is preferable.

Blood pressure, ventricular volume and number of cardiomyocyte nuclei in rats fed for 12 months on diets differing in fat composition.

Blood pressure (BP), body mass (BM), ventricular volume (V[vent]) and the number of ventricular cardiomyocyte nuclei (N[vcn]) were analysed in rats fed different dietary fats. A total of 20 Wistar male rats were studied from 21 days old to 12 months of age and divided in the groups: soybean oil (S), canola oil (CA), lard and egg yolk (LE) and canola oil+lard and egg yolk (CA+LE). The diets had the same basal diet that included cornstarch, casein, maize, egg white and mineral and vitamin mixtures. At the moment of the sacrifice, the LE group had the greatest BP and V[vent] which was significantly higher than the other groups, and the S group had the greatest BM. The myocardial structure was apparently normal in the S and CA groups while it showed areas of diffuse interstitial fibrosis and hypertrophied cardiomyocytes in the LE group, and intramyocardial coronaries with thick tunica media and little interstitial fibrosis in CA+LE group. The N[vcn] was significantly higher in the CA group and it was lower in the LE group. These results suggest that the different dietary fats affect the myocardial structure, and the canola oil diet reduces the cardiomyocyte loss in the old rats.

Dose dependency of L-arginine in neonatal myocardial protection: the nitric oxide paradox.

OBJECTIVES: Recent experimental studies have suggested that enriching cardioplegic solution with L-arginine improves myocardial protection by increasing nitric oxide production. Nitric oxide, however, also generates the toxic oxygen-derived free radical peroxynitrite; thus these beneficial effects may be dose dependent, especially in vulnerable (stressed) hearts. METHODS: Fifteen neonatal piglets underwent 60 minutes of ventilator hypoxia (inspired oxygen fraction 8%-10%) followed by 20 minutes of normothermic ischemia on cardiopulmonary bypass (stress). They were then protected for 70 minutes with multiple doses of blood cardioplegic solution. In 5 (group 1), the cardioplegic solution contained no L-arginine, in 5 (group 2), it was enriched with a 4 mmol/L concentration of L-arginine, and in 5 (group 3), a 10 mmol/L concentration of L-arginine. Myocardial function was assessed by means of pressure volume loops and expressed as a percentage of control, and coronary vascular resistance and conjugated diene production were measured during infusions of cardioplegic solution. RESULTS: Compared with the protection afforded by blood cardioplegic solution without L-arginine (group 1), the addition of a 4 mmol/L concentration of L-arginine (group 2) significantly improved myocardial protection, resulting in complete return of systolic function (end-systolic elastance 38% vs 100%; P <.001 vs 4 mmol/L L-arginine) and preload recruitable stroke work (40% vs 100%; P <. 001 vs 4 mmol/L L-arginine); minimal increase in diastolic stiffness (239% vs 158%; P <.001 vs 4 mmol/L L-arginine); and lower coronary vascular resistance, conjugated diene production, and myeloperoxidase activity (P <.001 vs 4 mmol/L L-arginine in each case). Conversely, supplementing the cardioplegic solution with a 10 mmol/L dose of L-arginine (group 3) negated these beneficial effects, resulting in depressed systolic function (end-systolic elastance 41% +/- 2%; P <.001 vs 4 mmol/L L-arginine) and preload recruitable stroke work (40% +/- 2%; P <.001 vs 4 mmol/L L-arginine); increased diastolic stiffness (246% +/- 7%; P <.001 vs 4 mmol/L L-arginine); and higher conjugated diene production, myeloperoxidase activity, and coronary vascular resistance (P <.001 vs 4 mmol/L L-arginine in each case). CONCLUSIONS: Enriching cardioplegic solution with a 4 mmol/L concentration of L-arginine significantly improves myocardial protection by reducing oxygen-derived free radical formation by white blood cells, thus preserving vascular and myocardial function. However, these beneficial effects are dose dependent because 10 mmol/L concentrations of L-arginine increase oxygen-derived free radical production, resulting in vascular and myocardial dysfunction.

Poststorage diastolic abnormalities of heart transplants: is vascular dysfunction or myocardial contracture the culprit?

BACKGROUND: Vascular dysfunction and myocardial contracture can both contribute to posttransplantation diastolic abnormalities commonly exhibited by heart transplants, but their respective importance remains incompletely elucidated. To address this issue, we assessed the effects of supplementing a new heart preservation solution, Celsior, with a nitric oxide precursor (L-arginine) and a compound known to uncouple excitation from contraction (2, 3-butanedione monoxime). METHODS: Fifty isolated buffer-perfused rat hearts were divided into four groups. In group 1, hearts were arrested with St. Thomas' Hospital solution No. 2 (Plegisol) and stored in normal saline solution. In group 2, Celsior solution was used for cardiac arrest and storage. Group 3 hearts were arrested with and stored in Celsior solution supplemented with 2 mmol/L of L-arginine. In group 4, Celsior solution used for arrest and storage was supplemented with both 2 mmol/L of L-arginine and 30 mmol/L of 2, 3-butanedione monoxime. All hearts were stored for 10 hours, subsequently reperfused for 1 hour on a Langendorff column, and left ventricular pressure-volume curves were constructed. 5-Hydroxytryptamine (10(-7) mol/L) and papaverine (5 x 10(-6) mol/L) were used to test changes in endothelium-dependent and endothelium-independent coronary vascular responses, respectively, and compared with those obtained during the preischemic period. RESULTS: After 10 hours of cold storage, a major postischemic contracture was found in group 1. Left ventricular diastolic function was best preserved in group 4 at the end of storage and over the entire period of reperfusion. Coronary vasodilatory response to 5-hydroxytryptamine was completely lost in all groups after cold storage and reperfusion. Endothelium-independent vasodilatory response to papaverine was preserved in 2, 3-butanedione monoxime-treated hearts, whereas it was reduced in other groups. CONCLUSIONS: Our results suggest that myocardial contracture plays a major role in posttransplantation diastolic abnormalities shown by cardiac allografts. Alleviation of contracture significantly improves the responsiveness of coronary smooth muscles but does not affect that of the vascular endothelium which needs to be handled by separate interventions.

Cardiovascular effect of oral calcium supplementation: echocardiographic study in patients with essential hypertension.

Oral calcium (Ca) supplementation mildly reduces blood pressure. The authors studied the effects of Ca supplementation on the cardiovascular system in patients with mild to moderate essential hypertension. Twelve patients aged forty-nine to seventy years (7 men and 5 women, mean age with 60.3 +/- 7.2 years) participated. The investigators orally administered Ca (1.0 g/day for one week) under hospitalization, adding to a dietary intake of Ca (0.6 g/day). Left ventricular function and systemic arterial compliance were evaluated by M-mode and pulsed Doppler echocardiographies before and after seven days of Ca supplementation. Left ventricular contractility and afterload were not changed. Preload indicated by end-diastolic volume was significantly decreased after Ca supplementation (109.6 +/- 8.5 vs 107.3 +/- 8.2 mL, P < 0.05). Myocardial relaxation evaluated by IIa-mitral valve opening time (87.7 +/- 6.7 vs 82.1 +/- 6.2 ms, P < 0.01) and maximum descending rate of the left ventricular posterior wall (10.6 +/- 1.0 vs 12.4 +/- 1.0 cm/s, P < 0.01), and atrioventricular net compliance assessed by the descending slope of rapid filling flow in the left ventricular inflow tract (2.63 +/- 0.24 vs 2.26 +/- 0.17 m/s2, P <0.05), as well as systemic arterial compliance (2.05 +/- 0.20 vs 2.73 +/- 0.26 mL/mmHg, P < 0.01) were significantly improved by Ca supplementation. Oral Ca supplementation improved the disturbed left ventricular diastolic function and systemic arterial compliance.

Oxidative stress as a mechanism of cardiac failure in chronic volume overload in canine model.

We investigated the effects of chronic volume overload in the absence or presence of vitamin E supplements on the cardiac function and contractility, cardiac malondialdehyde (MDA)--a lipid peroxidation product--cardiac antioxidant enzyme activity and antioxidant reserve in canine model. The dogs were divided into three groups of seven dogs each: group I, control; group II, mitral regurgitation (MR) of 4 months duration; and group III, MR of 4 months duration receiving vitamin E (40 U/kg/daily) orally. MR was created by detaching two or more chordae tendinae to raise left atrial pressure to 2.5 to three times normal. MR produced a decrease in the index of myocardial contractility with little change in myocardial function. Decrease in myocardial (left and right ventricles) contractility was associated with an increase in cardiac MDA, and a decrease in cardiac antioxidant reserve and antioxidant enzyme activity. Prevention of volume overload-induced decrease in myocardial contractility by vitamin E was associated with a decrease in cardiac MDA and an increase in cardiac antioxidant reserve and glutathione peroxidase activity towards control levels. Superoxide dismutase and catalase activity remained depressed in vitamin E-treated group. The results indicate that chronic volume overload decreases the contractility of both right and left ventricles and is associated with oxidative stress in both ventricles. These results support the hypothesis that oxygen free radicals are involved in the chronic volume overload-induced cardiac depression.

Effect of short-term antihypertensive therapy on left ventricular wall tension. A double-blind comparison of isradipine and nifedipine.

The comparative efficacy of the calcium antagonists isradipine and nifedipine in reducing left ventricular peak systolic wall tension was assessed in 25 patients with essential hypertension (20 men, 5 women; mean age: 49 years). After 2 weeks of treatment with either isradipine (2.5 mg twice daily) or slow-release nifedipine (20 mg twice daily), blood pressure was similarly reduced in both groups of patients whereas the thickness of the interventricular septum and left ventricular free wall did not change. Echocardiographic end-diastolic volume of the left ventricle showed no change whereas end-systolic volume significantly decreased with isradipine, but not with nifedipine retard. This led to a significant reduction in peak systolic wall tension in the isradipine group, but not in the nifedipine group. In conclusion, antihypertensive treatment with isradipine produces a reduction in peak systolic wall tension which is not seen with nifedipine, probably because of its negative inotropic effect.

Increased blood kynurenine level as a factor inhibiting the therapeutic effect of antihypertensive agents in combined long-term treatment of essential hypertension.

Results of a three-year antihypertensive combined treatment of 24 male patients with essential hypertension aged 35-55 years are presented. In all patients the blood serum kynurenine level after tryptophan load was determined before treatment and after the 1st, 2nd and 3rd years of therapy. It was found that in a part of patients the long-term administration of antihypertensive drugs led to an increased accumulation of kynurenine as a manifestation of pyridoxal-5-phosphate deficiency. The development and preservation of an increased blood kynurenine level interferes with the positive effects of antihypertensive therapy as regards both blood pressure and left ventricular myocardial mass reduction.

[Regression of left heart hypertrophy in hypertensive patients as a result of antihypertensive therapy]. / Regression der Linksherzhypertrophie Hochdruckkranker durch antihypertensive Therapie.

In a previous study (1) we could show a significantly more pronounced reversal of LVH with metoprolol than with gallopamil, whereas the combined therapy with atenolol and nifedipine was even more effective. We now report in 121 previously untreated hypertensive patients the longterm effect of the beta-blocker metoprolol (200 mg/die); 25 patients, mean age 43.6 yrs., follow-up 32.1 +/- 3.5 months, group A); the calcium antagonist gallopamil, 26 patients, mean age 49.7 yrs., follow-up 36.2 +/- 2.6 months, group B); the combined therapy with 50 mg atenolol and 20 mg nifedipine, 35 patients, mean age 44.5 yrs., follow-up 31.7 +/- 1.1 months, group C); 200 mg acebutolol and 20 mg nifedipine, mean age 52.1 yrs., follow-up 31.8 +/- 1.8 months, group D); 50 mg atenolol and 10 mg enalapril, mean age 43.3 yrs., follow-up 31.9 +/- 1.3 months, group E). Similar results were obtained for intraventricular septal and posterior wall thickness. Left ventricular enddiastolic dimensions remained unchanged but fractional shortenings were significantly (p less than 0.05-p less than 0.01) increased after 32 months of treatment.

Effect of the second-generation calcium channel blocker nisoldipine on left ventricular contractility in cardiac failure.

We studied the acute effects of nisoldipine, a new second-generation calcium channel-blocking drug, on cardiac hemodynamics and left ventricular (LV) contractility in 10 patients with grade 2 to 4 cardiac failure. Pressures were measured from an arterial line and a flow-guided catheter in the pulmonary artery, cardiac output by thermodilution, and LV ejection fraction simultaneously by radionuclide ventriculography. Ventricular loading conditions were altered by sublingual nitroglycerin to facilitate construction of LV end-systolic pressure (radial stress)-volume and stress-shortening curves. Nisoldipine, given by continuous intravenous infusion (0.12 micrograms/kg/min), reduced mean arterial pressure (p = 0.001), systemic vascular resistance (p less than 0.05), and the double product, a measurement of myocardial oxygen demand (p less than 0.01). Cardiac index, stroke index, and LV ejection fraction increased in 8 of the 10 patients. LV contractility was initially greatly reduced and was unchanged or slightly decreased during the administration of nisoldipine. Emax, the slope of the end-systolic pressure-volume curve, was unaltered in half of the patients and decreased in the others (NS), whereas the end-systolic stress-shortening curve did not change. In summary, nisoldipine has a potentially useful acute hemodynamic profile in patients with cardiac failure; it increases forward blood flow in most patients, decreases the determinants of myocardial oxygen demand, and produces little measurable changes in the inotropic state of the left ventricle.

[Effect of corinfar on hemodynamics in ischemic heart disease]. / Deistvie korinfara na gemodinamiku pri ishemicheskoi bolezni serdtsa.

During examination on the basis of a double blind test corinfar administered sublingually at a dose of 10-30 mg decreases significantly in 1 hour systolic and diastolic arterial pressure, general peripheral resistance, increases the heart rate, the blood stroke and minute volumes and a medium rate of the circular contraction of the muscular fibers in CHD patients. An increase in systolic discharge is associated with lowered arteriole tension.

[Verapamil, diltiazem or nifedipine in severe left ventricular functional disorder? A comparative study of the immediate hemodynamic effects]. / Verapamil, Diltiazem oder Nifedipin bei schwerer linksventrikulärer Funktionsstörung? Eine Vergleichsstudie der hämodynamischen Akutwirkungen.

High doses of verapamil, diltiazem or nifedipin were administered to three groups of eight patients each, with severely abnormal left-ventricular (LV) function (mean ejection fraction 0.29). Various haemodynamic measurements were made immediately before and 30 minutes after drug administration: LV ejection fraction, ratio of peak systolic pressure to endsystolic volume index, stroke index, pulmonary capillary closing pressure, and maximal diastolic filling rate. None of these were reduced. In fact, ejection fraction rose by a mean of 0.05, stroke index by a mean of 5 ml/m2, while p.c. closing pressure and contractility did not alter significantly. Verapamil and diltiazem reduced the pressure X rate product (an important determinant of oxygen consumption); nifedipine reduced total systemic resistance. It is concluded that verapamil and diltiazem can be used with advantage in cases of unstable angina, if there are severe abnormalities of LV function; they are to be preferred to beta-blockers in this situation. Nifedipin is the calcium antagonist of choice in hypertension and abnormal LV function.

Afterload reduction with nifedipine in aortic insufficiency.

The acute hemodynamic effects of nifedipine were assessed in 12 patients with severe aortic insufficiency during control conditions and 30 minutes after administration of nifedipine (20 mg sublingually). Left ventricular end-diastolic pressure decreased from 19 +/- 8 (mean +/- standard deviation) to 9 +/- 5 mm Hg (probability [p] less than 0.0001), mean aortic pressure from 98 +/- 12 to 80 +/- 9 mm Hg (p less than 0.00001), systemic vascular resistance from 1,135 +/- 280 to 794 +/- 176 dynes . s. cm-5 (p less than 0.0002) and rate-pressure product from 11,732 +/- 1,727 to 10,022 +/- 1,103 mm Hg beats/min (p less than 0.01). Forward cardiac index increased by 24 percent, from 3.8 +/- 1.1 to 4.4 to 0.8 liters/min per m2 (p less than 0.04). Left ventricular end-diastolic volume, ejection fraction and total stroke work index did not change significantly. Regurgitant fraction, measured in five patients, changed parallel with systemic vascular resistance. Left ventricular function was maintained while both preload and afterload were decreased. Regurgitant flow was moderated and myocardial oxygen demand decreased. This hemodynamically favorable condition, due to nifedipine, is clinically important and suggests the need for further therapeutic trials.

[Clinical experiences with the acute normovalemic hemodilution (author's transl)]. / Klinische Erfahrungen mit der akuten normovolämischen Hämodilution

Acute normavolemic hemodilution is a mean of autotransfusion and allow hepatitis prophylaxis in major surgical procedures which general require homologous blood transfusions. The dilutional drop in blood viscosity is followed by an increased cardiac output, while blood pressure and heart rate remain stable. The CO incerase compensates for the reduced oxygen capacity of the diluted blood. Hemodilution was applied in a total of 88 patients. In 46 cases thorough circulatory and laboratory investigations were performed. While an average of 1785 ml blood was withdrawn and replaced synchronically by plasma substitutes, hematocrit was lowered to 24.8% mean and CO rose from 4.4 to 6.01 l/min. In one half of the patients side reactions were observed that occurred in combination as a syndrome in 8 patients: rise in systemic blood pressure and pulmonary artery pressure, disproportional CO increase, peripheral vasoconstriction, and ST-depression in ECG. The possible pathomechanisms of these side reactions are discussed. A sympathetic adrenergic reaction could be excluded by catecholamine estimation. Hyposia may be assumed to be the more probable reason. Since severe side reactions only occured at hematocrit levels below 26%, the dilution waslimited lately to hct 27%. Patients with coronary heart disease, age greater than 70 years, and anemia less than 12 g% hgb were excepted. In 70% of major surgical procedures, e.g. colonic surgery, homologous blood becomes necessary, in 50% in the amount of 2-4 units. The corresponding blood loss of 1000-2000 ml may be compensated by acute normovolemic hemodilution and autotransfusion. In fact, only 15% of our patients required homologous blood transfusions.

Improved myocardial performance following high 2-3 diphosphoglycerate red cell transfusions.

Twenty-two matched coronary bypass surgery (CABS) patients were randomly divided into two groups; 11 patients in the control group received CPD-stored or fresh blood (mean age, 5.5 days) containing 70 percent of normal 2-3 diphosphoglycerate (2-3 DPG) and 11 patients received 2-3 DPG-enriched previously frozen, washed, concentrated red cells (2-3 DPG 150 percent of normal). Coming off cardiopulmonary bypass, when given a volume load, the high 2-3 DPG patients had a significant increase in cardiac index (2.95 L. per minute vs. 2.18 L. per minute, p smaller than 0.001) at similar filling pressures. At this time body oxygen consumption, in vivo P50, red cell 2-3 DPG, and arterial-venous oxygen content difference were all increased, but P minus vo2 was normal. Improved oxygen delivery occurred without decreasing mixed venous oxygen tension. The results suggest that, with volume loading, function in the heart with coronary artery disease is limited in part by available oxygen. By decreasing oxygen affinity for hemoglobin by altering red blood cells biochemically, myocardial performance can be improved safely.