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Biomedical subjects

J A Kline

Publications and source records attributed to J A Kline.

At least 19 recordsLinked to original sources
PubMed2006

Contrast nephropathy following computed tomography angiography of the chest for pulmonary embolism in the emergency department.

OBJECTIVE: To estimate the frequency of contrast nephropathy after computed tomography angiography (CTA) to rule out pulmonary embolism (PE) in the emergency department (ED) setting. METHODS: We prospectively followed patients undergoing CTA for PE, while in the ED, for 45 days. Patients who refused follow-up or were receiving hemodialysis were excluded. Severe renal failure was defined as an increase in creatinine > or = 3.0 mg dL(-1) or a need for hemodialysis within the follow-up period. Patients were also followed for laboratory-defined contrast nephropathy, defined as an increase in creatinine of > 0.5 mg dL(-1) or > 25%, within seven days following CTA. RESULTS: A total of 1224 patients were followed, and 354 [29%, 95% confidence interval (CI): 26-32%] patients had paired (preCTA and post-CTA) creatinine measurements. None developed renal failure (0/1224; 0%, CI: 0-0.3%). 44 patients developed laboratory-defined contrast nephropathy, corresponding to an overall frequency of 4% (44/1224; CI: 3-5%) and 12% (44/354; 95% CI: 9-16%) among those with paired creatinine measurements. CONCLUSIONS: Following CTA for PE, the incidence of severe renal failure was very low, but the incidence of laboratory-defined contrast nephropathy (4% overall and 12% of those with paired measurements) was higher than expected.

Angiography↗
PubMed2004

Metabolic dysfunction and depletion of mitochondria in hearts of septic rats.

Our previous studies indicate that hearts from septic rats have decreased work with oxygen wasting. The present studies test if there is energy deficit, changes in cardiac mitochondrial content and caspase activation during sepsis. Anesthetized, male Sprague-Dawley rats received no surgical treatment (control), laparotomy (sham), or laparotomy with cecal ligation and puncture (CLP) to induce polymicrobial septic shock. Hearts were isolated 12-14 h later. Cardiac work, oxygen consumption, substrate oxidation and energy stores were measured in perfused hearts. Normalized density of mitochondria was determined in ventricles without perfusion by morphometric analysis with electron microscopy. Citrate synthase activity was assessed in homogenates and isolated mitochondria. Cardiac work decreased significantly in CLP (47%), while oxygen consumption and glucose oxidation were unchanged compared with control or sham hearts (oxygen and substrate wasting). Tissue adenosine triphosphate, creatine phosphate and glycogen were lower in CLP hearts (energy deficit). Mitochondrial grid intersects decreased significantly from 151 +/- 8 sham to 130 +/- 4 CLP out of 361 possible intersects and autophagy was observed in CLP hearts. Total activity of citrate synthase decreased in homogenates (99 +/- 8 micromol/min/g wet weight sham vs. 62 +/- 7 CLP, P < 0.05) and in the mitochondrial fraction (27 +/- 1 micromol/min/g wet weight sham to 22 +/- 1 CLP, P < 0.05). Calculated mitochondrial content decreased from 63 +/- 4 mg protein/g wet weight sham to 46 +/- 5 CLP, P < 0.05 (mitochondrial depletion). Caspase-3 activity doubled and tumor necrosis factor alpha content tripled in CLP hearts. CONCLUSIONS. - Oxygen and substrate wasting in CLP occurs with fewer mitochondria and energy deficit, processes that are coincident with caspase-3 activation.

Animals↗
PubMed2004

Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism.

Overuse of the d-dimer to screen for possible pulmonary embolism (PE) can have negative consequences. This study derives and tests clinical criteria to justify not ordering a d-dimer. The test threshold was estimated at 1.8% using the method of Pauker and Kassirer. The PE rule-out criteria were derived from logistic regression analysis with stepwise backward elimination of 21 variables collected on 3148 emergency department patients evaluated for PE at 10 US hospitals. Eight variables were included in a block rule: Age < 50 years, pulse < 100 bpm, SaO(2) > 94%, no unilateral leg swelling, no hemoptysis, no recent trauma or surgery, no prior PE or DVT, no hormone use. The rule was then prospectively tested in a low-risk group (1427 patients from two hospitals initially tested for PE with a d-dimer) and a very low-risk group (convenience sample of 382 patients with chief complaint of dyspnea, PE not suspected). The prevalence of PE was 8% (95% confidence interval: 7-9%) in the low-risk group and 2% (1-4%) in the very low-risk group on longitudinal follow-up. Application of the rule in the low-risk and very low-risk populations yielded sensitivities of 96% and 100% and specificities of 27% and 15%, respectively. The prevalence of PE in those who met the rule criteria was 1.4% (0.5-3.0%) and 0% (0-6.2%), respectively. The derived eight-factor block rule reduced the pretest probability below the test threshold for d-dimer in two validation populations, but the rule's utility was limited by low specificity.

Adult↗
PubMed2003

Contribution of indirect computed tomography venography to computed tomography angiography of the chest for the diagnosis of thromboembolic disease in two United States emergency departments.

Recent reports suggest that physicians in non-ambulatory settings can use indirect CT venography (CTV) of the lower extremities immediately following spiral CT angiography (CTA) of the chest to identify patients with a negative CTA who have thromboembolic disease identified on CTV. We sought to determine the frequency of isolated deep venous thrombosis (DVT) discovered on CTV in emergency department (ED) patients with complaints suggestive of pulmonary embolism (PE) yet having a negative CTA. This study was conducted in a suburban and urban ED where patients with symptoms suspicious for PE were primarily evaluated with CTA and CTV. A total of 800 patients were studied, including 360 from the suburban ED and 440 from the urban ED. 88 (11%) patients were diagnosed with thromboembolic disease by CTA, or CTV, or both. Seventy-three patients had a CTA of the chest that was positive for PE, 42 (5.2%) of whom had evidence of both PE on CTA and DVT on CTV. Fifteen patients (2%, 95% CI = 1-3%) had a negative CTA and were subsequently found to have isolated DVT on CTV, all of whom received anticoagulation therapy. These data suggest that indirect CT venography of immediately following CT angiography of the chest significantly increased the frequency of diagnosed thromboembolic disease requiring anticoagulation in ED patients with suspected PE.

Adult↗
PubMed2001

Diagnostic accuracy of a bedside D-dimer assay and alveolar dead-space measurement for rapid exclusion of pulmonary embolism: a multicenter study.

CONTEXT: A previous study suggested that the combination of a normal D-dimer assay and normal alveolar dead-space fraction is a highly sensitive screening test for pulmonary embolism (PE). OBJECTIVE: To determine if the combination of a normal alveolar dead-space fraction (volume of alveolar dead space/tidal volume </=20%) and a normal whole-blood agglutination D-dimer assay can exclude PE in emergency department (ED) patients. DESIGN: Prospective, noninterventional study conducted in 1998-1999. Study data were obtained prior to standard testing for PE, consisting of radionuclide lung scanning or contrast-enhanced computed tomography and 6-month follow-up plus selective use of venous ultrasonography and pulmonary angiography. Imaging studies were interpreted by blinded observers. SETTING: Six urban teaching hospitals in the United States. PATIENTS: A total of 380 hemodynamically stable ED patients aged 18 years or older with suspected acute PE. MAIN OUTCOME MEASURES: Sensitivity and specificity for PE with a positive test defined as having either alveolar dead-space fraction or D-dimer assay results abnormal. Alveolar dead-space fraction was determined by subtracting airway dead space from physiological dead space (determined using the modified Bohr equation) and D-dimer assay, assayed at bedside using 20 microL of arterial blood. RESULTS: Pulmonary embolism was diagnosed in 64 patients (16.8%), of those 20 had an abnormal D-dimer assay result, 3 had an abnormal alveolar dead-space fraction, 40 had abnormal results in both, and 1 had normal results for both tests. The sensitivity for diagnosis of PE was 98.4% (95% confidence interval [CI], 91.6%-100.0%). Among the 316 patients without PE, both D-dimer and dead-space results were normal in 163, for a specificity of 51.6% (95% CI, 46.1%-57.1%). Posterior probability of PE with normal results on both tests was 0.75% (95% CI, 0%-3.4%). CONCLUSION: In this multicenter study of ED patients, a normal D-dimer assay result plus a normal alveolar dead-space fraction was associated with a low prevalence of PE.

Adult↗
PubMed2001

Pulseless electrical activity with witnessed arrest as a predictor of sudden death from massive pulmonary embolism in outpatients.

BACKGROUND: the objective was to determine clinical characteristics that can quickly distinguish sudden death from massive pulmonary embolism (MPE) from other causes of sudden death. METHODS AND RESULTS: all medical examiner reports from Charlotte, NC from 1992 to 1999 (n=4926) were hand-searched for cases of sudden death which met the inclusion criteria: non-traumatic death, age 18-65 years, transported to an emergency department (ED), and autopsy performed. Supplemental data from ED and prehospital records were retrieved to complete documentation. Data were analyzed by univariate odds ratios (OR) followed by chi-square (chi(2)) recursive partitioning for decision tree construction. Three hundred eighty four cases met inclusion criteria; MPE was the second most frequent cause of cardiac arrest in this cohort (37/384, 9.6%). The mean age of subjects with MPE (40.2+/-11.1 years) was significantly lower compared with non-PE subjects (46.5+/-9.9 years). Pulseless electrical activity was observed as the initial arrest rhythm (primary PEA) in 52/384 (13.5%) subjects. Out of 52 subjects with primary PEA, 28 (53%) died from MPE. Odds ratio data indicated significant association of MPE with female gender, arrest witnessed by medical providers, presence of primary PEA, and return of spontaneous circulation. The most accurate decision rule to recognize MPE consisted of witnessed arrest+primary PEA. This rule generated sensitivity=67.6% and specificity=94.5% and yielded a posttest probability of MPE of 57%. CONCLUSIONS: outpatients with witnessed cardiac arrest and primary PEA carry a high probability of MPE.

Adolescent↗
PubMed2001

Role of fatty acids in the recovery of cardiac function during resuscitation from hemorrhagic shock.

This study tested the hypothesis that removal of fatty acids as a fuel source would improve cardiac efficiency at the expense of reduced cardiac contractile function in the isolated working heart after hemorrhage-retransfusion. Non-heparinized male Sprague-Dawley rats were anesthetized with ketamine-xylazine and were hemorrhaged to a mean arterial blood pressure of 40 mmHg for 1 h. Two-thirds volume of shed blood was reinfused together with 0.9% NaCl in a volume equal to 2.3 times the shed blood volume, followed by continuous infusion of 0.9% NaCl at 10 mL/kg per h for 3 h. Hearts were removed and perfused in closed, recirculating working mode for 60 min to measure hydraulic work and cardiac efficiency. Rates of glycolysis and glucose oxidation were assessed with [5-3H/U-14C] glucose (11 mM) in the absence or presence of 0.4 mM palmitate. Compared to baseline measurements, hemorrhage-retransfusion significantly reduced arterial blood glucose (228+/-7 versus 118+/-12 mg/dL) and non-esterified fatty acid concentrations (0.36+/-0.01 versus 0.30+/-0.02 mM), while elevating blood lactate (0.8+/-0.1 versus 2.5+/-0.4 mM). Perfusion of sham hearts with glucose-only did not alter cardiac work compared to shams perfused with glucose plus palmitate. However, shocked hearts perfused with glucose-only demonstrated a significant reduction in cardiac work compared to shocked hearts perfused with glucose plus palmitate and compared to sham hearts perfused with glucose only (P < 0.05, repeated measures ANOVA). Shocked hearts perfused with glucose plus palmitate showed no reduction in cardiac work compared to shams. Shocked hearts perfused with glucose-only had increased glucose oxidation rates compared to shams perfused with glucose plus palmitate. In sham hearts perfused with glucose-only, myocardial glycogen and triacylglycerol contents were significantly reduced compared to hearts freeze-clamped in situ. These endogenous fuels were not decreased in shocked hearts. These data indicate that hemorrhagic shock renders the heart unable to mobilize endogenous fuels, and suggest that withdrawal of fatty acid oxidation will impair myocardial energy metabolism during resuscitation.

Animals↗
PubMed2001

Research fundamentals: choosing an appropriate journal, manuscript preparation, and interactions with editors.

This article, the last in a series on research methodology prepared by the Research Committee of the Society for Academic Emergency Medicine (SAEM), describes the process of journal selection, manuscript preparation, manuscript submission, and responding to editorial and reviewer comments. Methods for completing each step of this process are described. Following these methods will increase the chance of publishing one's work in the highest-quality and most appropriate journal.

Humans↗
PubMed2001

Identification of prearrest clinical factors associated with outpatient fatal pulmonary embolism.

UNLABELLED: Massive pulmonary embolism (MPE) is an important cause of outpatient sudden death, and description of these patients is critical for identification and treatment. OBJECTIVE: To test whether MPE patients can be distinguished from patients suffering sudden death from other causes based on clinical, demographic, and historical data. The hypothesis was that MPE cases would be more likely to manifest components of a clinical triad of 1) overt dyspnea, 2) alteration of mental status or syncope, and 3) shock index (pulse divided by systolic blood pressure) >0.8. METHODS: Retrospective case-control study of medical examiner data from 1992 to 1999 including all patients with nontraumatic death, aged 18-65 years, transported to an emergency department, with autopsy-determined cause of death. Analysis was done by 95% confidence interval (95% CI) for difference in proportions and multivariate logistic regression for odds ratios. RESULTS: The MPE patients (n = 37) were younger than the control subjects (n = 347) (40.2 vs 46.5 years, unpaired t-test p < 0.001). At least two of the three components of the triad were present in 56.8% of MPE cases vs 3.5% of controls (95% CI for difference in proportions = 37.3% to 68.0%). Significant variables (and odds ratios) for MPE after multivariate analysis included: dyspnea (13.8), shock index >0.8 (23.6), immobilization or fracture (14.6), seen by a physician within two weeks (5.1), and African American female status (6.4). CONCLUSIONS: Patients in this community with fatal MPE were young with risk factors for pulmonary embolism, and commonly manifested components of a triad including: dyspnea, alteration of mental status/syncope, and shock prior to death.

Adolescent↗
PubMed2001

Activation of poly(ADP-ribose) polymerase in severe hemorrhagic shock and resuscitation.

This study examines activation of poly(ADP-ribose) polymerase (PARP) in the ileum during hemorrhage and resuscitation and determines if inhibition of PARP reduces organ dysfunction and metabolic acidosis. Awake, nonheparinized rats were hemorrhaged (40 mmHg, 60 min). Resuscitation used Ringer's solution (2 1/3 x shed volume) and packed red blood cells (2/3 shed volume). Ileal PARP activity was elevated at the end of hemorrhage (3.6-fold) and 10 min of resuscitation (5-fold). The subsequent decline in PARP activity observed after 60 min of resuscitation was not due to cleavage by caspase-3. Ileum permeability increased 10-fold and circulating liver enzymes increased 4- to 6-fold following 60 min of resuscitation in animals pretreated with 3-aminobenzoic acid, a structural analog that does not inhibit PARP. Pretreatment with 3-aminobenzamide (3-AB), a PARP inhibitor, reduced these changes, whereas posttreatment with a bolus of 3-AB was ineffective. Metabolic acidosis, accumulation of lactate, and base deficit was reduced by pretreatment with 3-AB. PARP is activated in the ileum by hemorrhage and by resuscitation. Activation of PARP contributes to organ dysfunction in the ileum and liver and appears to be central to the development of metabolic acidosis.

Acidosis↗
PubMed2001

Biventricular cardiac dysfunction after acute massive pulmonary embolism in the rat.

Cardiac dysfunction has been documented in vivo after acute massive pulmonary embolism (AMPE). The present study tests whether intrinsic ventricular dysfunction occurs in rat hearts isolated after AMPE. AMPE was induced in spontaneously breathing ketamine-xylazine-anesthetized rats by thrombus infusion until mean arterial blood pressure (MAP) was approximately 40% of basal measurement. A hypotensive control group underwent controlled blood withdrawal to produce MAP approximately 40% of basal levels. Shams underwent identical surgical and anesthesia preparation but without pulmonary embolization. Hearts were perfused in isovolumetric mode, and simultaneous right ventricular (RV) and left ventricular (LV) pressures were measured. AMPE caused arterial hypotension with hypoxemia (PO(2) = 50 +/- 14 Torr), acidemia (pH = 7.26 +/- 0.11), and high lactate concentration (6.9 +/- 1.7 mM). Starling curves from both ventricles demonstrated that AMPE significantly reduced ex vivo systolic contractile function in the RV (P = 0.031) and LV (P = 0.008) compared with both the hypotensive control and sham hearts. AMPE did not alter coronary flow or compliance in either ventricle. Soluble tumor necrosis factor-alpha decreased in the RV (P = 0.043) and LV (P = 0.005) tissue. These data support the hypothesis that AMPE produces intrinsic biventricular dysfunction and suggest that arterial hypotension is not the principal mechanism of this dysfunction.

Animals↗
PubMed2001

Assessment of cardiac stress from massive pulmonary embolism with 12-lead ECG.

BACKGROUND: Massive pulmonary embolism (PE) that causes severe pulmonary hypertension can produce specific ECG abnormalities. We hypothesized that an ECG scoring system would vary in proportion to the severity of pulmonary hypertension and would help to distinguish patients with massive PE from patients with smaller PE and those without PE. METHODS: A 21-point ECG scoring system was derived (relative weights in parentheses): sinus tachycardia (2), incomplete right bundle branch block (2), complete right bundle branch block (3), T-wave inversion in leads V(1) through V(4) (0 to 12), S wave in lead I (0), Q wave in lead III (1), inverted T in lead III (1), and entire S(1)Q(3)T(3) complex (2). ECGs obtained within 48 h prior to pulmonary arteriography were located for 60 patients (26 positive for PE, 34 negative for PE) and for 25 patients with fatal PE. RESULTS: Interobserver agreement (11 readers) for ECG score was good (Spearman r = 0.74). The ECG score showed significant positive relationship to systolic pulmonary arterial pressure (sPAP) in patients with PE (r = 0.387, p < 0.001), whereas no significant relationship was seen in patients without PE (r = - 0.08, p = 0.122). When patients were grouped by severity of pulmonary hypertension (low, moderate, severe), only patients with severe pulmonary hypertension from PE had a significantly higher ECG score (mean, 5.8 +/- 4.9). At a cutoff of 10 points, the ECG score was 23.5% (95% confidence interval [CI], 16 to 31%) sensitive and 97.7% (95% CI, 96 to 99%) specific for the recognition of severe pulmonary hypertension (sPAP > 50 mm Hg) secondary to PE. In 25 patients with fatal PE, the ECG score was 9.5 +/- 5.2. CONCLUSIONS: The derived ECG score increases with severity of pulmonary hypertension from PE, and a score > or = 10 is highly suggestive of severe pulmonary hypertension from PE.

Blood Pressure↗
PubMed2001

Pulmonary dysfunction in patients with femoral shaft fracture treated with intramedullary nailing.

BACKGROUND: This study was undertaken to determine whether alveolar dead space increases during intramedullary nailing of femoral shaft fractures and whether alveolar dead space predicts postoperative pulmonary dysfunction in patients undergoing intramedullary nailing of a femoral shaft fracture. METHODS: All patients with a femoral shaft fracture were prospectively enrolled in the study unless there was evidence of acute myocardial infarction, shock, or heart failure. Arterial blood gases were measured at three consecutive time-periods after induction of general anesthesia: before intramedullary nailing and ten and thirty minutes after intramedullary nailing. The end-tidal carbon-dioxide level, minute ventilation, positive end-expiratory pressure, and percent of inspired and expired inhalation agent were recorded simultaneously with the blood-gas measurement. Postoperatively, all subjects were monitored for evidence of pulmonary dysfunction, defined as the need for mechanical ventilation or supplemental oxygen (at a fraction of inspired oxygen of >40%) in the presence of clinical signs of a respiratory rate of >20 breaths/min or the use of accessory muscles of respiration. RESULTS: Seventy-four patients with a total of eighty femoral shaft fractures completed the study. Fifty fractures (62.5%) underwent nailing after reaming, and thirty fractures (37.5%) underwent nailing with minimal or no reaming. The mean alveolar dead-space measurements before canal opening and at ten and thirty minutes after canal opening were 14.5%, 15.8%, and 15.2% in the total series of seventy-four patients (general linear model, p = 0.2) and 20.5%, 22.7%, and 24.2% in the twenty patients with postoperative pulmonary dysfunction (general linear model, p = 0.05). Of the twenty-one patients with an alveolar dead-space measurement of >20% thirty minutes after nailing, sixteen had postoperative pulmonary dysfunction. According to univariate and multivariate analysis, the alveolar dead-space measurement was strongly associated with postoperative pulmonary dysfunction. CONCLUSIONS: According to our data, intramedullary nailing of femoral shaft fractures did not significantly increase alveolar dead space, and the amount of alveolar dead space can predict which patients will have pulmonary dysfunction postoperatively.

Adolescent↗
PubMed2000

New diagnostic tests for pulmonary embolism.

In 1990, the multicenter Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED), sponsored by the National Institutes of Health, compared the diagnostic value of the radioisotopic ventilation-perfusion lung scan (V/Q scan) with that of pulmonary angiography for the diagnosis of pulmonary embolism (PE). Despite the endurance of the radioisotopic V/Q scan as the most widely used test for evaluation of pulmonary embolism (PE), a better screening tool is clearly needed for use in the emergency department. During the past decade, several new modalities have emerged for evaluation of patients with suspected PE. We evaluate the diagnostic utility of the D-dimer test and the alveolar dead space determination as potential screening tests and of spiral computed tomography, magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography as potential confirmatory tests for PE. For comparison, recent data on the diagnostic utility of the alveolar-arterial oxygen gradient and the V/Q scan are included. The potential application of these new tests to a hypothetical ED population is described.

Angiography↗
PubMed2000

Depletion of lactate by dichloroacetate reduces cardiac efficiency after hemorrhagic shock.

We have demonstrated previously that dichloroacetate (DCA) treatment in rodents ameliorates, via activation of the pyruvate dehydrogenase complex, the cardiovascular depression observed after hemorrhagic shock. To explore the mechanism of this effect, we administered DCA in a large animal model of hemorrhagic shock. Mongrel hounds were anesthetized with 1.5% isoflurane and were measured for hemodynamics, myocardial contractility, and myocardial substrate utilization. They were hemorrhaged to a mean arterial pressure of 35 mm Hg for 90 min or until arterial lactate levels reached 7.0 mM (1137 +/- 47 mL or 49 +/- 2% total blood volume). Animals were chosen at random to receive DCA dissolved in water or an equal volume of saline at the onset of resuscitation. Two-thirds of the shed blood volume was returned immediately after giving an equivalent volume of saline. Two hours after the onset of resuscitation, mean arterial pressure was not different between DCA and control groups (79 +/- 3 vs. 82 +/- 3 mm Hg, respectively). Arterial lactate levels were significantly reduced by DCA (0.5 +/- 0.06 vs. 2.0 +/- 0.2 mM). However, DCA treatment was associated with a decreased stroke volume index (0.56 +/- 0.06 vs. 0.82 +/- 0.08 mL/kg/beat) and a decreased myocardial efficiency (19 vs. 41 L x mm Hg/mL/100 g tissue). During resuscitation by DCA, myocardial lactate consumption was reduced (21.4 +/- 3.7 vs. 70.7 +/- 16.3 micromole/min/100 g tissue) despite a three-fold increase in myocardial pyruvate dehydrogenase activity, while free fatty acid levels actually began to rise. Although increased lactate oxidation should be beneficial during resuscitation, we propose that DCA treatment led to a deprivation of myocardial lactate supply, which reduced net myocardial lactate oxidation, thus compromising myocardial function during resuscitation from hemorrhagic shock.

Acidosis, Lactic↗
PubMed2000

Lactate improves cardiac efficiency after hemorrhagic shock.

This study was undertaken to examine the role of lactate on cardiac function and metabolism after severe acute hemorrhagic shock. Anesthetized, nonheparinized rats were bled to a mean arterial pressure of 25-30 mm Hg for 1 h; controls were not bled. Their hearts were removed, and cardiac work and efficiency (work/oxygen consumption) were measured in the isolated working heart mode for 60 min. The hearts were perfused with one of five substrate combinations: 1) glucose (11 mM), 2) glucose + 0.4 mM palmitate, 3) glucose + 0.4 mM palmitate + 8.0 mM lactate, 4) glucose + 1.2 mM palmitate, or 5) glucose + 1.2 mM palmitate + 8.0 mM lactate. After perfusion, hearts were freeze-clamped, and tissue contents of free coenzyme-A (CoA), acetyl CoA, and succinyl CoA were measured, as was myocardial pyruvate dehydrogenase (PDH) activity. The addition of 8.0 mM lactate significantly improved cardiac work in shocked hearts perfused with 0.4 mM palmitate and increased cardiac efficiency in the presence of either 0.4 mM or 1.2 mM palmitate. Compared to control hearts, shocked hearts exhibited a 20-30% decrease in PDH activity. Shocked hearts perfused with lactate demonstrated no increase in acetyl CoA content but did have a significant increase in tissue succinyl CoA compared to control hearts perfused with lactate or shocked hearts perfused without lactate. In the heart recovering from severe hemorrhagic shock, lactate improves cardiac efficiency in the presence of free fatty acids, possibly by a anaplerosis of the tricarboxylic acid cycle.

Acetyl Coenzyme A↗