Nitric oxide is synthesized from an essential amino acid L-arginine in vascular endothelial cells, vascular smooth muscle cells, and cardiac tissues. Nitric oxide induces vasorelaxation, anti-growth effects, and negative inotropic effects. Therefore, nitric oxide is regarded as an important regulator for the cardiovascular system including atherosclerosis. This brief article reviews new information on nitric oxide, and discusses the clinical implications of nitric oxide for cardiovascular disease.

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Plasma fibrinopeptide A (FPA), fibrinopeptide B β 15-42 (FPB β 15-42), and fibrin/fibrinogen degradation products (FDP) were measured before treatment for the determination of the diagnostic value of coagulation and fibrinolytic molecular markers in patients with pulmonary thromboembolism (n=16) and myocardial infarction (n=8). The levels of all markers measured prior to treatment were significantly higher in patients with pulmonaly thromboembolism than those in the patients with acute myocardial infarction, irrespective of shock (FPA, 40.0±22.1vs. 17.9±24.8ng·ml^-1, p=0.0085; FBP β 15-42, 34.1±20.8vs. 12.8±8.7ng·ml^-1, p=0.0044; FDP, 37.5±36.7vs. 6.3±6.5μg·ml^-1, p=0.0022). All of the markers had high sensitivity, specificity and predictive values for the diagnosis of pulmonary thromboembolism when the cut off points of FPA, FPB β 15-42 and FDP were set at 20ng·ml^-1, 15ng·ml^-1 and 10μg·ml^-1, respectively. We concluded that: 1) the markers measured in this study are all useful for the differential diagnosis of pulmonaly thromboembolism and acute myocardial infarction, and 2) pulmonaly thromboembolism is the most likely diagnosis when any of the following is positive: FPA>20ng·ml^-1, FPB β 15-42>15ng·ml^-1 or FDP>10μg·ml^-1.

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Cyclic 3', 5'-guanosine monophosphate (cGMP) stimulated by increased nitric oxide (NO) is responsible for the hypotension associated with low vascular tone and disturbance of gas exchange in a septic hyperdynamic state. We hypothesized that methylene blue (MB), a soluble guanylate cyclase inhibitor, would improve systemic circulation and gas exchange. In order to achieve this aim, we administered MB to eight septic patients in a hyperdynamic state (cardiac index>3.5L·min.^-1·m^-2).
Hemodynamic data before MB infusion showed low vascular resistance and hypotension despite the administration of catecholamines. A high respiratory index (RI) and intrapulmonary shunt (QVA/QT) were also demonstrated. MB 2mg·Kg^-1 was continuously administered for 30 minutes. Systemic and pulmonary hemodynamics and respiratory parameters were measured and blood cyclic 3', 5'-adenosine monophosphate (cAMP) and cGMP were also assessed before, at the end of, and one hour, two hours and 24 hours after MB infusion.
Mean arterial pressure (mAP) and the systemic vascular resistance index (SVRI) increased significantly, whereas mean pulmonary arterial pressure (mPAP), the pulmonary vascular resistance index (PVRI), Q_VA/Q_t and RI did not change following MB administration. MB significantly incerased mAP and SVRI up to 24 hours with the maximum increase occurring at the end of MB infusion. The blood cGMP levels decreased significantly two hours after MB administration, but the blood cAMP levels showed no significant change.
These results suggest that MB improves systemic circulation but does not alter gas exchange in patients with septic shock.

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44 patients underwent surgery on a lower extremity under the use of tourniquet. Blood samples were obtained from the radial artery and the femoral vein on the involved leg, at the time of the inflation of tourniquet and one hour after its release. Activated partial thromboplastin time (APTT), prothrombin time (PT), fibrinogen (Fbg), antithrombin III (AT III), solubule fibrin monomer complex (SFMC), thrombin-antithrombin III complex (TAT), D-dimer, plasminogen (Plg), α₂-plasmin-inhibiter (PI) and plasmin-plasmin inhibitor complex (PIC) were measured as analyses of coagulofibrinolysis. Total CK activity (CK), CK isoform ratio (IR) and myoglobin (Mb) were measured as a indicator of tissue injury.
TAT denoted always a significantly higher value in venous sample. After the release of tourniquet, APTT shortened and PT ratio decreased both significantly. Fbg and AT III showed significant decreases and TAT significantly increased. Plg and PI showed significant decreases and PIC significantly increased. CK, IR and Mb showed significant increases. TAT showed positive correlations with CK, IR and Mb. PIC showed positive correlation with CK, IR and Mb. Only IR in venous sample was correlated with the duration of tourniquet.
The values of APTT, PT, Fbg, AT III, TAT, Plg, PI and PIC suggest changes caused by a local hypercoagulofibrinolytic state. We should follow serial changes of these values to estimate the coagulofibrinolytic system in the patient with a local hypercoagulofibrinolytic state.

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To assess the efficacy of percutaneous cardiopulmonary support system (PCPS), we studied 16 patients supported urgently by PCPS (11 males, 5 females, mean age: 61 years). The reasons for indicating PCPS were cardiogenic shock in 10 patients, cardiac rupture in 3 patients and ventricular fibrillation (Vf) in 3 patients. Fourteen patients (88%) had ischemic heart disease (IHD). The remaining 2 patients had dilated cadiomyopathy and valvular heart disease, respectively. In five patients (31%), PCPS was used in combination with intraaortic balloon pump support. Finally, 4 patients (25%) survived: 1 patient with Vf and 3 patients with IHD. All of these 3 patients with IHD succeeded in coronary revascularization under the support of PCPS. The remaining patient succeeded in the termination of Vf after operating PCPS. No patient studied in the present study had vascular injury. However, 2 patients had severe mediastinal bleeding due to cardiopulmonary resuscitation, one of whom died of hemorrhagic shock. In conclusion, early coronary revascularization following PCPS is important to recover from cardiogenic shock because cardioprotective effect of PCPS is poor. Anti-coagulation therapy in operating PCPS sometimes induces severe hemorrhagic complications, to which we should pay attention.

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The aim of this study was to evaluate cardiac functions following cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest survivors.
Twelve of 151 patients who received CPR from October 1990 to February 1994 were assessed by a twelve-lead electrocardiograms (ECG), two-dimensional echocardiograms and hemodynamics measured with a Swan-Ganz catheter.
ECG on admission showed ventricular fibrillation in 5 patients and cardiac standstill in 6. Counter-shock was successfully performed in 7 patients. Post-CPR ECGs showed elevations of the ST-segments in eight patients and abnormal Q waves in one. One week later, the number of patients with the former phenomenon decreased, whereas those with the latter and negative T waves increased.
Post-CPR echocardiograms showed segmental left ventricular (LV) wall motion abnormalities in eight patients and global hypokinesis in one. One week later, LV wall motion normalized in two of these nine patients.
Decreased cardiac output and/or increased pulmonary artery wedge pressure were common when CPR exceeded 30 minutes.
In conclusion, the majority of cardiac arrest survivors showed significant left ventricular dysfunction indicating the need to evaluate cardiac function in post-CPR patients.

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A case of thrombotic thrombocytopenic purpura (TTP) is reported. The patient (32yrs) underwent cesarean section because of severe eclampsia, then developed TTP in the postpartum period. She was treated aggressively with plasma exchange, antiplatelet agents, anticoagulants and steroids. Her platelet count recovered after the second plasma exchange and her condition was well managed for about 10 days. However, TTP became worse on the 21st postoperative day due to infection. Despite further treatment, including plasma exchange, the patient died on the 29th postoperative day.
Nine cases of TTP in pregnancy and the postpartum period from the past 10 years are also reviewed.

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