Sebastian Huber

Nifedipine reduces the incidence of myocardial infarction and transient ischemia in patients undergoing coronary bypass grafting.

A randomized study was performed on 104 patients undergoing elective coronary artery bypass grafting to examine whether the infusion of nifedipine (n = 53) reduces the incidence of perioperative myocardial ischemia and necrosis in the early postoperative period. Continuous hemodynamic and three-channel Holter monitoring was performed for 24 hours and serial assessment of serum enzymes and 12-lead electrocardiography were performed for 36 hours postoperatively. Nifedipine (minimum dose, 10 micrograms/kg/hr for 24 hours) was applied from the onset of extracorporal circulation. The control group (n = 51) received nitroglycerin (minimum dose, 1 micrograms/kg/min for 24 hours). Using the combined analyses of electrocardiography and Holter recordings, myocardial ischemia was defined as being either a transient ischemic event (TIE), transient coronary spasm (TCS), or myocardial infarction (MI). The two groups did not differ with respect to preoperative New York Heart Association classification, age, history of myocardial infarction, extracorporal circulation and aortic cross-clamp time, number of distal anastomoses, or systemic and pulmonary hemodynamics. The incidence of perioperative myocardial ischemia was substantially lower in the nifedipine than in the nitroglycerin group [TIE: three of 53 patients (6%) versus nine of 50 patients (18%), p less than 0.001; MI: two of 53 patients (4%) versus six of 50 patients (12%), p less than 0.001; and TCS: none of 53 patients (0%) versus two of 50 patients (4%), p = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

Infusion of nifedipine after coronary artery bypass grafting decreases the incidence of early postoperative myocardial ischemia

We performed a randomized study on patients undergoing elective coronary bypass grafting to examine whether postoperative infusion of nifedipine (n = 25) could reduce the incidence of isolated transient myocardial ischemia, myocardial infarction, or both. The control group (n = 25) received nitroglycerin. Hemodynamic and Holter monitoring and serial assessment of enzymatic and electrocardiographic changes were performed for all patients. Both groups showed comparable preoperative and operative data. The incidence of myocardial infarction was significantly lower in the nifedipine group (n = 1) as compared with the control group (n = 4), whereas the number of patients with isolated transient myocardial ischemia was similar in both groups (nifedipine, 3; control, 4). At the time of peak activity, levels of creatine kinase (350 +/- 129 versus 511 +/- 287 IU/mL), creatine kinase-MB (8.4 +/- 5.4 versus 17.1 +/- 11.0 IU/mL), and glutamate-oxaloacetate-transaminase (30.4 +/- 4.4 versus 41.0 +/- 7.9 IU/mL) were markedly lower in the nifedipine group (p less than 0.05). We conclude that infusion of nifedipine after elective coronary artery bypass grafting effectively decreases the incidence of myocardial infarction and the extent of myocardial necrosis during the early postoperative period.

Simultaneous assessment of cardiac output with pulsed Doppler and electromagnetic flowmeters during cardiac stimulation

The aim of this study was to test the accuracy of cardiac output assessment by Doppler and electromagnetic flowmetry in dogs during states of (1) marked enhancement in cardiac output, which was obtained by means of either isoprenaline infusion or treadmill exercise, or (2) reduction in cardiac output obtained by administration of phenylephrine. Additionally, in vitro comparisons were undertaken between Doppler and electromagnetic flow-probes and assessment of flow by direct volumetric measurement. These in vitro experiments showed a good correlation between timed volume collections and electromagnetic flow assessment up to high flow velocities. Doppler flow measurements underestimated the flow at high velocities. In both the resting dog and after phenylephrine, that is, at states with low heart rate and cardiac output, the waveforms of electromagnetic flow and Doppler velocity were similar for both phasic and mean flow, respectively. During states of cardiac stimulation Doppler flow showed a decrease in maximum velocity in the ascending aorta. Due to this decrease in peak flow velocity, mean Doppler blood flow did not increase despite of increased heart rate. This result cannot be explained on the basis of the deviation of Doppler measurements at high velocities in the in vitro experiments. Although our results are in contradiction with earlier studies, electromagnetic assessment seems to be more reliable in blood flow measurements in the ascending aorta. Hence, Doppler flow measurements should not be used uncritically for such quantitative flow assessment in large vessels as determination of cardiac output.

Oral NG-nitro-L-arginine in conscious dogs: 24 hour hypertensive response in relation to plasma levels

SummaryHaemodynamic changes after oral administration of 30 mg/kg NG-nitro-L-arginine (L-NNA) were studied in conscious chronically instrumented mongrel dogs throughout a 24 h observation period in order to evaluate the long-term efficacy of L-NNA-induced inhibition of endothelium-dependent relaxation and its relation to plasma L-NNA level. Diastolic blood pressure remained elevated for the entire 24 h observation period, but systolic blood pressure was raised only up to the 6 h value. The hypertensive response was accompanied by bradycardia. The increase in blood pressure and the plasma L-NNA level both reached their maxima at 3 h. The plasma L-NNA level at the end of the observation period was diminished by only 21.7% with respect to the maximum increase, whilst the maximum increase in mean arterial blood pressure was attenuated by 72.2% at 24 h. These data show a dissociation between plasma L-NNA level and the respective blood pressure.

Cardiovascular and side effects of flesinoxan in conscious hypertensive dogs. Modulation by prazosin

Previous studies on anaesthetized animals indicate that flesinoxan exerts hypotensive effects via stimulation of central 5-HT1A receptors. The purpose of the present study was to investigate the cardiovascular and side effects of flesinoxan in conscious, renal hypertensive dogs at rest and during exercise. Animals were pretreated with prazosin (2.5 or 7.5 nmol/kg) to verify a reduction of dose-dependent side effects, as occurred in normotensive dogs. A decrease in blood pressure without reflex tachycardia was observed only with the lower dose of flesinoxan (0.1 mumol/kg). The higher dose (0.2 mumol/kg) led to an increase in blood pressure and heart rate. The increase in heart rate during exercise was diminished by 0.2 mumol/kg flesinoxan. Pretreatment with prazosin resulted in an additive hypotensive effect at rest. Side effects, occurring primarily after the higher dose of flesinoxan, were not influenced by prazosin. It is concluded that flesinoxan is not likely to be efficacious in antihypertensive therapy.