Biomedical subjects
Publications and source records attributed to P Raatikainen.
A method and a sensor device were developed to detect dynamic laser speckle pattern for monitoring of deformation of pharmaceutical tablets after compression. Temporal variations in optical signal revealed local surface deformation of the ibuprofen and the starch acetate tablets as well as anisotropy of tablet surfaces at the inspection location.
Optical inspection techniques for estimation of surface roughness and surface quality of flat punches, which are used in the pharmaceutical industry for tablet compression, were studied. It was observed that a simple specular reflection technique is useful for surface roughness assessment of flat punches. A diffractive element based sensor was used for the surface quality detection, such as mirror property or flatness, with the aid of image information of a test pattern. It was observed that a new punch may have a poorer surface quality than a used one.
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Optical surface roughness of starch acetate compacts was investigated by specular reflection of a laser beam as a function of angle of incidence. The intensity data was fitted using the model of Gaussian and Lorentzian curves to solve numerical values for optical surface roughness which was observed to be order of 1 microm with the present samples.
It has been suggested that the myocardium is able to recruit endogenous protective mechanisms in response to repeated ischemia and reperfusion. We set out to study whether this is manifested in patients with coronary artery disease in the form of fewer signs of myocardial ischemia during the second of two successive exercise tests and whether any relations exist between ischemia adaptation and findings at cardiac catheterization. Twenty-one patients with typical angina pectoris symptoms underwent two repeated bicycle exercise tests with identical protocols, followed by cardiac catheterization and coronary angiography the next day. The first exercise test was discontinued whenever a 2 mm ST depression in the electrocardiogram (ECG) was achieved or further exercise was limited by symptoms. The second exercise test was performed after disappearance of the symptoms or ST depression or both. Kaplan-Meier survival analysis for the appearance of a 1 mm ST depression demonstrated improved ischemia tolerance during the second test, when the required time for its appearance was significantly longer (6.5 +/- 0.8 min vs 4.5 +/- 0.5 min; p = 0.005). The maximal intensity of anginal pain was lower during the second exercise (2.2 +/- 1.0 min vs 0.7 +/- 0.3 min in Borg's scale; p < 0.001), and the time required for disappearance of the ST depression was shorter after this exercise (3.0 +/- 0.8 min vs 6.2 +/- 0.9 min; p = 0.003), with a similar tendency in the disappearance of angina. The rate-pressure product on the appearance of a 1 mm ST depression was significantly higher during the second test (17,990 +/- 1210 mm Hg x min-1 vs 15,960 +/- 869 mm Hg x min-1; p = 0.009). Eighteen of the patients had three-vessel disease, as evidenced by coronary angiography, and the change in the time required for the appearance of a 1 mm ST depression in the repeated exercise tests was inversely correlated with the severity of the left anterior descending (LAD) coronary artery obstruction (r = -0.61; p = 0.006) and left ventricular end-diastolic pressure (r = -0.50; p = 0.03). No significant correlation with the degree of collateral vessels was found. We conclude that most patients with extensive coronary artery disease are able to increase their tolerance of ischemia during repeated dynamic exercise and that increased vasodilation and oxygen delivery are the major mechanisms for this warm-up phenomenon. On the other hand, collaterals visible in routine resting anglography do not predict the degree of adaptation to ischemia during repeated dynamic exercise.
BACKGROUND: Adenosine has been proposed as one mediator for the preconditioning effect in the myocardium of some animals, but recent investigations have shown that this may not be the mechanism in the rat heart, although the effect itself is clearly demonstrable. The cellular energy state has been shown to be better in preconditioned hearts, and the role of ATP consumption has been discussed. The role of inhibition of mitochondrial F1F0-ATPase as a mechanism for the preservation of ATP in preconditioned hearts remains controversial. METHODS AND RESULTS: Three-minute global ischemia followed by 9 minutes of reperfusion was used to precondition Langendorff-perfused rat hearts, and control hearts were perfused under normoxic conditions for the same time. The duration of sustained ischemia in both groups of hearts was 21 minutes, after which the hearts were reperfused for 15 minutes to evaluate their mechanical and metabolic recovery. Separate experiments were performed for tissue metabolite determinations, mitochondrial ATPase activity measurements, and 31P nuclear magnetic resonance studies. The recovery of the rate-pressure product was better in the preconditioned group. Three-minute preconditioning ischemia caused inhibition of the mitochondrial ATPase that persisted throughout the 9-minute intervening reperfusion so that at the early stages of sustained ischemia the enzyme activity was still more inhibited in preconditioned hearts. ATP was better preserved in preconditioned hearts than in control hearts during sustained ischemia. The accumulation of adenosine and its degradation products during sustained ischemia was greater in the control group. More lactate and H+ ions accumulated in this group, indicating higher anaerobic glycolysis. Also, inhibition of mitochondrial ATPase by oligomycin slowed ATP depletion during ischemia. CONCLUSIONS: The results indicate that preconditioning causes inhibition of rat heart mitochondrial ATPase that persists during reperfusion so that the enzyme is inhibited from the very beginning of the sustained ischemia. This inhibition leads to sparing of high-energy phosphates and improves the time-averaged energy state during ischemia. Although a causal relationship is difficult to prove, this reversible inhibition may contribute to postischemic recovery of the heart.
BACKGROUND: Continuous retrograde blood cardioplegia has been introduced as a promising alternative for myocardial protection during cardiac operations, although the optimal conditions for its delivery have been poorly studied. METHODS: We randomized a prospective series of 101 patients to receive either retrograde warm (37 degrees C) or mild hypothermic (28 degrees to 29 degrees C) blood cardioplegia during elective coronary artery bypass grafting. Warm blood cardioplegia was delivered to the aortic root until the heart was arrested, after which the regimen was switched to retrograde and continued either as warm or mild hypothermic cardioplegia. Oxygen consumption and transcardiac pH differences during aortic cross-clamping were determined, and postoperative creatine kinase-MB efflux, hemodynamic recovery, and clinical complications monitored. RESULTS: Clinical characteristics, cardioplegia delivery rates, aortic cross-clamp and cardiopulmonary bypass times, and the number of distal anastomoses were similar in both patient groups. Short intermissions in cardioplegia delivery during construction of distal anastomoses were allowed, the ischemia time in the mild hypothermic group being somewhat longer (8.3% +/- 1.1% versus 5.1% +/- 0.8% of cross-clamp time; p = 0.05). Myocardial oxygen consumption was lower in the mild hypothermic group (2.49 +/- 0.23 versus 3.93 +/- 0.33 mL/min at 30 minutes of cross-clamping; p < 0.01), and the transcardiac pH difference was smaller (0.05 +/- 0.01 versus 0.07 +/- 0.01 at 30 minutes of cross-clamping; p < 0.03). Postoperative creatine kinase-MB levels were higher in the normothermic group. Heart rate was higher and left ventricular stroke work index smaller in the warm group, but otherwise there were no major differences between the groups in hemodynamic recovery. The number of postoperative complications was also similar in both groups. CONCLUSIONS: Although both normothermic (37 degrees C) and mild hypothermic (28 degrees to 29 degrees C) retrograde blood cardioplegia, when delivered in near-continuous fashion, will offer safe myocardial protection during coronary artery bypass grafting, mild hypothermia seemed to provide somewhat better protection under the conditions prevailing here. The effects of different cardioplegia temperatures should perhaps be tested further in patients with recent myocardial infarction, unstable angina, or severely depressed left ventricular function.
BACKGROUND: Free radicals and lipid peroxidation have been suggested to play an important role in the pathophysiology of myocardial reperfusion injury. The purpose of the present study was to monitor myocardial malondialdehyde (MDA) production as an index of lipid peroxidation during ischemia-reperfusion sequences in patients undergoing elective coronary bypass grafting. There has been a lot of debate on the role of xanthine oxidase as a potential superoxide anion generator and thus lipid peroxidation in human myocardium. To evaluate the activity of xanthine oxidase pathway, we measured the changes in the transcardiac concentration differences in adenosine, inosine, hypoxanthine, xanthine, and uric acid. METHODS AND RESULTS: The coronary sinus-aortic root differences (CS-Ao) of MDA, oxypurines, and nucleosides were measured by a recently developed ion-pairing high-performance liquid chromatographic (HPLC) method. Fifteen patients were included in the study, and 13 of them demonstrated a more than 10-fold increase in net myocardial production of MDA on intermittent reperfusion during the aortic cross-clamp period. In 2 patients, MDA was not detectable in any of the CS or Ao samples. Before aortic cross-clamping, the CS-Ao concentration differences in adenosine, inosine, hypoxanthine, xanthine, and uric acid were 0.59 +/- 0.19, 0.23 +/- 0.05, 0.89 +/- 0.36, 0.58 +/- 0.32, and 11.4 +/- 4.9 mumol/L, respectively. After aortic cross-clamping, the sum of the transcardiac differences of these compounds increased up to 2.8-fold and then gradually decreased after declamping of the aorta. There was a weak positive correlation between transcardiac concentration differences of MDA and xanthine plus uric acid (r = .48, P < .01). The postoperative functional recovery or leakage of cardiac enzymes was not affected by the level of MDA net release during the aortic cross-clamp period, however. CONCLUSIONS: We conclude that myocardial lipid peroxidation, estimated as MDA formation, is common during intermittent ischemia-reperfusion sequences in coronary bypass surgery, although some patients may be better protected. Xanthine oxidase appears to be operative in human myocardium, and free radicals generated in this reaction might also be involved in the observed lipid peroxidation process. Increased degradation of myocardial adenine nucleotides and concomitant lipid peroxidation may play a specific role in the development of reperfusion injury. In this study, however, more extensive lipid peroxidation was not associated with impaired functional recovery.
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