[Induced, autogenic heart valves].
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Biomedical subjects
Publications and source records attributed to R S Reneman.
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The degradation of lipids by endogenous hydrolytic activity has been studied in rat cardiac tissue deliberately damaged by freezing and thawing prior to storage under anoxic conditions. Aliquots of the freeze-thawed material were kept at 37 degrees C under an atmosphere of N2 up to 120 minutes. Triacylglycerol was hydrolyzed at a rate of 0.14 mumol fatty acids per minute per gram dry weight of tissue. Hydrolysis of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) was associated with proportional production of lyso PC and lyso PE, respectively. This finding indicates that the activity of lysophospholipase is negligible in autolyzing cardiac tissue. The rate of hydrolysis of PC and PE was found to be 0.10 and 0.06 mumol per minute per gram dry weight of tissue. The observation that lyso PC and lyso PE mainly contained saturated and mono-unsaturated fatty acids indicates that phospholipase A2 rather than A1 is active in autolyzing cardiac tissue. The accumulation of fatty acids corresponded with the loss of triacylglycerol and phospholipids from the tissue during 120 minutes of autolysis.
The use of tannic acid has been proposed to improve the preservation of phospholipids in tissues. We investigated the effects of tannic acid on the preservation of small unilamellar vesicles, prepared from sonicated aqueous suspensions of phospholipids. With cryo-electron microscopy it is demonstrated that small unilamellar vesicles are formed after sonication of the phospholipid suspensions. Fixation of vesicles without tannic acid results in extraction of the phospholipids during dehydration and embedding. Fixation of vesicles containing phosphatidyl choline with tannic acid, with or without glutaraldehyde, results in a fast (within a second) aggregation of the vesicles and the resulting sediment can be dehydrated and embedded when a postfixation in osmium tetroxide is carried out. Small unilamellar vesicles fixed in this way are retrieved in thin sections as multilamellar vesicles with a periodicity of about 5 nm for dimyristoylphosphatidyl choline and about 6 nm for dioleoylphosphatidyl choline. By using 14C-phosphatidyl choline it was also demonstrated that tannic acid prevents to a large extent the extraction of phosphatidyl choline during fixation, dehydration and embedding. This dual effect of tannic acid on phosphatidyl choline, aggregation and fixation, should be considered when using tannic acid in tissue preparation.
The precise role of eicosanoids in the development of myocardial injury during ischemia and reperfusion is still a matter of debate. Enhanced local production of these bioactive compounds appears to be a common response to tissue injury. Most likely, the cardiac tissue has the capacity to generate prostaglandins, thromboxanes as well as leukotrienes. Prostacyclin (PGI2) is the major eicosanoid produced by the jeopardized myocardium. In addition, at sites of tissue injury activation of platelets and infiltrating leukocytes results in the formation of considerable amounts of thromboxanes and leukotrienes. The production of eicosanoids requires prior release of arachidonic acid (AA) from phospholipids. Both ischemia and reperfusion are associated with a rise in the tissue level of AA. The absence of a proportional relationship between the tissue level of AA and the amounts of PGI2 produced suggests that the sites of AA accumulation and PGI2 formation are different. It is conceivable that AA accumulation is mainly confined to myocytes, whereas the capacity to synthesize PGI2 mainly resides in vascular cells. Both beneficial and detrimental effects of eicosanoids on cardiac tissue have been described. Prostaglandins act as vasodilators. Besides, some of the prostaglandins, especially PGI2, are thought to possess cyto-protective properties. Thromboxanes and leukotrienes may impede blood supply by increasing smooth muscle tone. Besides, leukotrienes augment vascular permeability. Experimental studies, designed to evaluate the effect of pharmacological agents, like PGI2-analogues and lipoxygenase and cyclo-oxygenase inhibitors, indicate that eicosanoids influence the outcome of myocardial injury.(ABSTRACT TRUNCATED AT 250 WORDS)
A simple but still versatile datalogging system based on a VCR (video cassette recorder) has been developed. The VCR allows mass storage of data originating from a maximum of 256 channels as used, for example, in the recording of the time-dependent potential distribution at the surface of the myocardium. Incorporated in the system is a display memory allowing on-line simultaneous visualization of the assessed recordings of 16 channels. On an interactive base display parameters (time-window, channel-selection) can be altered without loss of data. A link with a personal computer allows modification of system parameters and storage of data for off-line analysis of the recorded data. The high data rate to and from the VCR (4.3 MHz) fully utilizes the bandwidth available. A normal videotape can, therefore, contain up to 2 Gigabyte of data. Despite this, the use of the tapecounter and the decoding of the time-code inserted into the signal allows quick retrieval of the stored data without needing expensive equipment. The system described brings mass data logging within the reach of a vast number of laboratoria and cardiovascular centers.
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An animal model for the induction of coronary artery stenosis is described. In this model the degree of stenosis, as induced with commercially available hydraulic occluders, can be easily controlled by keeping constant the mean perfusion pressure (pcor) distal to the site of stenosis. This pcor is the input signal for a servo-system feeding a motor-pump, which determines the degree of inflation of the cuff around the left anterior interventricular coronary artery (LAICA). In each experiment pcor did not vary more than 2 mm Hg from the preset value of about 25 mm Hg. In 60 anesthetized open-chest dogs the time course of standard hemodynamic variables and regional myocardial blood flow in the center of the underperfused area, using the radioactive microsphere technique, were determined. Within 1 min after induction of stenosis heart rate and end-diastolic left ventricular pressure (plved) increased (by 20 and 60%, respectively) and mean aortic pressure and dplv/dtmax decreased (by 10 and 25%, respectively). After the initial decrease median myocardial blood flow further decreased between 1 and 5 min of stenosis from 0.63 to 0.32 ml.min-1.g-1 in the outer layers (P less than 0.05) and from 0.26 to 0.15 ml.min-1.g-1 in the inner layers (P less than 0.05), despite constant hemodynamic conditions and pcor. Between 5 and 120 min of stenosis these values remained unchanged in the outer layers, but decreased further in the inner layers to 0.08 ml.min-1.g-1 (P less than 0.05). The accurate control of pcor, the reproducibility of the levels of residual blood flow and the ease of handling the stenosis system indicate that coronary artery stenosis controlled by perfusion pressure distal to the stenosis is a useful animal model to study events during regional myocardial ischemia. With the use of this model of low flow ischemia a biphasic increase of myocardial vascular resistance was observed, which is initiated during the first minutes of coronary artery stenosis.