Biomedical subjects

J E Guilmette

Publications and source records attributed to J E Guilmette.

8 recordsLinked to original sources

PubMed1983

Experimental hyperthermic isolation-perfusion using cis-diamminedichloroplatinum(II).

The intent of this study was to determine whether or not local control and/or cure of rabbits bearing the VX-2 carcinoma could be achieved with regional hyperthermia and chemotherapy. A model of isolation-perfusion used cis-diamminedichloroplatinum(II) (DDP). Five different experimental groups were studied, each group receiving progressively smaller tumor inocula and shorter treatment intervals. Although local control and cure improved as the tumor inocula became smaller and treatment interval became shorter, there was no benefit demonstrated when compared to sham-operated animals. DDP appeared to be well tolerated in animals perfused as normothermic temperatures. However, animals perfused at hyperthermic temperature with DDP experienced necrosis of normal as well as neoplastic tissue, resulting in early demise of the animal. This final observation suggests that the amount of DDP utilized in clinical isolation-perfusion should be approached with caution.

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PubMed1982

Experimental evaluation of magnesium cardioplegia.

The effectiveness of magnesium solution in protecting ischemic myocardium was evaluated in a blood-perfused, isolated rabbit papillary muscle preparation. Anoxic cardioplegia was induced by either a control solution containing no magnesium or a test solution containing a magnesium concentration of 160 mEq/L. The magnesium solution induced a very rapid cardiac arrest, less than 1 minute, in contrast to more than 10 minutes with the control solution. Restarting time was not affected by magnesium cardioplegia. Following 30 minutes of anoxic cardioplegia, the magnesium group showed significantly (p less than 0.01) better recovery of myocardial contractility, 91.3% +/- 8.3% (n = 6), than the control group, 77.7% +/- 4.1% (n = 6). These protective effects of magnesium were lost when the ischemic time was longer than 45 minutes.

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PubMed1980

Experimental evaluation of myocardial preservation techniques: V. A. membrane-stabilizing agent, procaine hydrochloride.

The protective effects of procaine hydrochloride on the anoxic heart were investigated using the papillary muscle contractility of an isolated, blood-perfused rabbit heart as an index of myocardial function. Fifty-four experiments were divided into nine groups of six experiments each, in which anoxic periods (30, 45, 60 minutes) and concentration of procaine (solution 3, 0.3%) were the variables. The hearts arrested significantly faster with solution 3 compared with solution 2 or 1 (p < 0.01). After 30 minutes of anoxia, the recovery of the contractility was 81.1 +/- 4.2% with solution 1, 90.7 +/- 3.4% with solution 2, and 90.6 +/- 3.3% with solution 3. After 45 minutes of anoxia, the recovery was 31.8 +/- 19.0% with control, 67.5 +/- 15.8% with 0.03% procaine, and 58.1 +/- 22.8% with 0.3% procaine. After 60 minutes of anoxia, the recovery was 2.2 +/- 2.7% with control, 18.7 +/- 14.1% with 0.03% procaine, and 5.0 +/- 7.3% with 0.3% procaine. After each anoxic period, the best recovery occurred with those hearts arrested by solution 2. Although the difference in recovery between the procaine groups was not statistically significant, a longer time was required for the hearts arrested with solution 3 to reach full functional recovery. This study indicated that procaine per se has a protective effect on the anoxic hearts and that although high concentration (0.3%) of procaine arrests the heart rapidly, it delays the recovery of contractions. We recommend the use of 0.03% procaine in cardioplegic solution.

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PubMed1979

Experimental evaluation of myocardial preservation techniques: IV. Potassium cardioplegia.

To investigate whether potassium per se plays a significant role in cold potassium cardioplegia, isolated blood-perfused rabbit papillary muscle preparations were used to determine the recovery of myocardial contractility after normothermic anoxia. Cardioplegia was induced by infusing an isotonic electrolyte solution containing either 5 or 40 mEq/liter of potassium chloride. Anoxic periods of 30 minutes (9 experiments each) 45 minutes (10 experiments each), and 60 minutes (1 experiment each) were compared. Hearts stopped contracting in 45 seconds with infusion of a 40mEq/liter of potassium chloride solution compared to 5 minutes with a 5 mEq/liter solution. After 30 minutes of anoxia, myocardial recovery was 65.39 +/- 24.48 per cent with 5 mEq/liter of potassium chloride and 90.05 +/- 6.40 per cent with 40mEq/liter of potassium chloride. The difference was highly significant (p less than 0.01). After 45 minutes of anoxia the same trend as just described was noted, but the difference was statistically insignificant. After 60 minutes of anoxia, recovery was extremely poor regardless of the potassium concentration of the cardioplegic solution. Our conclusion was that a high potassium solution will arrest the heart rapidly and provide protection against anoxic injury of the myocardium. Its protective effect becomes less significant, however, as the anoxic time is prolonged.

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PubMed1979

Experimental evaluation of hypothermic intermittent coronary perfusion.

The recovery of the myocardial contractility of blood-perfused papillary muscle from the rabbit hearts was used to determine if hypothermia would minimize the myocardial injury associated with intermittent aortic cross-clamping (IACC). Continuous normothermic coronary perfusion for 2 hours with either cross circulation or a membrane oxygenator had only minimal adverse effects on contractility. None of the hearts tolerated normothermic IACC (45 minutes of anoxia and 10 minutes of reperfusion, repeated twice), When the myocardial temperature was reduced to 32 degrees C., the recovery following IACC was 41.25 +/- 11.21 percent (n=8). With hypothermia of 28 degrees C., it was 70.43 +/- 13.03 percent (cross circulation group, n=7) or 68.36 +/- 13.11 percent (membrane oxygenator group, n=7). If the hearts were cooled to 24 degrees C., the recovery of the myocardial contractility following IACC was 90.95 +/- 5.42 percent (n=11). The improvement of the degree of recovery by hypothermia was statistically highly significant (p less than 0.005). Creatine phosphokinase (CPK) and isoenzymes (CPK-MB) were also measured in some groups, but the results warrrant further studies before they can be correlated with the myocardial function.

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PubMed1978

Temporary cardiopulmonary bypass for the treatment of endotoxic shock.

New Zealand white rabbits were employed in the laboratory to evaluate the efficacy of temporary cardiopulmonary bypass in the prevention of pulmonary injury from endotoxin. Partial cardiopulmonary bypass using peripheral cannulation was carried out for 15 minutes after intraarterial administration of E coli endotoxin of LD90 doses. A significantly better long-term (1 month) survival rate of the treated animals (60 per cent) versus the untreated animals (10 per cent) as well as less severe pulmonary changes in those that succumbed after treatment were observed. It would appear that temporary cardiopulmonary bypass by peripheral cannulation warrants further study in the treatment of patients identified early as suffering from otherwise irreversible septicemic shock.

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PubMed1978

Functional evaluation of normothermic intermittent coronary perfusion.

The myocardial contractility of papillary muscle from rabbit hearts was used to evaluate various techniques of normothermic intermittent coronary perfusion. A progressive decline of the myocardial contractility was noted as aortic cross-clamping and coronary reperfusion were repeated. After a net anoxic period of 90 minutes, the contractility fell to 58.67, 60.2, and 40 percent of the base line when single aortic cross-clamping time was 5, 10, and 15 minutes, respectively, interrupted by 5 minutes of reperfusion. Repeated application of single cross-clamping of 20 minutes or longer was not tolerated by the rabbit hearts. When the heart was reperfused for 10 minutes, between 15 minute periods of anoxia, the final recovery of contractility was 62 percent. Normothermic intermittent coronary perfusion has a significant adverse effect on the myocardial contractility. If this technique is to be used, single anoxic times should not be longer than 15 minutes and the heart must be reperfused for at least 10 minutes.

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PubMed1976

Effect of hypothermic anoxic cardioplegia on myocardial contractility.

A study was undertaken to ascertain the protective effect of topical hypothermia on the anoxic heart. The presence or absence of myocardial damage was judged by myocardial contractility. The papillary muscle of an excised rabbit heart was detached from the mitral annulus and interposed between a fixed point and a force/displacement transducer. The maximal net developed tension (TNmax) of the papillary muscle with normothermic coronary perfusion was used as an index of myocardial contractility. With each temperature drop of 10 degrees C, the anoxia time that resulted in the same recovery level of TNmax was prolonged by a factor of 2.8. A nomogram was constructed correlating percent of myocardial recovery seen with different degrees of myocardial hypothermia during various anoxic periods. Optimum protection was noted at a myocardial temperature of 18 degrees C.

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