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Biomedical subjects

M Jellinek

Publications and source records attributed to M Jellinek.

At least 73 records · Page 4Linked to original sources
PubMed1977

Topical cardiac hypothermia for myocardial preservation.

We compared moderate (29 degrees C.) and profound (5 degrees C.) (ice chips) cardiac hypothermia for myocardial preservation during aortic cross-clamping for 30 or 60 minutes in a canine right heart bypass preparation. Ventricular function deteriorated significantly at 29 degrees C. but not at 5 degrees C. Maximum dp/dt declined only after 60 minutes of ischemia at 29 degrees C., and Vmax decreased after one hour at either temperature. Lactate and pyruvate washout were greater after 29 degrees C., and pyruvate production persisted after 60 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C., and total coronary flow remained elevated after 60 minutes of ischemia at 29 degrees C. Coronary flow distribution was not altered by hypothermia. Ultrastructural changes were primarily time dependent and not temperature dependent. Ice-induced subepicardial injury was not evident in the ultrastructure or by flow distribution. Sixty minutes of profound topical cardiac hypothermia is moderately well tolerated by the canine heart, but functional and structural alterations are evident.

Animals↗
PubMed1976

Effect of the histamine (H2) inhibitor metiamide on histamine-stimulated bile flow in dogs.

The effects of the histamine H2-receptor inhibitor metiamide on histamine-stimulated canine bile flow and gastric hydrogen ion output were evaluated. Histamine was found to stimulate bile volume in doses comparable to those that stimulated gastric hydrogen ion output; both responses appeared to have the same maximal response dose, 150 mug/kg per h. Metiamide alone did not alter hepatic bile flow. Administration of metiamide, 2 mg/kg per h, along with various doses of histamine demonstrated that the H2-receptor antagonist decreased bile volume and gastric hydrogen ion output from values obtained with histamine administration alone. The D50 of histamine for bile flow was 16.3 mug/kg per h and the D50 for hydrogen ion output was 44.2 mug/kg per h, Kinetic analysis suggests that the decrease in histamine-stimulated hydrogen ion output produced by metiamide is the result of competitive inhibition; the decrease in histamine-stimulated bile volume by metiamide which is different from the hydrogen ion inhibition, suggests noncompetitive inhibition. These data indicate that the mechanism of histamine choleresis is different from the mechanism of histamine-stimulated gastric acid output and that histamine-stimulated bile flow may not be the result of direct hormone-receptor interaction.

Animals↗
PubMed1975

Phosphorylated beta-guanidinopropionate as a substitute for phosphocreatine in rat muscle.

To evaluate phosphorylated beta-guanidinopropionate (beta-GPAP) as a substitute for phosphocreatine (PC), hypoxic tibialis anterior muscles were stimulated to contract isometrically in situ until twitch tension fell to 25 percent of the peak value. Muscles from rats fed beta-guanidinopropionic acid (beta-GPA) failed to exhibit the staircase phenomenon, and they developed 28 percent less tension than control muscles. In control muscles lactate increased from 0.75 to 20.99, ADP increased from 0.89 to 1.20, ATP decreased from 5.09 to 2.73, and PC decreased from 15.78 to 1.52 mumol/g. In muscles from rats fed beta-GPA, lactate increased from 0.85 to 14.31, ADP increased from 0.86 to 1.05, ATP decreased from 2.69 to 1.71, PC decreased from 0.73 to 0.30, and beta-GPAP decreased from 30.34 to 19.45 mumol/g. From these measurements, the use of high-energy phosphate was calculated to be reduced 32 percent in muscles from rats fed beta-GPA. The relationships between the use of high-energy phosphate was calculated to be reduced 32 percent in muscles from rats fed beta-GPA. The relationships between the use of high-energy phosphate and tension development confirm experimentally the ability of beta-GPAP to substitute for PC as a source of energy to sustain muscle contraction.

Adenosine Diphosphate↗
PubMed1975

Effect of glucagon on secretin-stimulated bile flow.

The effect of glucagon on secretin-stimulated bile flow was evaluated in dogs with chronic biliary and gastric fistulas. Evaluation of the effects of secretin and glucagon alone on hepatic bile flow indicated that the calculated maximal response (CMR) values of the two agents were similar. Secretin increased the bicarbonate concentration in hepatic bile whereas glucagon did not, suggesting basic differences in mechanism of action. Administration of glucagon to secretin-stimulated bile flow produced an increase in bile flow while decreasing the bicarbonate concentration in secretin-stimulated bile. Since the maximal response for bile flow to glucagon and secretin was significantly greater than the maximal response to either agent alone, glucagon produced potentiation of secretin-stimulated bile. Glucagon increased the CMR value of secretin-stimulated bile from 513 mul/min for secretin alone to 692 mul/min for secretin and glucagon. This was associated with no significant change in the values of the respective D50S. These data suggest that glucagon produced a noncompetitive augmentation of secretin-stimulated bile flow and suggest that the two agents do not utilize the same receptor to stimulate bile flow.

Animals↗