Effect of imipramine on the norepinephrine and histamine-induced capillary response in the rat

1967 ◽  
Vol 23 (3) ◽  
pp. 211-212 ◽  
Author(s):  
B. Gözsy ◽  
L. Kátó ◽  
A. St-Jean
Keyword(s):  
1957 ◽  
Vol 188 (2) ◽  
pp. 387-394 ◽  
Author(s):  
Jenö Kramár ◽  
William V. Meyers ◽  
Harry H. McCarthy ◽  
Nicholas Dietz ◽  
Margarete Simay-Kramár ◽  
...  

Two possibilities may be considered for the mechanism of the immediate capillary stress response: the direct nervous origin, and the humoral. The latter was investigated in this study. Immediate capillary stress response was found in the absence of the adrenal, pituitary or thyroid glands, and after removal of both the adrenals and the pituitary. Among the 10 physiologic substances considered as playing a potential role in this phenomenon, three were found to possess capillary activity. Vasopressin as well as oxytocin increases capillary resistance. Histamine gives rise to a biphasic response, involving a decrease of capillary resistance (primary effect) followed by an increase (due to vasopressin elicited by histamine). By means of these substances it is possible to duplicate the immediate capillary stress response. During the immediate capillary response plasma has antidiuretic and chloruretic properties—a finding compatible with an increased vasopressin concentration and with the assumption that vasopressin is discharged rather regularly in the first phase of the stress response. The immediate capillary stress response seems to be the result of an interplay between vasopressin-oxytocin, and histamine. Species and individual differences in the sensitivity to these substances may account for the various patterns of the capillary response. The possible significance of the immediate capillary response and of the increased vasopressin activity in some clinical conditions is discussed.


1996 ◽  
Vol 271 (5) ◽  
pp. H1755-H1761 ◽  
Author(s):  
N. R. Harris ◽  
D. N. Granger

Fluid filtration rate (Jv/S) from individual mesenteric capillaries in normocholesterolemic and hypercholesterolemic rats was measured before and after 30 min each of ischemia and reperfusion (I/R). The median I/R-induced increase in Jv/S (I/R vs. baseline) was 44% in normocholesterolemic rats (n = 11) and 97% in hypercholesterolemic rats (n = 11). A positive correlation slope of 0.20% per mg/dl resulted when the percent Jv/S increase vs. plasma cholesterol concentration (P = 0.02) was plotted, demonstrating that hypercholesterolemia enhances the capillary response to I/R. Because microvascular pressure did not change significantly after I/R in either group of rats, the increments in Jv/S likely reflect increased capillary permeability. In hypercholesterolemic rats rendered neutropenic with antineutrophil serum, I/R did not elicit a significant increase in Jv/S, suggesting that activated neutrophils mediate the exaggerated endothelial barrier dysfunction associated with hypercholesterolemia.


1954 ◽  
Vol 16 (5) ◽  
pp. 393-397 ◽  
Author(s):  
JENO KRAMAR ◽  
DWAINE J. PEETZ ◽  
HARRY H. McCARTHY
Keyword(s):  

1995 ◽  
pp. 105-107
Author(s):  
A. M. Shutt ◽  
S. R. Dodds ◽  
A. R. Cowan ◽  
A. B. D. Chant

1958 ◽  
Vol 192 (3) ◽  
pp. 603-608 ◽  
Author(s):  
Jenö Kramár ◽  
Victor E. Levine ◽  
V. William Meyers ◽  
Robert N. Sass

In an attempt to elucidate further the relationship of capillary resistance to the adrenal corticosteroids, capillary resistance was studied in connection with the plasma concentration and excretion of the 17, 21-dihydroxycorticosteroids in three groups of experiments. The actual concentration of these steroids in the plasma of nonstressed subjects failed to show any correlation with the actual capillary resistance level. The stress-induced increase in capillary resistance (capillary stress response) was accompanied by simultaneous changes in the plasma concentration or excretion of these corticosteroids in some experiments. In other experiments, on the other hand, plasma concentration and elimination of the corticosteroids did not change despite marked capillary response. This failure to demonstrate a consistent correlation between capillary resistance and plasma concentration and urinary excretion of the 17, 21-dihydroxycorticosteroids militates against a direct relationship of capillary resistance to adrenocortical activity and suggests the existence of another factor as playing a role in the capillary resistance-corticosteroid relationship.


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