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M Cutaia

Publications and source records attributed to M Cutaia.

24 records · Page 2Linked to original sources
PubMed1992

Effects of Na-K-ATPase inhibition on catecholamine reactivity in rat pulmonary artery.

The objective of this study was to determine the effects of Na-K-adenosinetriphosphatase (ATPase) inhibition on aspects of vascular reactivity in rat pulmonary artery, including resting tone and catecholamine reactivity, loss of reactivity to repeated catecholamine stimulation, and contraction-relaxation kinetics. The effect of ATPase inhibition on resting tone and catecholamine reactivity was determined by comparing the responses to 10(-4) and 10(-3) M ouabain (Oua-4, Oua-3), 10(-4) M tyramine, and 10(-6) M norepinephrine (NE) pre- and postouabain. Loss of responsiveness to NE was induced by repeated cumulative doses of NE (NE I, NE II) with 60 min between exposures. ATPase inhibition was superimposed on this loss of reactivity by 1) administration of Oua-4 or Oua-3 15 min before NE II, 2) incubation in K(+)-free solution 15 min before NE II, and 3) incubation in K(+)-free solution 15 min before NE I for the entire protocol. The effect of ATPase inhibition on the response pattern after repetitive dosing with phenylephrine (PE) and KCl was also determined. To correlate ATPase activity with the loss of reactivity after catecholamine stimulation, we measured ATPase activity (86Rb uptake) at different time points after repeated NE administration. The effect of ATPase inhibition on contraction-relaxation rates after catecholamine stimulation was determined by analyzing the response to repeated single doses of NE in normal salt solution and after incubation in K(+)-free solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Reversal of vascular tachyphylaxis to catecholamines and histamine in the feline lung.

The pulmonary vascular responses to histamine, epinephrine, and norepinephrine demonstrate tachyphylaxis following repetitive exposure in the isolated blood-perfused cat lung. In the present study, we tested the hypothesis that this phenomenon was related to a change in the balance of antagonistic receptor activity. The protocol consisted of 5 consecutive dose-response maneuvers (DR I to V) to 1 amine in each animal separated by 1 h. Once the loss of the initial vasoconstrictor activity had occurred (DR I to IV), the animal was given a receptor blocking agent, either the beta blocker propranolol or the H2 blocker cimetidine, prior to a final dose-response maneuver (DR V). The dose-response relationships were analyzed in terms of 3 parameters: maximum response, slope, and ED50. All the experiments with norepinephrine (n = 6), epinephrine (n = 10), and histamine (n = 25) demonstrated a progressive loss of vasopressor activity as shown by reductions in the maximum response and slope between DR I to IV. In addition, histamine demonstrated a significant increase in ED50 from DR I to IV, which suggested a loss of sensitivity. The loss of vasoconstrictor activity to histamine and the catecholamines was restored by the administration of propranolol prior to DR V. In contrast, cimetidine did not restore the initial vasopressor activity of histamine. The loss of reactivity to histamine was not secondary to changes in circulating catecholamine levels, because the plasma catecholamine levels before DR I and immediately following DR V in a subset of animals (n = 5) were within the reported normal range for this species.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Hypoxia-induced alterations of norepinephrine vascular reactivity in isolated perfused cat lung.

Past work in the isolated perfused cat lung has shown that acute hypoxia (H) changes the response to norepinephrine (NE) from vasoconstriction to vasodilation but has no effect on the response to serotonin (S). These results could be related to the increase in pulmonary arterial pressure or vascular resistance during the hypoxic pressor response or a direct effect of H. We addressed this question, in the same preparation, by comparing responses to NE under four conditions in each experimental animal (n = 12): 1) NE infused during normoxia; 2) NE infused after vascular resistance (Rpv) was increased with serotonin; 3) NE infused after Rpv was increased by H; 4) NE infused after lobar pressure was raised by an increase in flow (P/F). PO2 values during H were varied (27-56 Torr). S and H produced a 137 +/- 35 and 43 +/- 8% delta Rpv increase in lobar vascular resistance, respectively. P/F increased lobar pressure 91 +/- 10%. Only NE infusion during H demonstrated significant differences in lobar pressure and Rpv compared with control normoxic periods. There was no correlation between responses to NE during S, H, and P/F and degree to which each stimulus increased Rpv or lobar pressure (r = 0.003, 0.28, 0.24). A significant relationship between response to NE during H vs. PO2 during H was observed (r = 0.78; P less than 0.001). In a subset of animals, we repeated the infusion of NE during H and P/F post-beta-blockade. The decrease in vascular response to NE during H and the correlation of PO2 with NE response were abolished (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Pregnancy- and gender-related changes in pulmonary vascular reactivity.

Pregnancy is a state of altered pulmonary vascular reactivity, but the conclusions about changes in reactivity have varied with the agents or species chosen for study. The present study was designed as a comprehensive analysis of pregnancy-induced and gender-related differences in pulmonary vascular reactivity in one species. Using an isolated perfused feline lung preparation, the pulmonary vascular responses to angiotensin II, serotonin, histamine, epinephrine, norepinephrine, and acute hypoxia (FIO2, 8%) were compared between males, females, and pregnant females. Vascular reactivity (maximum response) and drug sensitivity (ED50) were compared using cumulative dose-response data for each pharmacological agent. The results demonstrate that (1) reactivity to angiotensin II, serotonin, epinephrine, and acute hypoxia is decreased during pregnancy, while the response to norepinephrine remain unchanged, (2) drug sensitivity is unchanged with serotonin and the catecholamines, increased with histamine, and decreased with angiotensin II, and (3) the responses to acute hypoxia and histamine have significant gender-related differences in reactivity independent of the changes observed during pregnancy.

Angiotensin II↗
PubMed1983

Pulmonary vascular reactivity after repetitive exposure to selected biogenic amines.

The present study investigated the effects of repetitive exposure to a select group of biogenic amines (epinephrine, norepinephrine, histamine, and serotonin) on pulmonary vascular reactivity by constructing and analyzing a set of four sequential cumulative dose-response curves to one biogenic amine in the isolated blood-perfused left lower lobe of the cat lung in vivo. The dose-response curves were obtained under conditions of constant flow, insuring that the observed pressure changes in the lobe were pressor responses resulting from vasoconstriction rather than flow-related changes. Histamine and epinephrine demonstrated a progressive loss of initial vasoconstrictor activity, whereas the responses to serotonin remained unchanged after repetitive exposure. Norepinephrine demonstrated two different patterns of response, depending on the dose range employed; norepinephrine (0.068-2.27 nmol/ml) demonstrated a loss of the original vasoconstrictor activity, in a pattern similar to histamine and epinephrine, while higher doses of norepinephrine (0.34-9.1 nmol/ml) demonstrated no change in activity with a left shift in the concentration at which the maximal responses occurred, suggesting an increase in sensitivity as a result of repeated exposure. These results were obtained in the absence of significant alterations of arterial blood gases, changes in base-line tone in the experimental left lower lobe, or the development of severe pulmonary edema. These data suggest that only the agents that are capable of stimulating antagonistic vasoconstrictor and vasodilator receptors demonstrated a loss of pulmonary vasoconstrictor activity, which may result from a functional shift in the balance of antagonistic receptor activity with continued exposure.

Animals↗