What question did this study set out to answer?

To assess whether physiological concentrations of insulin can restore defective prostaglandin E1/I2 receptor binding and anti-aggregatory activity in platelets from patients with acute ischemic heart disease.

January 1, 1991Circulation Research

Restoration by insulin of impaired prostaglandin E1/I2 receptor activity of platelets in acute ischemic heart disease.

View Full Paper

Ask AI

Bookmark

Why the study?

Does in vitro insulin treatment restore impaired prostaglandin E1/I2 receptor activity in platelets from patients with acute ischemic heart disease?

Population

Platelet-rich plasma from normal subjects and patients with acute ischemic heart disease (n=43)

Comparison

In vitro treatment with insulin for 3 hours at… vs Nontreated, control platelet-rich plasma

Design

Preclinical

Authors

NKNighat N. KahnFox Chase Cancer Center HMHiltrud S. MuellerThe University of Texas at Austin ASAnjana SinhaRutgers, The State University of New Jersey

Discussion

Member takes

Implication

May warrant in vivo testing of insulin's platelet effects; leaves open clinical translation from this in vitro finding.

Key Points

To assess whether physiological concentrations of insulin can restore defective prostaglandin E1/I2 receptor binding and anti-aggregatory activity in platelets from patients with acute ischemic heart disease.
Treated platelet-rich plasma from healthy controls and patients with acute ischemic heart disease (N = 43) with physiological concentrations of insulin (100–200 µU/ml) for 3 hours at 23°C.
Measured prostaglandin E1 binding sites, intracellular cyclic AMP accumulation, and the minimum inhibitory concentration of prostaglandin required to inhibit platelet aggregation.
Insulin treatment restored prostaglandin E1 binding from 850 ± 100 to 1,790 ± 140 sites/10^8 platelets in 75% of acute ischemic heart disease cases, whereas 25% remained unresponsive.
Insulin augmented cyclic AMP production from 7.70 ± 2.0 to 23.87 ± 4.1 pmol/10^8 platelets in patients and from 16.35 ± 2.91 to 44.14 ± 3.1 pmol/10^8 platelets in healthy controls.
The minimum inhibitory concentration for prostanoid-mediated inhibition of aggregation decreased from 49 ± 15 to 32 ± 11 nM (p = 0.002) in responder patients and from 34 ± 14 to 15 ± 9 nM (p < 0.001) in healthy controls.

Structured PICO

Does in vitro insulin treatment restore impaired prostaglandin E1/I2 receptor activity in platelets from patients with acute ischemic heart disease?

Population

Platelet-rich plasma from normal subjects and patients with acute ischemic heart disease (n=43)

Intervention

In vitro treatment with insulin (100 to 200 microunits/ml) for 3 hours at 23 degrees C

Comparator

Nontreated, control platelet-rich plasma

Outcome

Prostaglandin E1 binding sites per 10^8 plateletssurrogate

In vitro insulin treatment restores impaired prostaglandin E1/I2 receptor activity and cyclic AMP production in platelets from a majority of patients with acute ischemic heart disease.

Cite This Study

Kahn et al. (1991) studied this question.

synapsesocial.com/papers/6a8279bc8d8b29c30f795ef9 https://doi.org/10.1161/01.res.68.1.245

View Full Paper

Ask AI

Bookmark

Restoration by insulin of impaired prostaglandin E1/I2 receptor activity of platelets in acute ischemic heart disease.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Restoration by insulin of impaired prostaglandin E1/I2 receptor activity of platelets in acute ischemic heart disease.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider