What question did this study set out to answer?

To determine whether systemic and regional hemodynamic changes induced by nitric oxide synthase inhibition are mediated by neurogenic pathways.

July 1, 1994AJP Regulatory Integrative and Comparative Physiology

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

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Why the study?

Does autonomic nervous system blockade alter the hemodynamic effects of nitric oxide synthase inhibition in rats?

Population

Rats anesthetized with Inactin (thiobutabarbital)

Comparison

Autonomic nervous system blockade with 20 mg/kg… vs Control animals receiving NO synthase inhibition…

Design

Preclinical

Authors

MHMin HuangCentral South University MLM. L. LeblancUniversity of Mississippi Medical Center RHRobert L. HesterCross-Cutting Cardiology

Discussion

Member takes

Implication

Nitric oxide synthase inhibition reduces cardiac output independently of autonomic tone in rats; hypothesis-generating and should not yet change practice.

Key Points

To determine whether systemic and regional hemodynamic changes induced by nitric oxide synthase inhibition are mediated by neurogenic pathways.
Measured blood pressure, cardiac output, and tissue flows using radioactive microspheres in anesthetized rats before and after nitric oxide synthase inhibition with 20 mg/kg L-NAME.
Compared intact control rats against a group with autonomic nervous system blockade induced by 20 mg/kg hexamethonium and stabilized with norepinephrine infusion.
L-NAME treatment significantly elevated mean arterial pressure and reduced cardiac output by approximately 50% in both intact and autonomic-blocked animals (P < 0.05).
L-NAME caused significant reductions in renal, hepatic artery, stomach, intestinal, and testicular blood flow across both groups, whereas autonomic blockade alone had no effect on tissue flows.

Structured PICO

Does autonomic nervous system blockade alter the hemodynamic effects of nitric oxide synthase inhibition in rats?

Population

Rats anesthetized with Inactin (thiobutabarbital)

Intervention

Autonomic nervous system blockade with 20 mg/kg hexamethonium (plus intravenous infusion of norepinephrine 20-140 ng/min to maintain normal blood pressure) prior to NO synthase inhibition with 20 mg/kg L-NAME

Comparator

Control animals (intact autonomic nervous system) receiving NO synthase inhibition with 20 mg/kg L-NAME

Outcome

Changes in mean arterial pressure, cardiac output, and tissue flowssurrogate

The increase in blood pressure and decreases in cardiac output and tissue flows following nitric oxide synthase inhibition with L-NAME are not dependent on a neurogenic mechanism.

Cite This Study

Huang et al. (1994) studied this question.

synapsesocial.com/papers/6a83f8474f77243e16b05e67 https://doi.org/10.1152/ajpregu.1994.267.1.r84

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Implication

Nitric oxide synthase inhibition reduces cardiac output independently of autonomic tone in rats; hypothesis-generating and should not yet change practice.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider