# VASCULAR TRANSPORT CAPACITY OF MUSCLE IN HEART FAILURE

> **NIH NIH R01** · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · 1992 · $45,323

## Abstract

Patients with heart failure (HF) typically demonstrate a reduced work
capacity when compared to normal individuals.  This reduced work capacity
has been attributed, in park to the early onset muscular fatigue and has
been correlated with reductions in blood flow to working skeletal muscle.
The primary objective of this proposal is to identify the factors
contributing to the reductions in skeletal muscle blood flow in the HF
state.  Towards this objective, a surgically induced myocardial
infarction (MI) or a sham operation (SHAM) will be performed on adult
female Wistar rats.  Following 6 weeks of recovery, the extent of LV
dysfunction and HF produced will be determined by measuring LV and RV
pressures in vivo in the awake resting animal.  The vascular transport
capacity (VTC) of the hind limb musculature will then be assessed using
the isolated hindquarters perfusion technique.  The different components
of the VTC, the vascular flow capacity and capillary exchange capacity,
will be determined in NU rats and analyzed as a function of LV infarct
size (small, medium, large and extensive infarcts) and compared to both
components in SHAM rats.  In addition, the flow component of the VTC of
the hind limb musculature will be examined in individual muscles with
radiolabeled microspheres.  This experimental approach will allow us to
determine if the decrement in the VTC of the hind limb musculature of MI
rats becomes greater as the size of the infarct becomes larger, the
amount of LV dysfunction worsens and as the degree of HF progresses from
the compensated to the decompensated congestive state.  We will also
determine whether the formation of interstitial edema is one of the
mechanisms responsible for limiting flow in the skeletal muscle of MI
rats by reducing the amount of fluid retained in the extravascular space
of rats with diuretic therapy and by examining the effects of this
intervention on the VTC of the hind limb musculature.  Finally, we will
determine whether endurance exercise training can ameliorate the
decrements in the VTC of the hind limb musculature of MI rats.
Altogether, these studies will corroborate our preliminary studies where
decrements in the vascular flow capacity of hind limb musculature of rats
with a large MI were found.  They will provide a better understanding of
the mechanisms involved that produce the decrements in skeletal muscle
blood flow in the BF state and they will prove useful in the development
of clinical strategies for mating this debilitating disease.

## Key facts

- **NIH application ID:** 3123446
- **Project number:** 1R01AG011535-01
- **Recipient organization:** PENNSYLVANIA STATE UNIV HERSHEY MED CTR
- **SAM.gov UEI:** TNKGNDAWB445
- **Principal Investigator:** TIMOTHY I MUSCH
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $45,323
- **Award type:** 1
- **Project period:** 1992-09-30 → 1993-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3123446

## Citation

> US National Institutes of Health, RePORTER application 3123446, VASCULAR TRANSPORT CAPACITY OF MUSCLE IN HEART FAILURE (1R01AG011535-01). Retrieved via MORVS 2026-10-26 from https://api.morvs.ai/grant/nih/3123446. Licensed CC0.

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