1936-P: Muscle Ischemia Impairs Insulin-Mediated Microvascular Recruitment

The experiments were performed on 280 male Wistar rats weighing 300-340 g. The design of the study included: modeling of compression injury of the soft tissues of the thigh, local injection of the preparation of hyaluronic acid "Gialift 3.5" into the area of damage 3 hours after the cessation of compression, taking into account the results after 7, 14 and 28 days. The introduction of hyaluronic acid into the area of compression injury of soft tissues reduces the severity of myoglobinemia, increases the immunohistochemical density of VEGF-positive cells, improves the perfusion characteristics of microcirculation, oxygen saturation, and specific oxygen consumption by tissues. Keywords: traumatic muscle ischemia, hyaluronic acid, myoglobin, microcirculation, metabolism, laser Doppler flowmetry, morphometry.

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Modulation of sympathetic nerve activity during posthandgrip muscle ischemia in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.1.h79 ◽

1994 ◽

Vol 266 (1) ◽

pp. H79-H83 ◽

Cited By ~ 16

Author(s):

C. A. Ray ◽

N. H. Secher ◽

A. L. Mark

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Muscle Sympathetic Nerve Activity ◽

Sensory Nerve ◽

Vascular Occlusion ◽

Voluntary Contraction ◽

Central Command ◽

Isometric Handgrip ◽

Nerve Activity ◽

Muscle Ischemia

To evaluate modulation of muscle sympathetic nerve activity (MSNA) during posthandgrip muscle ischemia (PHGMI), subjects performed 2 min of isometric handgrip at 33% of maximal voluntary contraction (MVC) followed by 2 min of PHGMI produced by forearm vascular occlusion. The response to PHGMI was studied in the absence and again during the addition of contralateral rhythmic handgrip (RHG; 40 times/min) at 15% (n = 6) and 30% (n = 10) MVC during the second minute of the PHGMI. Additionally, to isolate the effect of central command, response to PHGMI was studied during attempted RHG after sensory nerve blockade (n = 5). RHG for 2 min at 15 and 30% MVC and attempted RHG for 2 min did not increase MSNA. Isometric handgrip elicited an 130 +/- 48% increase in MSNA (P < 0.05), which was maintained during PHGMI. RHG at 15 and 30% MVC elicited an attenuation of MSNA (-10 +/- 7% and -14 +/- 6%, respectively) when performed during the second minute of PHGMI (P < 0.05). In contrast, attempted RHG did not significantly affect MSNA during PHGMI. The findings demonstrate modulation of MSNA during activation of the muscle metaboreflex. The attenuation of metaboreceptor-mediated increases in MSNA appear to be the result of mechanosensitive muscle afferents and not central command.

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ASIC3: A Lactic Acid Sensor for Cardiac Pain

The Scientific World JOURNAL ◽

10.1100/tsw.2001.254 ◽

2001 ◽

Vol 1 ◽

pp. 510-512 ◽

Cited By ~ 37

Author(s):

D.C. Immke ◽

E.W. McCleskey

Keyword(s):

Coronary Artery Disease ◽

Lactic Acid ◽

Sensory Neurons ◽

Heart Attack ◽

Anaerobic Metabolism ◽

Metabolic Demand ◽

Peripheral Artery ◽

Muscle Ischemia ◽

Artery Disease ◽

Cardiac Pain

Angina, the prototypic vasoocclusive pain, is a radiating chest pain that occurs when heart muscle gets insufficient blood because of coronary artery disease. Other examples of vasoocclusive pain include the acute pain of heart attack and the intermittent pains that accompany sickle cell anemia and peripheral artery disease. All these conditions cause ischemia � insufficient oxygen delivery for local metabolic demand — and this releases lactic acid as cells switch to anaerobic metabolism. Recent discoveries demonstrate that sensory neurons innervating the heart are richly endowed with an ion channel that is opened by, and perfectly tuned for, the lactic acid released by muscle ischemia[1,2].

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