Noninvasive Detection of Cardiac Sympathetic Nervous Dysfunction in Diabetic Patients Using [123I]Metaiodobenzylguanidine

Diabetes ◽  
1992 ◽  
Vol 41 (9) ◽  
pp. 1069-1075 ◽  
Author(s):  
M. Mantysaari ◽  
J. Kuikka ◽  
J. Mustonen ◽  
K. Tahvanainen ◽  
E. Vanninen ◽  
...  
Keyword(s):  
Noninvasive Detection ◽  
Diabetic Patients ◽  
Sympathetic Nervous

Noninvasive detection of cardiac sympathetic nervous dysfunction in diabetic patients using [123I]metaiodobenzylguanidine

Diabetes ◽  
1992 ◽  
Vol 41 (9) ◽  
pp. 1069-1075 ◽  
Author(s):  
M. Mantysaari ◽  
J. Kuikka ◽  
J. Mustonen ◽  
K. Tahvanainen ◽  
E. Vanninen ◽  
...  
Keyword(s):  
Noninvasive Detection ◽  
Diabetic Patients ◽  
Sympathetic Nervous

Transient outward potassium channel regulation in healthy and diabetic heartsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

2009 ◽  
Vol 87 (2) ◽  
pp. 77-83 ◽  
Author(s):  
Mónica Gallego ◽  
Aintzane Alday ◽  
Janire Urrutia ◽  
Oscar Casis
Keyword(s):  
Cardiac Arrhythmias ◽  
Functional Expression ◽  
Trophic Factors ◽  
Diabetic Patients ◽  
Special Issue ◽  
Channel Regulation ◽  
Research Workshop ◽  
Sympathetic Nervous ◽  
Selection Of

Diabetic patients have a higher incidence of cardiac arrhythmias, including ventricular fibrillation and sudden death, and show important alterations in the electrocardiogram, most of these related to the repolarization. In myocytes isolated from diabetic hearts, the transient outward K+ current (Ito) is the repolarizing current that is mainly affected. Type 1 diabetes alters Ito at 3 levels: the recovery of inactivation, the responsiveness to physiologic regulators, and the functional expression of the channel. Diabetes slows down Ito recovery of inactivation because it triggers the switching from fast-recovering Kv4.x channels to the slow-recovering Kv1.4. Diabetic animals also have decreased responsiveness of Ito towards the sympathetic nervous system; thus, the diabetic heart develops a resistance to its physiologic regulator. Finally, diabetes impairs support of various trophic factors required for the functional expression of the channel and reduces Ito amplitude by decreasing the amount of Kv4.2 and Kv4.3 proteins.

Microvascular oxygen partial pressure during hyperbaric oxygen in diabetic rat skeletal muscle

2015 ◽  
Vol 309 (12) ◽  
pp. R1512-R1520 ◽  
Author(s):  
Kohei Yamakoshi ◽  
Kazuyoshi Yagishita ◽  
Hirotsugu Tsuchimochi ◽  
Tadakatsu Inagaki ◽  
Mikiyasu Shirai ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Tibialis Anterior ◽  
Response Times ◽  
Dynamic Balance ◽  
Tibialis Anterior Muscle ◽  
Small Animal ◽  
Diabetic Rat ◽  
Diabetic Patients ◽  
Phosphorescence Quenching ◽  
Sympathetic Nervous

Hyperbaric oxygen (HBO) is a major therapeutic treatment for ischemic ulcerations that perforate skin and underlying muscle in diabetic patients. These lesions do not heal effectively, in part, because of the hypoxic microvascular O2 partial pressures (PmvO2) resulting from diabetes-induced cardiovascular dysfunction, which alters the dynamic balance between O2 delivery (Q̇o2) and utilization (V̇o2) rates. We tested the hypothesis that HBO in diabetic muscle would exacerbate the hyperoxic PmvO2 dynamics due, in part, to a reduction or slowing of the cardiovascular, sympathetic nervous, and respiratory system responses to acute HBO exposure. Adult male Wistar rats were divided randomly into diabetic (DIA: streptozotocin ip) and healthy (control) groups. A small animal hyperbaric chamber was pressurized with oxygen (100% O2) to 3.0 atmospheres absolute (ATA) at 0.2 ATA/min. Phosphorescence quenching techniques were used to measure PmvO2 in tibialis anterior muscle of anesthetized rats during HBO. Lumbar sympathetic nerve activity (LSNA), heart rate (HR), and respiratory rate (RR) were measured electrophysiologically. During the normobaric hyperoxia and HBO, DIA tibialis anterior PmvO2 increased faster (mean response time, CONT 78 ± 8, DIA 55 ± 8 s, P < 0.05) than CONT. Subsequently, PmvO2 remained elevated at similar levels in CONT and DIA muscles until normobaric normoxic recovery where the DIA PmvO2 retained its hyperoxic level longer than CONT. Sympathetic nervous system and cardiac and respiratory responses to HBO were slower in DIA vs. CONT. Specifically the mean response times for RR (CONT: 6 ± 1 s, DIA: 29 ± 4 s, P < 0.05), HR (CONT: 16 ± 1 s, DIA: 45 ± 5 s, P < 0.05), and LSNA (CONT: 140 ± 16 s, DIA: 247 ± 34 s, P < 0.05) were greater following HBO onset in DIA than CONT. HBO treatment increases tibialis anterior muscle PmvO2 more rapidly and for a longer duration in DIA than CONT, but not to a greater level. Whereas respiratory, cardiovascular, and LSNA responses to HBO are profoundly slowed in DIA, only the cardiovascular arm (via HR) may contribute to the muscle vascular incompetence and these faster PmvO2 kinetics.

Sign in / Sign up

Export Citation Format

Share Document