TY - JOUR
T1 - Coronary vascular dysfunction associated with direct current shock injury
AU - Oltman, Christine L.
AU - Clark, Craig B.
AU - Kane, Neal L.
AU - Zhang, Yi
AU - Gutterman, David D.
AU - Dellsperger, Kevin C
AU - Kerber, Richard E.
PY - 2003/11
Y1 - 2003/11
N2 - DC shocks for cardioversion and defibrillation cause myocardial injury that may be free radical mediated. Objective: To determine if cardiac injury following DC shocks includes impairment of coronary vascular reactivity. Methods: 36 dogs (18-32 kg) were anesthetized and a thoracotomy was performed. Either antioxidant enzymes, superoxide dismutase (SOD, 15,000 U/kg) plus catalase (55,000 U/kg) or the NO synthase inhibitor NG-nitro-L-arginine (L-NNA, 5 mg/kg) was administered IV prior to sham (no shocks) or DC shock treatment, and the results were compared to dogs which did not receive SOD/catalase or L-NNA. In sham dogs, electrodes cradled the heart, but no shocks were delivered. In shock dogs, three 20 Joule DC shocks were delivered to the epicardium using hand-held paddles. Other dogs were allowed a 3-hour recovery period after the shocks. Epicardial microvessels and conduit rings were studied in vitro. Antagonists were not added to the bath of the study vessel. Internal diameter was measured in microvessels after constriction with endothelin. Tension of conduit arteries was measured after constriction with PGF2α. Responses to acetyicholine (Ach, 10-10 - 10-4 M), bradykinin (10-14 - 10-6 M), the calcium ionophore A23187 (A23187, 10-12 - 10-4 M) or nitroprusside (SNP, 10-10 - 10-4 M) were measured. Results: Bradykinin, A23187 and SNP dependent dilation was not different between vessels from sham and shocked animals. Dilation to Ach was attenuated in vessels from shocked dogs. Superoxide production probably contributed to the impaired dilation to Ach since treatment with SOD/catalase improved dilation. Treatment with L-NNA also improved vascular function after DC shock. Conclusion: DC shocks cause endothelial dysfunction, as demonstrated by impaired dilation to acetylcholine, in both canine coronary microvascular and conduit arteries. Since pretreatment with either SOD/catalase or L-NNA protects against this damage, a free radical mechanism, possibly involving eNOS, may contribute to endothelial dysfunction.
AB - DC shocks for cardioversion and defibrillation cause myocardial injury that may be free radical mediated. Objective: To determine if cardiac injury following DC shocks includes impairment of coronary vascular reactivity. Methods: 36 dogs (18-32 kg) were anesthetized and a thoracotomy was performed. Either antioxidant enzymes, superoxide dismutase (SOD, 15,000 U/kg) plus catalase (55,000 U/kg) or the NO synthase inhibitor NG-nitro-L-arginine (L-NNA, 5 mg/kg) was administered IV prior to sham (no shocks) or DC shock treatment, and the results were compared to dogs which did not receive SOD/catalase or L-NNA. In sham dogs, electrodes cradled the heart, but no shocks were delivered. In shock dogs, three 20 Joule DC shocks were delivered to the epicardium using hand-held paddles. Other dogs were allowed a 3-hour recovery period after the shocks. Epicardial microvessels and conduit rings were studied in vitro. Antagonists were not added to the bath of the study vessel. Internal diameter was measured in microvessels after constriction with endothelin. Tension of conduit arteries was measured after constriction with PGF2α. Responses to acetyicholine (Ach, 10-10 - 10-4 M), bradykinin (10-14 - 10-6 M), the calcium ionophore A23187 (A23187, 10-12 - 10-4 M) or nitroprusside (SNP, 10-10 - 10-4 M) were measured. Results: Bradykinin, A23187 and SNP dependent dilation was not different between vessels from sham and shocked animals. Dilation to Ach was attenuated in vessels from shocked dogs. Superoxide production probably contributed to the impaired dilation to Ach since treatment with SOD/catalase improved dilation. Treatment with L-NNA also improved vascular function after DC shock. Conclusion: DC shocks cause endothelial dysfunction, as demonstrated by impaired dilation to acetylcholine, in both canine coronary microvascular and conduit arteries. Since pretreatment with either SOD/catalase or L-NNA protects against this damage, a free radical mechanism, possibly involving eNOS, may contribute to endothelial dysfunction.
KW - Acetylcholine
KW - Coronary circulation
KW - Defibrillation
KW - Endothelial function
KW - Microcirculation
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U2 - 10.1007/s00395-003-0428-5
DO - 10.1007/s00395-003-0428-5
M3 - Article
C2 - 14556086
AN - SCOPUS:0242383501
SN - 0300-8428
VL - 98
SP - 406
EP - 415
JO - Basic Research in Cardiology
JF - Basic Research in Cardiology
IS - 6
ER -