Pathologic changes induced by 1-norepinephrine

Szakács, Comdr.JenöE.; Mehlman, Benjamin

doi:10.1016/0002-9149(60)90127-2

Cited by 155 publications

(33 citation statements)

References 10 publications

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“…Klouda and B^rynjolfsson 12 demonstrated that subendocardial hemorrhage and focal myocardial necrosis in dogs subjected to stellate ganglion stimulation and norepinephrine infusion intravenously produces focal myocarditis and subpericardial hemorrhage in dogs, cats and rabbits. 13 ' w The rostral connections for the sympathetic nervous system are located in the hypothalamus, stimulation of which in cats has been reported to result in electrocardiographic changes similar to those seen in patients with central nervous system lesions. 16 " 17 Hawkins and Clower 18 demonstrated that experimental intracranial hemorrhage in mice resulted in myocardial damage and that the incidence of such damage could be reduced by adrenalectomy or pretreatment with reserpine.…”

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confidence: 99%

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Benedict¹,

Loach²

1978

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SUMMARYIn patients with subarachnoid hemorrhage there were increased concentrations of plasma epinephrine and norepinephrine when compared with those concentrations in a group of patients admitted to hospital with other illness.Reassessment after a variable period showed that in patients whose eventual clinical result was poor the plasma epinephrine and norepinephrine concentrations increased further while in those with a good result those concentrations showed a decline. No such changes were evident in plasma dopamine-,8-hy droxylase activities which were within normal range.In a sub-group of patients who had neurosurgery after admission for clipping an aneurysm, the post-operative changes of plasma epinephrine and norepinephrine concentrations were related to the clinical condition of the patients.

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confidence: 99%

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Benedict¹,

Loach²

1978

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“…The hypothesis that very high plasma concentrations of FFA or a decrease in the rate of oxidation of fatty acids by the cell may result in accumulation of sufficient fatty acids to prove detrimental to cellular structure and function is an interesting concept. Diphtheria toxin produced acute myocardial lesions similar to those induced by catecholamines (6). This toxin also inhibited the oxidation of long chain fatty acids by heart homogenate preparations (33).…”

Section: Resultsmentioning

confidence: 88%

“…None of the changes in triglyceride concentrations were statistically significant. Although 6 of the 22 geese given glucagon died within 90 min after the injection, myocardial lesions were found in only two. Twelve in this group had fatty livers.…”

Section: Resultsmentioning

confidence: 93%

“…In others, sinus arrest, supraventricular tachycardia, ventricular tachycardia, and signs of myocardial ischemia were observed. In group III, 6 , , F I G U R E 5 --. glucagon-treated geese (group I) from 115 ±-31 to 182 +52 mg/100 ml at 90 min whereas the control values (group II) decreased from 176 ± 100 to 119 ±68.…”

Section: Resultsmentioning

confidence: 99%

“…Long chain fatty acids are known to produce cytotoxic effects in tissue cultures (3) and cause acute myocardial failure when injected intravenously in the unbound state into dogs (4). Infusion of norepinephrine has been associated with the development of fatty liver (5) and acute myocardial necrosis in dogs (6,7). These effects in dogs can be prevented by propranolol that inhibits the usual increase in FFA produced by catecholamines.…”

Section: Introductionmentioning

confidence: 99%

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Toxic effects of glucagon-induced acute lipid mobilization in geese

Hoak¹,

Connor²,

Warner³

1968

J. Clin. Invest.

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A B S T R A C T The toxic effects associated with rapid lipid mobilization and a high plasma free fatty acid (FFA) concentration produced by glucagon were evaluated. Glucagon (0.5 mg/kg of body wt) was injected intravenously into nonfasting geese. The geese developed rapid respirations and high plasma FFA levels within 15 min after the glucagon injection; three of eleven died. Control geese, injected with saline, did not exhibit toxic signs. Peak FFA concentrations developed 15 min after glucagon and high levels persisted for over 90 min. Geese injected with glucagon frequently developed electrocardiographic abnormalities that included supraventricular tachycardia, premature ventricular contractions, and signs of myocardial ischemia. Light and electron microscopy revealed acute myocardial degeneration and fatty infiltration of the liver. The increase in plasma FFA concentrations and toxic effects were not prevented by pretreatment with nicotinic acid or propranolol.

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Thyrotoxic Mitral Regurgitation

Reynolds¹

1971

Am J Dis Child

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Mitral regurgitation is reported in three children with hyperthyroidism. The regurgitation was demonstrated by left-ventricular cineangiography in one patient, the first known case of demonstrated thyrotoxic mitral regurgitation. We propose that excess thyroid hormone induces intrinsic papillary muscle disease by its direct effects on the heart and circulation. Mitral regurgitation disappeared in these three patients two to ten months after hyperthyroidism was treated. Recognition of a mitral-thyrotoxicosis nexus is of help in the differential diagnosis of mitral regurgitation.Whether hyperthyroidism can be the sole cause of heart disease has historically been controversial. Recent opinion, reviewed by de Groot and Leonard,1 indicates that it defi¬

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Pathologic changes induced by 1-norepinephrine

Cited by 155 publications

References 10 publications

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Sympathetic nervous system activity in patients with subarachnoid hemorrhage.

Toxic effects of glucagon-induced acute lipid mobilization in geese

Thyrotoxic Mitral Regurgitation

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