Seasonal anestrus in the ewe results from two effects of inhibitory photoperiods: a steroid-dependent effect by which estradiol gains the capacity to suppress LH pulse frequency and a steroid-independent effect that decreases LH pulse frequency in ovariectomized ewes. We have previously proposed that these effects of anestrous photoperiods result from the activation of inhibitory neuronal mechanisms at this time of year. In the present study, we used specific receptor antagonists to test this hypothesis and identify the neurotransmitters involved. Initially, eight receptor antagonists were screened for their ability to increase pulsatile LH secretion in ovary-intact anestrous ewes. Of these, only pimozide, a dopaminergic antagonist, and phenoxybenzamine, an alpha-adrenergic antagonist, increased LH pulse frequency. In contrast, neither pimozide nor phenoxybenzamine increased pulsatile LH secretion in midluteal phase ewes during the breeding season. These drugs did, however, produce other biological responses at this time of year; pimozide increased serum PRL levels, and phenoxybenzamine decreased arterial blood pressure. Pimozide also increased pulsatile LH secretion in ovariectomized ewes treated with estradiol in anestrus to suppress LH pulse frequency, but phenoxybenzamine was ineffective in these animals. Neither drug increased LH in ovariectomized ewes not treated with estradiol. The seasonal variation in the ability of pimozide and phenoxybenzamine to increase LH secretion in ovary-intact ewes supports the hypothesis that inhibitory neural mechanisms suppressing GnRH are activated during anestrus and suggests that dopaminergic and/or alpha-adrenergic neurons are involved. In addition, the steroid-dependent effect of anestrous photoperiods may be exerted through the ability of estradiol to stimulate inhibitory dopaminergic neurons which are only active at this time of year.
Technetium-99m stannous pyrophosphate was utilized for myocardial imaging in 202 patients admitted to the hospital with chest pain of uncertain etiology. One hundred and one patients had clinical and evolved electrocardiographic and enzymatic evidence of acute myocardial infarction. Ninety-six of these 101 patients had increased myocardial uptake of the technetium stannous pyrophosphate and positive myocardial scintigrams; there was nearly precise correlation between the ECG and myocardial imaging localization of the area of infarction for acute transmural myocardial infarctions. In the five patients with negative myocardial images the scintigrams were obtained after seven or more days had elapsed following the myocardial infarction. In the remaining 101 patients no clinical, ECG, or enzymatic evidence of infarction developed; 92 of these patients had negative myocardial scintigrams. Seven of the remaining nine patients were admitted with "unstable angina pectoris", and despite the absence of diagnostic ECG and enzyme evolution each of these patients had faintly and diffusely positive myocardial scintigrams. The remaining two patients had positive myocardial scintigrams but no definite ECG or enzymatic evidence of acute myocardial infarction. Thus the technetium pyrophosphate imaging technique appears safe, inexpensive and to correlate well with ECG and enzyme identification of the presence of infarction and with ECG localization of myocardial infarction. In addition the positive myocardial scintigrams in some patients with "unstable angina" suggest that there may be limited myocardial necrosis that is ordinarily undetected by ECG and enzymes in these patients. The incidence of false positive and false negative scintigrams appears to be small.
A new method of visualizing acute myocardial infarction in humans following intravenous injection of 15 mCi-5 mg of 99mTc stannous pyrophosphate in 23 patients is reported. Fifteen patients had histories suggestive of acute myocardial infarction and subsequently developed electrocardiogram and enzyme changes that confirmed the clinical diagnosis. Eleven of the 15 patients were scanned 3-5 days postinfarction, and all had positive scintigrams. The four remaining patients were scanned 7-10 days after their myocardial infarction; two had positive scintigrams. In those 8 patients with chest pain but without ECG and enzyme changes suggestive of myocardial infarction, scintigrams were negative. Positive scintigrams in the patients with myocardial infarction are thought to be due to incorporation of pyrophosphate into the crystalline structure of the hydroxyapatite found within the mitochondria of irreversibly damaged myocardial cells. The location of the acute myocardial infarction by scintigram correlated well with ECG localization in the 13 patients with positive scintigrams. This imaging method shows promise in 1) identifying the presence of acute myocardial infarction in patients with chest pain, 2) determining the location of acute myocardial infarction with a high degree of accuracy, 3) detecting the extension of the infarction, and 4) the possibility of determining the size of acute myocardial infarctions.From the
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.