Force patterns of hypoxic myocardium applied to oxygenated muscle preparations: Comparison with effects of regional ischemia on the contraction of non-ischemic myocardium

Objective: To examine the basis for local wall motion abnormalities commonly seen in patients with ischemic heart disease, computer-controlled isolated muscle studies were carried out. Methods: Force patterns of physiologically sequenced contractions (PSCs) from rat left ventricular muscle preparations under well-oxygenated conditions and during periods of hypoxia and reoxygenation were recorded and stored in a computer. Force patterns of hypoxic-reoxygenating and oxygenated myocardium were applied to oxygenated and hypoxic-reoxygenating myocardium, respectively. Results: Observed patterns of shortening and lengthening closely resemble those obtained from ischemic and non-ischemic myocardial segments using ultrasonic crystals in intact dog hearts during coronary occlusion and reperfusion, and are similar to findings reported in angiographic studies of humans with coronary artery disease. Conclusion: The current study, demonstrating motions of oxygenated isolated muscle preparations which are similar to those in perfused segments of intact hearts with regional ischemia, supports the concept that the multiple motions of both ischemic and non-ischemic segments seen in regional myocardial disease can be explained by interactions of strongly and weakly contracting muscle during the physiologic cardiac cycle.

Electrocardiographic evaluation and serum cardiac troponin I levels in anemic dogs with blood parasitosis

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Thyroid State and Tolerance of Mammalian Myocardium to Hypoxia

Thyroid hormone is known to affect myocardial glycogen stores and thereby possibly limit anaerobic performance of mammalian cardiac muscle. Thyroid hormone administration (3,5,T-triiodo-L-thyroxine, 300 mu g/kg/day, sc) for 10 days decreased left ventricle (LV) glycogen concentration relative to euthyroid animals (2.78 +/- 0.46 vs. 4.28 +/- 0.29 mg/g of LV (mean +/- SEM)) while increasing the percent of V(1) myosin isozyi-ne, contractile activity and cardiac mass. In contrast, thyroidectomy increased myocardial glycogen stores (8.50 +/- 0.56 mg/g of LV) and shifted the myosin isozyme toward V(3), prolonged contractile activity and decreased LV mass. Thyroxine administration for 3, 7 and 10 days to thyroidectomized animals progressively decreased contractile duration and increased LV mass. Thyroxine administration for 3 or 7 days to thyroidectomized rats did not reduce glycogen stores (7.75 +/- 1.02 and 9.62 +/- 1.16 mg/g of LV, respectively), whereas myocardial glycogen declined to 3.30 +/- 0.58 mg/g of LV after 10 days of treatment. During hypoxia, cardiac muscle from thyroidectomized rats maintained greater active force and developed less contracture relative to euthyroid and, to a greater extent, than hyperthyroid rats. Removal of glucose from the bath decreased anaerobic performance and impaired recovery; however, myocardium from thyroidectomized rats remained more tolerant to hypoxia than the euthyroid group. Overall, the intrinsic LV glycogen content was positively correlated to anaerobic performance. These data demonstrate that the thyroid state profoundly affects myocardial growth, contractility and anaerobic performance of rat myocardium. Although energy demand may affect function during hypoxia, anaerobic substrate reserve (cardiac glycogen concentration) appears to be the primary factor determining tolerance to hypoxic stress. J. Exp. Zool. 311A:399-407, 2009. (C) 2009 Wiley-Liss, Inc.

Physiological response of American bullfrog tadpoles to stressor conditions of capture and hypoxia

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Profile of cortisol, glycaemia, and blood parameters of American Bullfrog tadpoles Lithobates catesbeianus exposed to density and hypoxia stressors

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Involvement of serotoninergic receptors in the anteroventral preoptic region on hypoxia-induced hypothermia

Hypoxia causes a regulated decrease in body temperature (Tb). There is circumstantial evidence that the neurotransmitter serotonin (5-HT) in the anteroventral preoptic region (AVPO) mediates this response. However, which 5-HT receptor(s) is (are) involved in this response has not been assessed. Thus, we investigated the participation of the 5-HT receptors (5-HT(1), 5-HT(2), and 5-HT(7)) in the AVPO in hypoxic hypothermia. To this end, Tb of conscious Wistar rats was monitored by biotelemetry before and after intra-AVPO microinjection of methysergide (a 5-HT(1) and 5-HT(2) receptor antagonist, 0.2 and 2 mu g/100 nL), WAY-100635 (a 5-HT(1A) receptor antagonist, 0.3 and 3 mu g/100 nL), and SB-269970 (a 5-HT(7) receptor antagonist, 0.4 and 4 mu/100 nL), followed by 60 min of hypoxia exposure (7% O(2)). During the experiments, the mean chamber temperature was 24.6 +/- 0.7 degrees C (mean +/- SE) and the mean room temperature was 23.5 +/- 0.8 degrees C (mean +/- SE). Intra-AVPO microinjection of vehicle or 5-HT antagonists did not change Tb during normoxic conditions. Exposure of rats to 7% of inspired oxygen evoked typical hypoxia-induced hypothermia after vehicle microinjection, which was not affected by both doses of methysergide. However, WAY-100635 and SB-269970 treatment attenuated the drop in Tb in response to hypoxia. The effect was more pronounced with the 5-HT7 antagonist since both doses (0.4 and 4 mu g/0.1 mu L) were capable of attenuating the hypothermic response. As to the 5-HT(1A) antagonist, the attenuation of hypoxia-induced hypothermia was only observed at the higher dose. Therefore, the present results are consistent with the notion that 5-HT acts on both 5-HT(1A) and 5-HT7 receptors in the AVPO to induce hypothermia, during hypoxia. (c) 2005 Elsevier B.V All rights reserved.

Anapyrexia during hypoxia

Reducing body temperature has been found to improve survival not only due to hypoxia (the main focus of this review) but also to ischemia, shock, and many other types of insults. Under these conditions, there is a reduced oxygen delivery to the brain. To compensate the hypoxia, a regulated hypothermia (anapyrexia-Glossary of terms for Thermal Physiology, Commission for Thermal Physiology, 2001) takes place, which has been reported as a beneficial response since the drop in body temperature causes a reduced oxygen demand. The objective of the present article is to review the current knowledge of the mechanisms of hypoxia-induced anapyrexia, focusing on its neurochemical control mainly at the preoptic region of the anterior hypothalamus. (c) 2005 Elsevier Ltd. All rights reserved.

Role of Locus coeruleus noradrenergic neurons in cardiorespiratory and thermal control during hypoxia

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Ionotropic glutamatergic receptors in the rostral medullary raphe modulate hypoxia and hypercapnia-induced hyperpnea

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Opioid mu-receptors in the rostral medullary raphe modulate hypoxia-induced hyperpnea in unanesthetized rats

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Role of preoptic opioid receptors in the body temperature reduction during hypoxia

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The breathing pattern and the ventilatory response to aquatic and aerial hypoxia and hypercarbia in the frog Pipa carvalhoi

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