The American journal of physiology
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An efficient new technique was developed to investigate heart rate control at all physiologically relevant frequencies by using respiratory activity as a frequency probe of the autonomic nervous response. The transfer function from respiratory activity to heart rate was determined during 6-min periods in which the respiratory rate was voluntarily controlled in a predetermined but erratic fashion. Changes in posture were used to manipulate autonomic balance. ⋯ Physiol. 256 (Heart Circ. Physiol. 25): H142-H152, 1989], suggests that the magnitude and phase characteristics of the subjects in the supine and upright postures differ because of relatively increased sympathetic outflow in the upright posture. A precise and efficient characterization of respiratory sinus arrhythmia can yield considerable insight into the autonomic regulation of the heart.
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Platelet-activating factor (PAF-acether) is a lipid mediator that can exhibit potent vasoconstrictor influence in the pulmonary vessels. Therefore, the release of PAF-acether during inflammatory conditions in newborns might cause deleterious increases in pulmonary vascular tone. Thirty-four anesthetized open-chest newborn piglets were given 0.01-1 nmol PAF-acether iv. ⋯ Treatment with indomethacin or SQ 29548 prevented the decrease in cardiac index and attenuated the PAF-acether-induced rises in PAP and PVRI. Vehicle and LY 171883 had no effect. The inhibitory influence of indomethacin and SQ 29548 suggests that an important component of PAF-acether's pulmonary vasoconstrictor action is mediated (at least in the newborn piglet) by cyclooxygenase products, most likely thromboxane.
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Comparative Study
Cardiovascular responses to intrathecal vasopressin in conscious and anesthesized rats.
Increases in mean arterial pressure and heart rate have been documented after the intrathecal administration of [Arg8]vasopressin (AVP) in rats. Prior studies in our laboratories with conscious rats indicated that these cardiovascular changes were associated with a marked hindlimb sensorimotor dysfunction. In this study, which represents the first systematic comparison of the effects of intrathecal AVP in conscious and anesthesized rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the motor dysfunction induced by intrathecal AVP is accompanied by a rise in mean arterial pressure that is significantly greater than that produced by an equal intravenous dose of AVP, and 2) both paralytic and pressor effects of intrathecal but not intravenous AVP are blocked by the intrathecal administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT) but are not blocked by intravenous phenoxybenzamine, hexamethonium, or [Sar1, Thr8]angiotensin II, an angiotensin II antagonist. ⋯ Furthermore, conscious but not anesthesized rats exhibited a tachyphylaxis to intrathecal AVP. These results indicate that intrathecal AVP produces both the cardiovascular changes and the sensorimotor deficits through interactions with centrally located V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate the rise in mean arterial pressure produced by intrathecal AVP in anesthesized rats, but they do not in conscious rats.
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Unilateral pneumonectomy in rats causes compensatory growth of the remaining lung. This growth involves rapid production of collagen and noncollagen proteins, but the mechanisms for these changes have not been fully investigated. Rates of collagen metabolism were measured using previously validated in vivo methods. ⋯ Noncollagen protein synthesis and degradation rates both increased by approximately 80% (control 44.3 +/- 3.4%/day, pneumonectomy 80.3 +/- 10.2%/day) with a slightly greater increase in synthesis that led to an 85% increase in noncollagen protein content 28 days after pneumonectomy. The data obtained show dramatic changes in protein synthesis and degradation during compensatory lung growth and indicate extensive remodeling of structural elements in lung tissue. The changes for intracellular collagen degradation provide further evidence that this pathway may have an important role in regulating collagen deposition.
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We used awake, unsedated rats with indwelling cardiovascular catheters to study the role of endothelial injury and increased pulmonary vascular reactivity in the pathogenesis of monocrotaline (MC)-induced pulmonary hypertension. Hemodynamic findings were correlated with morphometric analyses of alterations in the vascular endothelium assessed by electron microscopy and of muscularization of pulmonary arteries assessed by light microscopy. Male Sprague-Dawley rats (200-250 g) were injected with MC (60 mg/kg) or with saline vehicle. ⋯ Endothelial injury was observed as early as 4 days postinjection with pallor and swelling evident qualitatively and by a decreased proportion of microfilaments (P less than 0.05) assessed quantitatively. By light microscopy, extension of smooth muscle into normally nonmuscularized pulmonary arteries was evident by 8 days postinjection. By 12 days postinjection there was marked extension of smooth muscle present (P less than 0.01) with medial hypertrophy of muscular arteries.(ABSTRACT TRUNCATED AT 250 WORDS)