The American journal of physiology
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To test the hypothesis that atrial natriuretic factor (ANF) increases total body venous compliance through venodilation and thereby reduces cardiac preload, we compared the systemic hemodynamic effects of ANF (99-126) with the venodilator nitroglycerin in conscious rats with myocardial infarction (mean infarct size 25%) induced by coronary artery ligation 3 wk previously. A 30-min ANF infusion (0.5 microgram.kg-1.min-1) decreased mean arterial pressure, central venous pressure, and blood volume by 11 mmHg, 0.8 mmHg, and 3 ml/kg, respectively (P less than 0.02). Nitroglycerin (10 micrograms.kg-1.min-1) similarly reduced arterial and venous pressures (7 and 0.6 mmHg; P less than 0.02) but increased blood volume by 2 ml/kg (P less than 0.05). ⋯ Compared with vehicle infusion, nitroglycerin increased total body vascular compliance as derived from serial MCFP measurements taken during 10% blood volume changes (2.09 +/- 0.12 vs. 2.76 +/- 0.32 ml.kg-1.mmHg-1; P less than 0.05) and reduced extrapolated unstressed volume (34.96 +/- 1.10 vs. 23.79 +/- 3.80 ml/kg; P less than 0.02). In contrast, ANF had no effect on either measurement. These data suggest that ANF and nitroglycerin reduced cardiac filling pressure through different mechanisms; the lack of effects of ANF on total body venous compliance and unstressed volume does not support its venodilating effect in these rats postmyocardial infarction.
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Although Ringer lactate (RL) is routinely used for resuscitation, it is not known whether the volume of RL that restores cardiac output after severe hemorrhagic shock also restores the depressed effective hepatic blood flow (EHBF). To study this, a 5-cm midline laparotomy was performed in rats (i.e., trauma induced), and the animals were then bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximum bleedout volume was returned in the form of RL. Animals were then resuscitated with four or five times the volume of maximum bleedout with RL. ⋯ Results indicate that resuscitation markedly improved but did not restore the depressed EHBF after trauma and hemorrhagic shock despite the fact that cardiac output was restored. Similar changes in EHBF, HMBF, and hepatic blood flow as determined by microspheres were observed, suggesting that the in vivo ICG clearance is a reliable method to assess effective hepatic perfusion. Thus the lack of restoration of EHBF may be responsible for the subsequent hepatocellular dysfunction after trauma and severe hemorrhage.
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The overall objective of this study was to determine whether leukocyte adherence and/or emigration is a prerequisite for the increased vascular protein leakage associated with acute inflammation. An in vivo preparation was used to monitor intestinal vascular protein leakage as well as polymorphonuclear leukocyte (PMN) adhesion and emigration in feline mesenteric microvessels exposed to platelet-activating factor (PAF) and leukotriene B4 (LTB4). Local intra-arterial infusion of PAF (4 ng/min) produced a fourfold increase in vascular protein leakage. ⋯ Both PAF and LTB4 caused degranulation of cat PMNs in vitro, yet superoxide production was stimulated by PAF only. The data derived from these in vivo and in vitro studies indicate that leukocyte adhesion per se does not necessarily lead to increased vascular protein leakage and leukocyte emigration. Adhesion-dependent PMN functions such as emigration and superoxide production may play an important role in producing the alterations in vascular integrity observed in inflamed microvessels.
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The effect of beta-adrenergic agonists on splanchnic intravascular volume (SIV), measured with radionuclide imaging, and the subsequent influence of such volume changes on cardiac output (CO) were examined in 40 anesthetized dogs. Isoproterenol (6 micrograms/min) caused a decrease in total SIV of 12 +/- 1% (P less than 0.001). The decrease was due entirely to a decrease in splenic volume of 24 +/- 3% (P less than 0.001), since volume increased in the remainder of the splanchnic vasculature [hepatic and mesenteric volume increased 12 +/- 2% (P less than 0.001) and 11 +/- 3% (P less than 0.02), respectively]. ⋯ After subsequent alpha-adrenergic inhibition with phenoxybenzamine, terbutaline caused no change in SIV and an attenuated (P less than 0.05) increase in CO. Thus beta-adrenergic agonist administration causes a decrease in total SIV due entirely to a decrease in splenic volume. The SIV decrement is dependent on beta 2- and alpha-adrenoceptor stimulation and appears to enhance CO only if beta 1-adrenergic effects are minimized.
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We have demonstrated previously that transfer function analysis can be used to precisely characterize the respiratory sinus arrhythmia (RSA) in normal humans. To further investigate the role of the autonomic nervous system in RSA and to understand the complex links between respiratory activity and arterial pressure, we determined the transfer functions between respiration, heart rate (HR), and phasic, systolic, diastolic, and pulse arterial pressures in 14 healthy subjects during 6-min periods in which the respiratory rate was controlled in a predetermined but erratic fashion. ⋯ We found that 1) the pure sympathetic (standing + atropine) HR response is characterized by markedly reduced magnitude at frequencies greater than 0.1 Hz and a phase delay, whereas pure vagal (supine + propranolol) modulation of HR is characterized by higher magnitude at all frequencies and no phase delay; 2) both the mechanical links between respiration and arterial pressure and the RSA contribute significantly to the effects of respiration on arterial pressure; 3) the RSA contribution to arterial pressure fluctuations is significant for vagal but not for sympathetic modulation of HR; 4) the mechanical effects of respiration on arterial pressure are related to the negative rate of change of instantaneous lung volume; 5) the mechanical effects have a higher magnitude during systole than during diastole; and 6) the mechanical effects are larger in teh standing than the supine position. Most of these findings can be explained by a simple model of circulatory control based on previously published experimental transfer functions from our laboratory.