Platelet-activating factor (PAF) is a phospholipid with a wide range of biological activities. We studied PAF metabolism and PAF receptor (PAFR) signaling in perinatal ovine lungs to understand PAF's role in transition of the perinatal pulmonary hemodynamics and pathophysiology of persistent pulmonary hypertension of the newborn. We hypothesized that downregulation of PAF synthesis with upregulation of PAF catabolism by acetylhydrolase (PAF-Ah) in the newborn lung is needed for fetus-to-newborn pulmonary adaptation. Studies were conducted on fetal and newborn lamb pulmonary arteries (PA), veins (PV) and smooth muscle cells (SMC). PAF metabolism, PAFR binding and cell proliferation were studied by cell culture; gene expression was studied by qPCR. Fetal lungs synthesized 60% more PAF than newborn lungs. Compared with the fetal PVs and SMCs, PAF-Ah activity in newborn was 40–60% greater. PAF-Ah mRNA expression in newborn vessels was different from the expression by fetal PA. PAF-Ah gene clone activity confirmed deletion of hypoxia-sensitive site. PAFR mRNA expression by the PVs and SMC-PV of the fetus and newborn was greater than by corresponding PAs and SMC-PA. Q-PCR study of PAFR expression by the SMC-PV of both groups was greater than SMC-PA. Fetal SMCs bound more PAF than the newborn SMCs. PAFR antagonist, CV-3988, inhibited PAFR binding and DNA synthesis by the fetal SMCs, but augmented binding and DNA synthesis by newborn cells. We show different PAF–PAFR mediated effects in perinatal lungs, suggesting both transcriptional and translational regulation of PAF-Ah and PAFR expression in the perinatal lamb lungs. These indicate that the downregulation of PAF-mediated effects postnatally protects against persistent pulmonary hypertension of the newborn.

Background: Definition of normative data of the great arteries from neonatal to adult ages may aid in assessment of the growth of cardiovascular structures, thus guiding the timing and type of intervention in patients with congenital cardiac disease. Methods: We calculated the cross-sectional areas of the arterial roots at the basal attachment of the valvar leaflets, the sinuses, and standardized distal sites using cineangiograms of 59 normal children and adolescents with mean age of 5.4 plus or minus 4.7 years and a range from 0.1 to 16 years, the children having a mean weight of 21.2 plus or minus 15.7 kilograms, with a range from 2.2 to 68 kilograms, and mean height of 108 plus or minus 35 centimetres, with a range from 43 to 184 centimetres. Values at each site were calculated averaging end-diastolic and end-systolic measurements, and indexed to body surface area. Results are expressed as the mean plus or minus the standard deviation. Results: The diameter of the aortic root at the basal attachment of the leaflets was 249 plus or minus 26, the midpoint of the sinuses 379 plus or minus 59, the sinutubular junction 290 plus or minus 58, the isthmus 158 plus or minus 36, the postisthmic region 152 plus or minus 33, and the descending aorta at the level of diaphragm 130 plus or minus 18 millimetres squared per metre squared. The pulmonary root measured at the basal attachment of the leaflets was 253 plus or minus 28, the midpoint of the sinuses 352 plus or minus 58, the sinutubular junction 293 plus or minus 58, the right pulmonary artery 176 plus or minus 25, the left pulmonary artery 153 plus or minus 20, and sum of right and left pulmonary arteries 330 plus or minus 37 millimetres squared per metre squared. All indexes were consistent over a wide range for body surface areas. Conclusions: Definition of normative data of the great vessels may aid in the evaluation of congenital or acquired abnormalities, serving as guidelines for intervention during medical or surgical management and follow-up.

Background and objective: The arterial thermodilution technique offers the ability to measure cardiac output using only central venous and arterial catheters. However, the technique has been reported to overestimate cardiac output because of a higher loss of cold indicator due to the increased distance between the sites of injection and measurement. In this study, the two techniques were compared with respect to conditions of low cardiac output in which a longer passage time may further increase loss of indicator.

Methods: Seventeen anaesthetized dogs were studied during hypovolaemic shock and fluid resuscitation. Cardiac output measurements were carried out simultaneously by arterial and pulmonary artery thermodilution techniques.

Results: One-hundred-and-two measurements were performed. The mean cardiac output was 2.28 ± 1.4 L min−1 by the pulmonary arterial technique and 2.29 ± 1.56 L min−1 by the arterial thermodilution technique. The correlation coefficient between the two measurements was 0.95, the precision −0.04 ± 0.41 L min−1 and the limits of agreement from −0.86 to 0.78 L min−1. The agreement was also consistent at low cardiac outputs.

Conclusions: The arterial thermodilution technique may serve as a less invasive cardiac output monitor in conditions of severe bleeding and shock.

To elucidate if an effect of propofol on endothelium-dependent relaxation could contribute to propofol-induced vasodilation, smooth muscle relaxation of isolated human omental artery and vein segments precontracted by endothelin-1 were measured. Substance P induced a concentration-dependent relaxation (mean ±SEM) in both artery (63 ± 8.4% of precontraction, n=9) and vein (60 ± 11%, n=7). The relaxation was enhanced by 10−6 M propofol (artery, 72 a 9.5%, n=9; vein, 81 ± 12%, n=7) but not affected by 10−7, 10−5 and 10−4 M propofol. In the presence of Nω-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), 10−6 M propofol still enhanced the substance P-induced relaxation in arteries but not veins, whereas 10−4 M propofol inhibited the relaxation in both arteries (rightward shift of the concentration-response curve) and veins (28 ± 7.5%, n=8). In the presence of potassium chloride (to prevent hyperpolarization), the enhancement of substance P-induced relaxation by 10−6 M propofol was abolished in both arteries and veins whereas 10−5 and 10−4 M propofol reduced the relaxation in arteries (38 ± 13% at 10−5 M, n=6; 30 ± 11% at 10−4 M, n=6) but not in veins. These results demonstrate that propofol, at lower, clinically relevant concentrations, promotes endothelium-dependent relaxation mediated via hyperpolarization in human omental arteries and via both nitric oxide and hyperpolarization in human omental veins.

We describe a patient with aortic dissection extending into the right coronary artery who was successfully resuscitated and operated upon after a cardiac arrest during transfer to the operating room. The use of transoesophageal echocardiography was particularly helpful for rapid diagnosis of aortic type A dissection and urgent surgical treatment.

The effects of propofol and thiopental on three vasoconstrictors, acetylcholine, histamine, and serotonin were studied in isolated porcine and human coronary artery rings. Propofol and thiopental attenuated the contractile response to all mediators in a dose-dependent manner. This dilating effect was fairly weak using low concentrations (propofol 1 μg mL−1 and 10 μg mL−1, thiopental 5 μg mL−1 and 10 μg mL−1). In the presence of high concentrations (propofol 100 μg mL−1, thiopental 50 μg mL−1) marked relaxation was observed (propofol −32% up to −49%, P < 0,05; thiopental −23% up to −67%, P < 0.05). These dilating effects were seen both in intact and denuded rings, the differences were not significant. Human coronary artery segments were relaxed by thiopental (−22% to −76%) and propofol (−11% to −67%) to a similar extent. Our data indicate that propofol and thiopental relax isolated coronary segments in a dose-dependent manner, and that there is no evidence that these effects are dependent of endothelial factors.

The aim of this study was to elucidate the influence of four neuromuscular blocking substances on coronary vascular tone using the model of isolated porcine coronary artery segments. We studied the effects of four muscle relaxants, atracurium, pancuronium, rocuronium, and vecuronium (0.1, 1, and 10 μg mL−1 each), on the contractile response to three vasoconstrictors: acetylcholine, histamine, and serotonin. None of the neuromuscular blocking agents under investigation exerted a significant influence on the vasoconstricting effects of these mediators except for pancuronium, which dose-dependently attenuated acetylcholine-mediated contractions (−10.8% attenuation for 10 μg mL−1 pancuronium, P < 0.05). There was no difference between vessels with intact endothelium and denuded preparations. It is concluded that high-dose pancuronium exerts an antimuscarinic effect in vascular smooth muscle. The other neuromuscular agents studied do not alter vascular reactivity of isolated porcine coronary arteries.

The present study was designed to determine the direct effects of halothane, isoflurane and sevoflurane on the bovine epicardial coronary artery as well as their mode of action. We chose serotonin as the vasoconstrictor because it also causes endothelium-dependent relaxation of coronary arteries. Isolated spiral strips of bovine epicardial coronary artery with and without endothelium were suspended for isotonic contraction recordings in Tyrode's solution. KCl (80.4 mm) solution induced maximal contraction, regarded as the reference value (100%). The muscle strips were then exposed to increasing concentrations of serotonin from 10−8 to 10−4 m in the presence and absence of 1.5 MAC halothane, isoflurane or sevoflurane. All three drugs attenuated serotonin-evoked contraction in the coronary artery strips both those strips with and without endothelium (P < 0.05−0.001). However, there were no significant differences in the attenuation of serotonin-induced contraction of the strips, both with and without endothelium, in each drug group. The attenuation potency of halothane was more than that of isoflurane and sevoflurane. The results demonstrate that halothane, isoflurane and sevoflurane attenuate contractile responses evoked by serotonin in bovine epicardial coronary artery both with and without endothelium.