The relation of pulmonary hemodynamics to pathological change in the pulmonary vasculature was examined in a model of unilateral pulmonary venous (PV) obstruction. The left upper pulmonary vein (A group, n=6) or both the left upper and left lower pulmonary veins (B group, n=6) of two-week-old piglets were banded; the control group (n=6) was sham operated. At eight weeks after PV banding, mean pulmonary arterial pressure was highest in the B group, intermediate in the A group and lowest in the control group. In all groups, the media of the pulmonary artery was equally thickened in both lungs, whereas the media of the pulmonary vein was thickened only in those lung lobes having stenotic pulmonary veins. For all animals from three groups, left pulmonary arterial wedge pressure (PAWP) correlated with medial thickness of the pulmonary arteries of the right lung (r=0.76, p=0.003), the left upper lobe (r=0.54, p<0.03), the left lower lobe (r=0.49, p=0.04). This finding suggests that the pathogenesis of PAWP-related medial thickening of the bilateral lung pulmonary artery begins with the sensing by the bilateral lung of PV pressure buildup in the unilateral lung.

Animals↗

PubMedDate not supplied

Hypoxia and cold stress on pulmonary venous obstruction.

Hemodynamic changes induced by hypoxia and cold stress were examined on the model of pulmonary venous obstruction (PVO) to investigate the mechanism of pulmonary hypertensive crisis. Bilateral pulmonary venous stenosis was surgically created in 7 newborn piglets of the PVO group. Sham operations were performed on 6 piglets of the control group. Following the baseline hemodynamic measurement (FiO2 = 0.3) at 8 weeks after the operation, the piglets were exposed to hypoxia (FiO2 = 0.14) for 10 minutes, and were also exposed to cold stress for 20 minutes. Hypoxia significantly increased mean pulmonary arterial pressure in the PVO group. Hypoxia increased not only pulmonary arterial resistance, but also pulmonary venous resistance in the PVO group. Cold stress did not change pulmonary arterial resistance or pulmonary venous resistance in each group. In the lungs of the PVO group, the medial muscular layer of the pulmonary arteries and pulmonary veins were thickened. This probably accelerates hypoxia-induced vasoconstriction, which in turn increases pulmonary arterial and venous resistances.

Animals↗

PubMedDate not supplied

A new method for detecting diatoms in human organs.

A new method for diatom detection is described. It includes an ultrasonic irradiation procedure with the use of a tissue solubilizer. The method is easy to carry out and is less time-consuming than previous techniques.

Aged↗

PubMedDate not supplied

Molecular chaperone function of mammalian Hsp70 and Hsp40--a review.

Virtually all organisms respond to up-shifts in temperature (heat shock) by synthesizing a set of proteins called heat shock proteins (HSPs). The HSPs are induced not only by heat shock but also by various other environmental stresses. Induction of HSPs is regulated by the trans-acting heat shock factors (HSFs) and cis-acting heat shock element (HSE) present at the promoter region of each heat shock gene. Usually, HSPs are also expressed constitutively at normal growth temperatures and have basic and indispensable functions in the life cycle of proteins as molecular chaperones, as well as playing a role in protecting cells from the deleterious stresses. Molecular chaperones are able to inhibit the aggregation of partially denatured proteins and refold them using the energy of ATP. Recently, there are expectations for the use of molecular chaperones for the protection against and therapeutic treatment of inherited diseases caused by protein misfolding. In this review, the focus will be on the mammalian Hsp40, a homologue of bacterial DnaJ heat shock protein, and the beneficial functions of molecular chaperones.

Animals↗

PubMedDate not supplied

The role of pulsatility in end-organ microcirculation after cardiogenic shock.

To estimate the effectiveness of pulsatility in end-organ microcirculation after cardiogenic shock, experimental studies using swine were done. Cardiogenic shock was produced in 14 pigs by ligating the left anterior descending branches so that mean aortic pressure dropped to 60% of the control value. After inducing shock, left atrial to ascending Ao bypass was initiated. A pneumatic pulsatile pump (Zeon Medical Inc, Tokyo, Japan) was used in seven pigs (Group P) and a centrifugal pump (BP-80, BioMedicus Inc, Minneapolis, MN) in seven (Group NP). In both groups, about half the usual cardiac output was supported for 3 hr, maintaining mean aortic pressure at approximately 100 mm Hg. The pulse pressure was 36.6 +/- 4.6 mm Hg in Group P, and 14.3 +/- 1.5 mm Hg in Group NP. Epicardial and endocardial regional flows recovered after assist in both groups. There were no significant differences between the two groups. However, liver tissue flow, renal cortex flow, and stomach mucous flow in Group P was significantly higher than those of Group NP after support (p < 0.05). In addition, arterial blood ketone ratio in Group P was 0.61 +/- 0.13 vs 0.39 +/- 0.06 in Group NP, a significant difference (p < 0.05). These results suggest that in uneven blood flow distribution of end organs after cardiogenic shock, pulsatility was effective in improving and maintaining function and microcirculation of end organs, preventing multiorgan failure.

Animals↗