Effects of changes in pH and CO2 on pulmonary arterial wall tension are not endothelium dependent

We examined thechanges in isolated pulmonary artery (PA) wall tension on switchingfrom control conditions (pH 7.38 ± 0.01, PCO₂ 32.9 ± 0.4 Torr) toisohydric hypercapnia (pH change 0.00 ± 0.01, PCO₂ change 24.9 ± 1.1 Torr) ornormocapnic acidosis (pH change 0.28 ± 0.01, PCO₂ change 0.3 ± 0.04 Torr) and the role of the endothelium in these responses. In rat PA, submaximally contracted with phenylephrine, isohydric hypercapnia did not cause a significant change in mean (± SE) tension [3.0 ± 1.8% maximal phenylephrine-induced tension(P_o)]. Endothelial removal did not alter this response. In aorticpreparations, isohydric hypercapnia caused significant(P < 0.01) relaxation (27.4 ± 3.2% P_o), which waslargely endothelium dependent. Normocapnic acidosis caused relaxationof PA (20.2 ± 2.6% P_o), which was less(P < 0.01) than that observed in aorticpreparations (35.7 ± 3.4%P_o). Endothelial removal leftthe pulmonary response unchanged while increasing(P < 0.01) the aortic relaxation(53.1 ± 4.4% P_o).These data show that isohydric hypercapnia does not alter PA tone.Reduction of PA tone in normocapnic acidosis is endothelium independentand substantially less than that of systemic vessels.

     

Mechanical output impedance of the lung determined from cardiogenic oscillations.

The beating heart naturally oscillates the lung because of the close juxtaposition between these organs producing cardiogenic oscillations in flow that can be measured at the mouth when the glottis is open. Correspondingly, if the mouth is occluded, the same phenomenon produces cardiogenic pressure oscillations that can be measured just distal to the site of occlusion. The Fourier-domain ratio of these oscillations in pressure and flow constitutes what we call cardiogenic respiratory impedance (Zc). We calculated Zc between about 1.5 and 10 Hz in relaxed normal subjects at functional residual capacity with open glottis. Zc was insensitive to heart rate changes induced by exercise and had an imaginary part close to zero at all frequencies investigated. Its real part was similar to or smaller than resistance determined by the forced oscillation technique. We speculate that Zc measures the flow resistance of the central and upper airways of the lung. Zc may be useful as a means of obtaining information about lung mechanics without the need for an external source of flow perturbations.     

pH oscillations in transport process.

The paper discusses in more detail four published crystal structures which were used (McGavin, 1971a) in supporting the idea that base pairs in nucleic acid structures might be able to pair with identical base pairs about dyad axes so that specific four-strand structures are formed. The improbability of pairing unlike base pairs in such structures is discussed in more detail. Specific four-strand models themselves are also briefly discussed.     

Relationship between hyperventilation and excessive CO2 output during recovery from repeated cycling sprints

The purpose of the present study was to examine whether excessive CO2 output (VCO2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (DeltaLa) were 11.17+/-2.57 mM from rest to 5.5 min during first recovery and 2.07+/-1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (VCO2) was significantly higher than O2 uptake (VO2) during both recovery periods. This difference was defined as VCO2excess. VCO2excess was significantly higher during first recovery than during second recovery. VCO2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). DeltaLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETCO2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETCO2 during first recovery was significantly higher than that during second recovery. It is concluded that VCO2excess is not simply determined by ventilation during recovery from repeated cycle sprints.     

Differences in pH influence the fate of CO2 in plants

Soils represent the largest and most stable carbon pools on Earth, exceeding even the carbon aggregate found in the atmosphere and global phytomass. However, our understanding of how CO₂ travels from the soil to the atmosphere, and the role of plants in this journey, is not fully understood. An article in this issue of Physiologia Plantarum (Shimono et al. 2019) sheds light on this process and unearths the dramatic effect pH can have on the fate of CO₂ in plants.     

The CO2/pH ventilatory drive in fish.

That ventilation in fish is driven by O2 has long been accepted. The O2 ventilatory drive reflects the much lower capacitance of water for O2 than for CO2, and is mediated by O2 receptors that are distributed throughout the gill arches and that monitor both internal and external O2 levels. In recent years, however, evidence has amassed in support of the existence of a ventilatory drive in fish that is keyed to CO2 and/or pH. While ventilatory responses to CO2/pH may be mediated in part by the O2 drive through CO2/pH-induced changes in blood O2 status, CO2/pH also appear to stimulate ventilation directly. The receptors involved in this pathway are as yet unknown, but the experimental evidence available to date supports the involvement of branchial CO2-sensitive chemoreceptors with an external orientation. Internally-oriented CO2-sensitive chemoreceptors may also be involved, although evidence on this point remains equivocal. In the present paper, the evidence for a CO2/pH-keyed ventilatory drive in fish will be reviewed.     

CO2-laser radiation damage of the arterial wall

This study describes the effects of CO2 laser radiation on the histology of the normal rabbit arterial wall, using models that simulate laser angioplasty and anastomosis. Rabbit arteries were exposed to laser treatments similar to those used clinically; 40, 0.5 sec pulses of 40-60 mW, CO2 continuous wavelength laser, or a 1/2-circumferential laser anastomosis with a 60-80 mW continuous pulse. Aneurysms developed in 8 of 22 femoral, 1 of 22 carotid, and no controls at 12 week. There were small breaks in the internal elastic lamina with atrophy, loss of muscularis, "packing" of the elastica, thinning of the muscularis at the damage site, and enlargement of the arterial diameter. Aneurysms developed in one femoral and no carotid anastomosed artery. Laser anastomoses demonstrated more muscle damage and loss, with extensive scarring and a wider area of elastic loss than the controls. The intima was reestablished with focal reduplication of the internal elastic lamina. There were no histologic differences between the arteries which developed aneurysms and those which did not in either series. These results suggest that low power laser damage of the arterial wall consists mainly of destruction of the muscularis propria, with minimal damage to the elastica.     

Regulation of arterial PCO2 during intravenous CO2 loading.

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by "conventional" airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite "sensitivity" when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.