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Biomedical subjects

R W Torrance

Publications and source records attributed to R W Torrance.

At least 19 recordsLinked to original sources
PubMed1998

Allometric algorithms and the work of the heart.

In mammals, blood velocity at the aortic root varies little with body mass, M, and so the kinetic work is a constant fraction of the total work of the heart, and also of the metabolic rate of the animal. This happens because body metabolism and the cross-sectional area of the aortic root vary to the same power of M. But if metabolism increased with M to a higher power than area, aortic velocity would increase and kinetic work would become a greater fraction of total work in a large animal. In larger animals it could exceed pressure work at rest and even more so in exercise. But there is a limit to how much an increase in aortic area can balance an increase in metabolism without the aorta becoming ridiculously large. Also aortic area should not exceed ventricular area. These factors could dictate how high the power of M is in relation to the metabolism of an animal.

Algorithms↗
PubMed1996

Haldane and indifferent gases: O2 secretion or CO excretion?

The method that Haldane used in 1911, when he claimed that O2 comes to be secreted into the pulmonary capillary blood after a few days at altitude, required that CO be an indifferent gas except for one property: it combines with Hb. But that is now known not to be true. CO is formed when Hb is katabolised, it reacts with many substances in the body, and it is involved in transmissions between cells. If, instead of supposing that CO is an indifferent gas, one proceeds from Barcroft's observation that PaO2 remains equal to PAO2 on going to altitude, the conclusion from Haldane's observations must be that he showed that CO has come to be actively excreted from the body after a few days at altitude. And that presumably happened because, as Killick (J. Physiol., London, 107: 27-44, 1948) suggested, Haldane's method required that the subject be repeatedly exposed to CO. The transport of CO around the body by Hb, and the possible effects on this, and on DLCO, of active excretion of CO, have to be considered.

Altitude↗
PubMed1996

Alveolar Pco2 and Po2 of high-altitude natives living at sea level.

This study was designed to determine whether subjects born at high altitude (HA; 2,000 m or above) who subsequently move to near sea level (SL) develop end-tidal PCO2 (PETCO2) and PO2 (PETO2) values that equal those of SL natives living near SL. A total of 108 male HA natives living near SL were identified by survey of a district in Lima, Peru, and a further 108 male SL natives from the same district were identified as control subjects. Of these subjects, satisfactory data for inclusion in the study were obtained from 93 HA and 82 SL subjects. Mean PETCO2 and PETO2 values were 37.7 +/- 2.5 (SD) and 104.7 +/- 3.2 Torr, respectively, in HA subjects and 37.7 +/- 2.2 and 104.8 +/- 3.0 Torr, respectively, in SL subjects. The average difference between SL natives and HA natives for PETCO2 was 0.07 Torr (-0.64 to 0.78; 95% confidence interval) and for PETO2 was 0.05 Torr (-0.89 to 0.99, 95% confidence interval). The average age and weight of the SL and HA subjects did not differ, but the HA subjects were shorter and tended to have larger vital capacities, consistent with their origin at HA. We conclude that the PETCO2 and PETO2 near SL of SL natives and HA natives do not differ.

Acclimatization↗
PubMed1991

Effect of waveforms of inspired gas tension on the respiratory oscillations of carotid body discharge.

The responses of carotid body chemoreceptor discharge to repeated ramps (20- to 60-s forcing cycle durations) of inspired gas tensions were studied in spontaneously breathing and in artificially ventilated pentobarbitone-anesthetized cats. In all animals the mean intensity of chemoreceptor discharge followed the frequency of the forcing cycle, and superimposed on this were oscillations at the frequency of ventilation (breath-by-breath oscillations). The amplitude of the breath-by-breath oscillations in discharge was often large, and it waxed and waned with the forcing cycle. It was greatest when the mean level of discharge was falling and smallest near the peak of mean discharge. No qualitative differences were observed between PO2-alone forcing in constant normocapnia and PCO2-alone forcing in constant hypoxia. The variation in the amplitudes of breath-by-breath oscillations was shown to be due primarily to variations in the amplitudes of the downslope component of the discharge oscillation. Variations in the upslope component of individual oscillations were small. The factors responsible for the breath-by-breath oscillations are discussed, and it is concluded that the shape of the waveform of arterial gas tensions that stimulate the peripheral chemoreceptors departs markedly from that of a line joining end-tidal gas tensions. This causes breath-by-breath oscillations of discharge to be very large after an "off" stimulus. Reflex studies involving the forcing of respiratory gases should therefore include consideration of these effects.

Animals↗
PubMed1988

Do oxygen tension variations contribute to the respiratory oscillations of chemoreceptor discharge in the cat?

1. A high-frequency high-flow ventilator has been developed which will produce abrupt changes in alveolar gas tensions. We have used it to study the individual contributions of PCO2 and PO2 in producing the oscillations which occur in the discharge of carotid chemoreceptors in the cat with respiration, by producing repeated end-tidal alternations (i) of PCO2 in constant hypoxia, (ii) of PO2 in constant normocapnia and (iii) of both PO2 and PCO2, i.e. of asphyxia. 2. The chemoreceptor response to alternations of PCO2 was always brisker than that to alternations of PO2 at 2, 4 or 8 s cycle durations. 3. An increase in the frequency of the alveolar alternation shortened the difference between the response times to PCO2 and PO2 but it increased the phase difference between the stimulus and the response waveforms. 4. With 4 s cycles, in normocapnic hypoxia, PCO2 was 2.9 times more effective (impulses s-1 Torr-1) than PO2 in producing oscillations in discharge. 5. The oscillations in discharge to simultaneous alternations of PO2 and PCO2 were not significantly different from the sum of individual oscillations to alternations of PCO2 and of PO2 alone. This was true with respect to timing and to amplitude of the oscillation. 6. Usually the amplitude of the chemoreceptor discharge oscillation in response to an asphyxial alternation was greater than the amplitude of the oscillation to either its PCO2 or its PO2 component alone. However, at the highest frequencies used, the phase relation between the PCO2 and PO2 components of the response could lead to the summed asphyxial response being less than its individual components. 7. The amplitudes and shapes of the oscillations in response to 4 s PCO2 alternations were not affected by changing either the steady-background PO2 or PCO2, but the amplitudes of the oscillations to pure PO2 alternations were enhanced by hypoxia and by hypercapnia. The importance of PO2 and PCO2 in giving rise to the natural respiratory oscillations in chemoreceptor discharge depends on the mean levels of the two gases. In normocapnic hypoxia (PO2 ca. 50 Torr) they are equally important but when PO2 is raised it becomes less important.

Action Potentials↗
PubMed1983

The effect on breathing of abruptly reducing the discharge of central chemoreceptors.

Tris, a powerful CO2 buffer, was injected through one vertebral artery directly at the central chemoreceptive region in bilaterally vagotomized pentobarbitone anaesthetized cats. This was intended to reduce central chemoreceptor drive abruptly. Injections in inspiration shortened that inspiration and prolonged the following expiration. Injections given early in expiration often prolonged that expiration and also the following inspiration, but most injections given in an expiration shortened that expiration and also shortened the following inspiration. Tidal volume (VT) was invariably reduced. A plot of VT against delay from an injection to the termination of inspiration shows that VT falls with a half time of about one second. The changes in the pattern of breathing were similar to those after abrupt removal of carotid body chemoreceptor discharge (Nye et al., 1981) though the latency to the first response of air flow was about 100 msec longer. These observations support the idea that peripheral and central chemoreceptors have similar connections with the respiratory centre.

Animals↗
PubMed1982

Arterial chemoreceptor inhibition by a single inspirate containing carbon monoxide is accounted for by raised arterial PO2.

Carbon monoxide (CO) slugs (10--100 ml) injected into the inspired air of 6 hypoxic, anaesthetized cats reduced carotid body chemoreceptor discharge. The inhibition was invariably associated with a sharp rise in Pa, O2 which was continuously recorded by a fast responding intravascular electrode. This suggests that CO in solution in the blood leaving the lungs displaces O2 from blood after it was left the exchange region and that the displaced O2 raises the Pa, O2 and inhibits chemoreceptor discharge. Our results provide no support for the idea that a haemoglobin-like pigment is involved in the mechanism of arterial chemoreceptor excitation.

Action Potentials↗
PubMed1982

The effects on respiration in the cat of the sudden excitation of cerebral vascular nociceptors by carbon dioxide.

1. Injection of CO2-saturated saline in a distal direction into either a vertebral artery or an internal maxillary artery in pentobarbitone-anaesthetized cats produced abrupt changes in respiration. Vertebral-artery injections produced a transient inhibition of respiration, followed by a stimulation of it. Internal-maxillary-artery injections produced only the inhibition. 2. Injections during inspiration usually shortened that inspiration, reduced its volume and prolonged the following expiration. In the first 30% of an expiration they prolonged that expiration, but given in the next 50% they shortened it. In the last 20% of expiration internal-maxillary-artery injections again slightly prolonged the expiration. 3. Phenyl diguanide injected into either a vertebral or an internal maxillary artery also produced abrupt effects on respiration. 4. The effects of CO2-saturated saline were abolished by intravenous acetazolamide, suggesting that nociceptors may be affected by a change in local pH. 5. The effects may arise from the excitation of vascular nociceptors, and our observations may suggest a way of studying in animals the receptors responsible for headache.

Acetazolamide↗
PubMed1981

The effect on breathing of abruptly stopping carotid body discharge.

In bilaterally vagotomized, decerebrate or pentobarbitone anaesthetized cats, intense carotid body discharge (FET O2 ca. 0.075) was abruptly removed by injections centrally of 100% O2-equilibrated Ringer into both external carotid arteries. In an inspiration the injections usually shortened that inspiration, reduced its volume and prolonged the immediately following expiration. Early in expiration they prolonged that expiration, but later in expiration they shortened it. The inspiratory results can be reconciled with von Euler's model of the inspiratory off-switch if the off-switch acts early because a reduction in chemoreceptor input lowers its threshold more rapidly than it reduces the input to it. The threshold falls to half of its final value in about one second. The respiratory centres respond to decreases in carotid body activity nearly as quickly as to increases, and expiration can be altered independently of the preceding inspiration. We present a simple model of the control of expiratory duration.

Animals↗
PubMed1981

Studies on the localization of pulmonary carbonic anhydrase in the cat.

1. We considered whether some of the carbonic anhydrase of the lung is on the surface of the pulmonary capillaries so that it acts directly on plasma as it traverses the pulmonary capillaries to accelerate CO2/pH equilibration. 2. Experiments were performed on spontaneously breathing cats or saline-perfused cat lungs. 3. In intact cats, Tris buffer injected suddenly into the right atrium transiently lowered end-tidal CO2, FET, CO2. The rate of CO2 uptake came within an order of magnitude of taxing the calculated diffusing capacity of the lungs. The fall in FET, CO2 was much reduced by giving the carbonic anhydrase inhibitors benzolamide or acetazolamide intravenously, or even by adding benzolamide to the injected Tris. The fall in FET, CO2 could be increased by adding carbonic anhydrase to the injected Tris. 4. In saline-perfused lungs ventilated with 5% CO2 in O2, Tris or alkalinized albumin solution injected into the pulmonary artery transiently lowered FET, CO2 and the effect was reduced by the addition of benzolamide or acetazolamide to the injectate. Injecting Tris bubbled with 15% CO2 caused a rise in FET, CO2, also reduced by benzolamide. 5. We conclude that pulmonary carbonic anhydrase is readily accessible to large or small molecular wight buffers in the capillaries and to inhibitors, and we suggest that it is located on the luminal surface of the capillary endothelium.

Acetazolamide↗
PubMed1981

The location of carbonic anhydrase in relation to the blood-brain barrier at the medullary chemoreceptors of the cat.

1. The role of carbonic anhydrase near the medullary chemoreceptors has been investigated in the cat. Vertebral artery injections have been used to cause abrupt changes in respiration as a result of changes in the activity of medullary chemoreceptors. 2. Injections of 100% CO2-saline were used to stimulate respiration and of Tris or alkalinized albumin solution to cause a reduction in respiration. 3. The injections gave rapid effects. We studied the effect on these of benzolamide (1-4 mg/kg i.v.) a carbonic anhydrase inhibitor which does not easily cross the blood-brain barrier and acetazolamide (50 mg/kg i.v.) an inhibitor which crosses the barrier more easily. 4. The effects of Tris were much reduced after benzolamide. Even addition of benzolamide to the injected Tris or albumin was sufficient to reduce their effects. 5. The effects of CO2-saline were reduced only after acetazolamide i.v. Whereas addition of carbonic anhydrase to injected Tris potentiated the effects on respiration, after acetazolamide this potentiation was much less marked. 6. It is concluded that carbonic anhydrase acts in the region of the medullary chemoreceptors at two sites: (a) outside the blood-brain barrier, probably at the luminal surface of the capillary endothelium, where it may act on plasma buffers, and (b) inside the barrier, in association with the chemoreceptors, where it may accelerate CO2/pH equilibration.

Animals↗