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B J Grant

Publications and source records attributed to B J Grant.

14 recordsLinked to original sources
PubMed1992

Compliance of the main pulmonary artery during the ventilatory cycle.

Transmural pulmonary arterial pressure (Ppa), diameter (D), and length (L) of a segment of the main pulmonary artery (MPA) were measured simultaneously in anesthetized open-chest dogs. The instantaneous volume was calculated from D and L. Pulmonary arterial elasticity for diameter (EpD) was calculated as the ratio of the amplitude of Ppa to D oscillation normalized by the mean D. Similar indexes were calculated for L (EpL) and V (Epv). Compliance per unit length was calculated from the dimensions and elasticity of the MPA. Under control conditions with 5 cmH2O positive end-expiratory pressure, EpD, EpL, and Epv at cardiac frequency were 175 +/- 27, 147 +/- 27, and 55 +/- 7 cmH2O, respectively. EpD increased with positive end-expiratory pressure, but EpL decreased and Epv was unaffected. EpD, EpL, Epv, and compliance per unit length were not significantly different between the start of inspiration and the start of expiration. In addition, there were no significant phase differences between the oscillations of Ppa and V at respiratory frequency. We conclude that the previously reported time variation of pulmonary arterial compliance during the ventilatory cycle is not due to time-varying properties of the MPA.

Animals↗
PubMed1979

Dependence of phrenic motoneurone output on the oscillatory component of arterial blood gas composition.

1. The hypothesis that respiratory oscillations of arterial blood gas composition influence ventilation has been examined. 2. Phrenic motoneurone output recorded in the C5 root of the left phrenic nerve and the respiratory oscillations of arterial pH in the right common carotid artery were measured in vagotomized anaesthetized dogs which had been paralysed and artificially ventilated. 3. The effect of a change in tidal volume for one or two breaths on phrenic motoneurone output was measured with the inspiratory pump set at a constant frequency similar to, and in phase with, the animal's own respiratory frequency. A reduction of tidal volume to zero or an increase by 30% led to a corresponding change of mean carotid artery pH level. The changes of carotid artery pH resulted in a change of phrenic motoneurone output, predominantly of expiratory time (Te) but to a lesser extent of inspiratory time (T1) and also peak amplitude of 'integrated' phrenic motoneurone output (Phr). Denervation of the carotid bifurcation blocked this response. 4. The onset of movement of the inspiratory pump was triggered by the onset of phrenic motoneurone output. When a time delay was interposed between them, the phase relationship between respiratory oscillations of arterial pH and phrenic motoneurone output altered. The dominant effect was to alter Te; smaller and less consistent changes of Phr and T1 were observed. 5. When the inspiratory pump was maintained at a constant frequency but independent of and slightly different from the animal's own respiratory frequency (as judged by phrenic motoneurone output), the phase relationship between phrenic motoneurone output and the respiratory oscillations of pH changed breath by breath over a sequence of 100-200 breaths, without change of the mean level of arterial blood gas composition. Te varied by up to 30% about its mean value depending on the phase relationship. Ti and Phr were also dependent on the phase relationship but varied to a lesser extent. The changes were comparable to the results obtained in paragraph 4. 6. It was concluded that phrenic motoneurone output is dependent in part on its relationship to the respiratory oscillations of arterial blood gas composition. 7. Information concerning a transient ventilatory disturbance is stored in the arterial blood in the form of an altered pattern of the respiratory oscillations of blood gas composition; this in turn can change breathing by an effect on the carotid bodies.

Action Potentials↗
PubMed1978

Endogenous and exogenous heptadecapeptide gastrin transport across the pig liver.

In vivo studies in the pig showed no net loss or gain of endogenous porcine gastrin during transport across the liver in fasting animals. Infusion of synthetic human heptadecapeptide gastrin (G-17) in doses of 0,25, 0,5 and 1,0 microgram/kg/min raised circulating gastrin levels to those found in the postprandial state. At no time was there a loss or gain of immunologically determined gastrin across the liver. Changes in the molecular size of gastrin, however, suggested that qualitative but not quantitative effects followed the administration of G-17 in vivo. The disappearance of gastrin from the circulation was biphasic, with an initial half-life of 3 minutes and a slower phase suggesting recirculation or multicompartment equilibration. The distribution at equilibrium was +/- 20% of body weight calculated from arterial levels, but 30-40% if portal or hepatic venous values were used. The mean blood production rate was +/- 125 microgram/day but the portal contribution was only 30 microgram/day, suggesting an important alternative source of gastrin.

Animals↗
PubMed1978

Metabolism of synthetic human heptadecapeptide gastrin by the isolated perfused rat liver.

Synthetic human heptadecapeptide gastrin-1 (SHG-17-1) and rat insulin were perfused cyclically through the isolated rat liver in a plasma-free medium. Synthetic human gastrin did not disappear from the medium at either physiological or supraphysiological levels, whereas rat insulin was cleared rapidly. Chromatography of perfusion samples showed that the SHG-17-U was neither lysed to smaller peptides nor changed to the larger molecular weight species. The isolated rat liver apparently plays no role in the metabolism of synthetic human heptadecapeptide gastrin-I.

Animals↗
PubMed1978

Bromhexine in severe asthma.

Fourteen patients with acute severe asthma necessitating hospital admission were all treated with a standard therapeutic regimen, and in addition received either bromhexine or placebo (initially intravenously and subsequently orally) double-blind. We were unable to show any significant improvement in the rate of recovery of the bromhexine-treated group, in terms of either arterial blood gases or change in peak expiratory flow rates.

Acute Disease↗
PubMed1976

Local regulation of pulmonary blood flow and ventilation-perfusion ratios in the coatimundi.

Small catheters (ca. 3 mm diam at tip) were wedged in subsegmental bronchi in anesthetized coatimundi (Nasua nasua) during spontaneous breathing. Mixed expired gases of a group of lobules were sampled continuously without contamination from neighboring units, and local tidal volume, frequency, carbon dioxide production, and oxygen consumption were measured, as well as mixed venous PO2 and PCO2. Local ventilation-perfusion ratio, alveolar PO2, PCO2, and blood flow were calculated. There was a 22% reduction (range 15-38) in local perfusion (as percent of flow at PAO2 100 mmHg) per 10 mmHg fall in local alveolar oxygen tension over the PAO2 range 150-36 mmHg. Local hypercapnia had little effect on local flow. Local tidal volume (ca. 1% of total tidal volume) was unaffected by changes in alveolar gas tensions. The contribution of vasoconstriction or vasodilatation, as a negative feedback system, to the stability of local PAO2 was greatest close to the physiologic range (65-85 mmHg) falloderate efficiency.

Animals↗
PubMed1975

Gastrins in human antrum, duodenum and peripheral circulation.

Previous studies have shown that arginine-stimulated gastrin release disappears after pyloric antrectomy in the human, while conflicting evidence indicates that gastrin is released by the human duodenum. The present study reconciles this conflict by showing that the major form of gastrin in the pyloric antrum is the heptadecpeptide form, while the duodenum contains mainly "big" and almost no heptadecapeptide gastrin. Fasting serum samples contain mostly "big" gastrins, while stimulated serum contains increased proportions of the heptadecapeptide and minigastrin species. It is suggested that local factors operative at the different G-cell sites determine the nature of gastrin released since "big" gastrins occur in most sites containing gastrin.

Chromatography, Gel↗
PubMed1975

Stimuli for heptadecapeptide gastrin release: a comparison of oral and intravenous arginiine-monochloride and oxo in normal, vagotomized and antrectomized patients.

Arginine, administered intravenously, was a more potent stimulus to gastrin release than oral Oxo-feeding, while oral arginine failed to elicit a response in normal subjects. Intravenous arginine stimulated a rise in serum gastrin only in normal subjects but not in antrectomized or vagotomized patients. The gastric antrum appears to be the major site of production of heptadecapeptide gastrin and 'mini' gastrin, as measured by the anti-serum used in our radio-immunoassay.

Administration, Oral↗