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Biomedical subjects

J F Green

Publications and source records attributed to J F Green.

At least 55 records · Page 3Linked to original sources
PubMed1984

Pulmonary C-fibers evoke both apnea and tachypnea of pulmonary chemoreflex.

Pulmonary C-fibers initiate the prompt apnea evoked by pulmonary arterial injections of capsaicin, but their role in the subsequent rapid shallow breathing of the pulmonary chemoreflex is disputed. To determine whether this reflex tachypnea is triggered by pulmonary C-fibers rather than by afferents further downstream, we separately perfused the pulmonary and systemic circulation in anesthetized dogs. When the lungs were rhythmically inflated, injection of capsaicin (0.5-20.0 micrograms X kg-1) into the isolated pulmonary circulation evoked an immediate cessation of phrenic nerve firing ("apnea") and when phrenic bursts resumed, a reduction in their amplitude. Phrenic burst frequency was usually entrained to the ventilator cycle and did not increase. By contrast, when entrainment of phrenic bursts was avoided by statically inflating the lungs at a transpulmonary pressure of 3 cmH2O, the injection of capsaicin evoked apnea, followed by a prolonged increase in phrenic burst frequency and a decrease in amplitude ("rapid shallow breathing"). The infusion of capsaicin (10-20 micrograms X kg-1 X min-1) also evoked rapid shallow breathing, but without apnea. Our results are consistent with the hypothesis that in spontaneously breathing animals, stimulation of pulmonary C-fibers evokes rapid shallow breathing.

Animals↗
PubMed1984

Peripheral limitations to exercise.

We present a computer simulation of a two-compartment model of the systemic circulation which demonstrates how this model can be used to understand the mechanism(s) for the maximal exercise cardiac output (Q). The model consists of two parallel vascular channels, the splanchnic channel (all blood draining through the hepatic veins) and the peripheral channel (all other vascular beds). The distinguishing characteristic of each channel is the product of its venous compliance and venous resistance. Model parameters for the human circulation were estimated from similar parameters obtained directly from animal experiments. "Exercise" was achieved by decreasing the compliance of both channels to 40% of their initial value and by redistributing the Q such that the fraction of Q perfusing the splanchnic channel fell from 38 to 5%, while that perfusing the peripheral channel (skeletal muscles) increased from 62 to 95%. These combined changes increased Q from 4.4 to 22.0 l X min-1 and suggest that maximal adjustments of the two-compartment model parameters lead to a prediction of a maximal Q that approaches the maximal Q usually obtained by humans during exercise.

Blood Circulation↗
PubMed1983

Documentation of a venous resistance in the baboon.

In the steady state, blood flow out of the heart must be the same as blood flow into the heart. Thus, flow in the cardiovascular system should depend not only on cardiac determinants of flow--pericardial pressure, afterload, heart rate, and contractility--but also on systemic venous determinants of flow as well. We studied the venous determinants of flow in nine baboons. The mean systemic pressure, the upstream driving pressure for venous return, was 10 mm Hg higher than the right atrial pressure. Flow generated by this upstream pressure was modulated by a venous resistance. This resistance acted as if it were interposed between the upstream capacitance vessels and the right atrium. These determinants of venous return in the baboon would be inadequately described by classical concepts of cardiovascular physiology. We suspect that classical concepts would be inadequate in man as well.

Animals↗
PubMed1983

Ventilatory changes associated with changes in pulmonary blood flow in dogs.

To examine the influence of pulmonary blood flow (Qp) on spontaneous ventilation (VE), we isolated the systemic and pulmonary circulations and controlled the arterial blood gases and blood flow (Q) in each circuit as we measured VE. Each dog was anesthetized with ketamine and maintained with halothane. Systemic Q was drained from the right atrium and pumped through an oxygenator and heat exchanger and returned to the aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and pumping it to the pulmonary artery. The heart was fibrillated, all cannulas were brought through the chest wall, and the median sternotomy was closed. The dog was then allowed to breathe spontaneously. The arterial O2 partial pressure (PO2) of both circuits was maintained greater than 300 Torr. Systemic Q was maintained at 0.080 l X min-1 X kg-1. Initially the arterial CO2 partial pressure (PCO2) of both circuits was set at 40 Torr as Qp was varied randomly between approximately 0.025 and 0.175 l X min-1 X kg-1. The average VE-Qp relationship was linear with a slope of 1.45 (P less than 0.0005). Increasing the arterial PCO2 of both circuits to 60 Torr elevated VE an average of 0.37 l X min-1 X kg-1 at each level of Qp (P less than 0.0005). Vagotomy abolished the effect of Qp on VE. Increasing Qp affected the systemic arterial PCO2-VE response curve by shifting it upward without altering its slope. These results demonstrate that increases in Qp are associated with increases in VE. This phenomenon may contribute to exercise hyperpnea.

Animals↗
PubMed1983

alpha-Adrenoreceptor stimulation of the systemic circulation in dogs.

The influence of phenylephrine (an alpha-adrenoreceptor agonist) on the arterial and venous systems of the systemic circulation was studied in 10 anesthetized dogs during a right ventricular bypass procedure. Phenylephrine (1 microgram X kg-1 of body weight X min-1) produced a significant (P less than 0.001) increase in arterial resistance, no change in venous resistance, and a mild decrease in venous compliance. Seemingly in the clinically normal dog, a dose of phenylephrine sufficient to double total peripheral resistance will redistribute a small amount of blood volume from the venous to arterial systems with a slight decrease in venous return and concomitant attenuation of cardiac output.

Animals↗
PubMed1983

The transition from oocyte-coded to embryo-coded glucose phosphate isomerase in the early mouse embryo.

The proportions of glucose phosphate isomerase (GPI-1) allozymes produced by early (Gpi-1sa/Gpi-1sb female X Gpi-1sc/Gpi-1sc male)F1 mouse embryos were analysed by quantitative cellulose acetate electrophoresis. Technical controls showed that this system is extremely sensitive, quantitatively reproducible and quite accurate. Genetic controls established that the Gpi-1sa/Gpi-1sb mothers were homozygous for the Gpi-1tb temporal allele, that produces relatively high GPI-1 activity in the oocyte. The oocyte-coded enzyme lasted until about 5 1/2 days post coitum (p.c.) or shortly thereafter. The maternally derived, embryonic Gpi-1s allele was expressed no earlier than the paternally derived allele. This was first expressed between 2 1/2 and 3 1/2 days p.c. In this cross, most of the transition from oocyte-coded to embryo-coded GPI-1 occurred between 2 1/2 and 5 1/2 days p.c.

Alleles↗
PubMed1982

Evidence for pulmonary CO2 chemosensitivity: effects on ventilation.

To determine whether there is a pulmonary chemoreceptor for CO2 that influences spontaneous ventilation (VE), we separated the systemic and pulmonary circulations and controlled partial pressure of CO2 (PCO2) independently in each circuit under hyperoxic conditions and measured VE. Dogs were anesthetized with ketamine and maintained with 1% halothane. Systemic venous return was drained from the right atrium and passed through an oxygenator and heat exchanger; blood was returned to the ascending aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery. The heart was fibrillated; all cannulas were brought through the chest wall; and the median sternotomy was closed. Blood flow through both circuits was maintained at 0.080 l . kg-1 . min-1. Systemic PCO2 (PSCO2) was held constant at three different nonoscillatory levels. At each level, pulmonary PCO2 (PpCO2) was randomly varied between approximately 7 and 85 Torr. With PSCO2 at 43.5 +/- 0.4 Torr, VE increased 2.67 +/- 0.61 l . min-1 as PpCO2 was varied between these limits. With PSCO2 at 63.8 +/- 2.5 Torr, VE increased 3.95 +/- 0.73 l . min-1 over these same limits of PpCO2. With PSCO2 below 25--30 Torr, the dogs were apneic and no longer responded to changes in PpCO2. The effect of PpCO2 on VE was abolished by vagotomy. These results suggest the presence of a CO2 chemoreceptor in the lung that interacts with the nonpulmonary chemoreceptors in the control of VE.

Animals↗
PubMed1980

Aporphines XXVI: GLC and mass spectrometric properties of trifluoracetyl derivatives of N-methyl-, N-propyl-, and noraporphines.

The O-trifluoroacetyl and N,O-trifluoroacetyl derivatives of a series of aporphine and noraporphine alkaloids were prepared, and their GLC and mass spectrometric characteristics were determined. The positional isomers apocodeine and isoapocodeine were resolved chromatographically as their trifluoroacetyl derivatives, and their mass spectra were distinctly different. Mass spectrometry fragmentation processes apparently unique to N-trifluoroacetyl derivatives of nonraporphines were observed. Plausible mechanisms for the formation of the major ions in the mass spectra of the various compounds are given.

Aporphines↗
PubMed1979

Aporphines. 25-trimethylislyl derivatives of N-methyl and N-propyl aporphines: gas chromatographic and mass spectrometric properties.

A series of synthetic, semisynthetic and naturally occurring aporphine alkaloids were converted to the O-trimethylsilyl derivatives, and analyzed by gas chromatography mass spectrometry. A discussion of structurally informative fragment ions along with gas chromatographic data is presented. Their applicability to the analysis of biological metabolites of apomorphine, a CNS active structural analog of dopamine, is discussed.

Apomorphine↗
PubMed1978

Mechanisms of pulsus paradoxus in upper airway obstruction.

Pulsus paradoxus, a greater than 10 Torr systolic pressure fluctuation during the respiratory cycle, is seen in upper airway obstruction. To test the hypotheses 1) that blood is pooled in the pulmonary circulation with reduced return to the left heart during inspiration and 2) that inspiration increases left ventricular afterload, the following was done. Esophageal pressure (Pes), pericardial pressure (Pp), left atrial transmural pressure (Platm), and left ventricular transmural pressure at end-isovolumic systole (Plvtm) were recorded during partially obstructed inspirations in spontaneously breathing dogs anesthetized with pentobarbital (25 mg/kg). Changes in Pes and Pp were nearly identical (r = 0.9883) confirming that changes in Pes adequately reflect changes in Pp. During inspiration Platm and Plvtm increased 0.5 and 0.4 Torr, respectively, per Torr decrease in Pes suggesting that increased blood return to left atrium and increased left ventricular afterload occur. Similar changes were observed during near constant thoracic volume (total airway block) and cardiac reflex blockade (atropine 0.05 mg/kg and propranolol 0.5 mg/kg). Thus mechanical factors including left ventricular afterload appear of major importance in producing pulsus paradoxus in upper airway obstruction.

Airway Obstruction↗