Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Ex Input:
Abstract: A clinical trial was undertaken to assess the effects of oral H1 (diphenhydramine hydrochloride) and H2 (cimetidine) histamine blockade on nasal resistance induced by topical histamine. Ten adult volunteers were tested on two separate occasions. Their noses were pretreated by oral administration of either combined H1 and H2 histamine antagonists or H1 antagonist and placebo. The nasal airflow resistive response to topical histamine was then determined. Combined histamine antagonism was significantly more effective in reducing the nasal resistive response to topical histamine than H1 antagonist alone (p less than 0.0001). Furthermore, ingestion of the oral H1 histamine antagonist, diphenhydramine hydrochloride, alone led to an increase in resistance of the unprovoked nose, whereas combined H1 and H2 antagonism did not lead to a significant change.

Ex Output:
The effects of combined H1 and H2 histamine antagonists on alterations in nasal airflow resistance induced by topical histamine provocation.

Ex Input:
Abstract: To determine the systemic absorption of epinephrine when it is given by inhalation, six normal volunteers were given 15 puffs, followed by 30 puffs, of epinephrine from a pressurized aerosol (160 micrograms epinephrine/puff). The peak mean (+/- SE) plasma epinephrine levels were 1.50 (+/- 0.61) and 4.22 (+/- 1.93) nmol/L 1 minute after each dose, respectively. The effect on physiologic finger tremor correlated with the plasma epinephrine level and returned to baseline 20 minutes after taking the higher dose. There was a small fall in mean plasma potassium levels of 0.45 mmol/L and a small rise in plasma glucose levels of 0.81 mmol/L. On a separate occasion an injection of 0.3 ml of 1/1000 (300 micrograms) epinephrine was given subcutaneously to the same individuals. This caused a peak plasma epinephrine level of 2.43 (+/- 0.47) nmol/L at 10 minutes, and this was still raised at 2.05 (+/- 0.41) nmol/L after 40 minutes. The maximum fall in the mean plasma potassium level was 0.43 mmol/L after the injection.

Ex Output:
Systemic absorption of inhaled epinephrine.

Ex Input:
Abstract: Slowly adapting pulmonary stretch receptors have been hypothesized to be the afferents mediating the vagally dependent, volume-related prolongation of expiratory time (TE) during expiratory loading. It has been further suggested that the vagal component of this prolongation of TE is due to the temporal summation of pulmonary stretch receptor (PSR) activity during expiratory loading. This hypothesis was tested in rabbits exposed to resistive and elastic single-breath expiratory loading while PSR's were simultaneously recorded. Both types of loads resulted in a decreased expired volume (VE) and increased expiratory duration (TE). The TE for resistive loads were significantly greater than for elastic loads for equivalent VE. Thus two different VE-TE relationships were found for resistive and elastic loads. When TE was plotted against the area under the expired volume trajectory, a single linear relationship was observed. PSR activity recorded during expiratory loading increased as VE decreased and TE increased. A single linear relationship resulted when the number of PSR spikes during the expiration was plotted against the associated TE for all types of loads. These findings demonstrate that the volume-related prolongation of TE with single-breath expiratory loads is associated with an increase in PSR discharge. These results support the hypothesis that the vagal component of load-dependent prolongation of TE is a function of both the temporal and spatial summation of PSR activity during the expiratory phase.

Ex Output:
Effect of expiratory loading on expiratory duration and pulmonary stretch receptor discharge.