Effect of gastric distension on cardiovascular parameters: gastrovascular reflex is attenuated in the elderly.

Stretching the stomach wall in young healthy subjects causes an increase in muscle sympathetic nerve activity and in blood pressure, the gastrovascular reflex. We compared healthy elderly subjects with healthy young subjects to find out whether the gastrovascular reflex attenuates in normal ageing and we studied whether there was a difference in autonomic function or gastric compliance that could explain this possible attenuation. Muscle sympathetic nerve activity, finger blood pressure and heart rate were continuously recorded during stepwise isobaric gastric distension using a barostat in eight healthy young (6 men and 2 women, 27 +/- 3.2 years, mean +/-s.e.m.) and eight healthy elderly subjects (7 men and 1 woman, 76 +/- 1.5 years). Changes in cardiac output and total peripheral arterial resistance were calculated from the blood pressure signal. The baseline mean arterial pressure and muscle sympathetic nerve activity were higher in the elderly group (both P < 0.05) and muscle sympathetic nerve activity increase during the cold pressor test was lower in the elderly group (P = 0.005). During stepwise gastric distension, the elderly subjects showed an attenuated increase in muscle sympathetic nerve activity compared to the young subjects (P < 0.01). The older group tended to show a higher increase in mean arterial pressure (P = 0.08), heart rate (P = 0.06) and total peripheral arterial resistance (P = 0.09) The cardiac output rose slightly in both groups without significant difference between groups. The fundic compliance did not differ between groups. We conclude that stepwise gastric distension caused an increase in muscle sympathetic nerve activity in both groups, but the increase in the elderly was attenuated.

The gastro-oesophageal pressure inversion point revisited.

BACKGROUND: The pressure inversion point (PIP) is defined as the point at which, during stationary pull-through manometry of the oesophago-gastric junction, the polarity of the respiratory-associated pressure variations changes. Traditionally, the PIP is ascribed to transition of the pressure sensor from the abdominal to the thoracic cavity. We used high-resolution manometry to investigate the validity of this concept in six healthy volunteers and six patients with a sliding hiatus hernia. METHODS: In the analysis, the position of the PIP was identified. When there was a second, more distal, PIP, its position was also noted. The amplitude of the respiratory-associated pressure variations, defined as the difference between end-expiratory and end-inspiratory pressure, was measured. RESULTS: Double PIPs were found both in healthy controls (23 +/- 8% of time) and in patients (38 +/- 9% of time). Amplitudes of the respiratory-associated pressure variations were significantly higher at the proximal and distal border of the PIP (3.36 +/- 0.2 kPa and 2.29 +/- 0.2 kPa) than in the oesophageal body (0.54 +/- 0.03 kPa, P < 0.001) and in the stomach (0.54 +/- 0.03 kPa, P < 0.001). We also observed a relationship between the localization of the highest end-expiratory pressure and the position of the PIP. During TLOSRs respiratory variation amplitudes at the proximal and distal border of the PIP decreased to 0.61 +/- 0.02 kPa and 0.29 +/- 0.01 kPa, approximating respiratory pressure variation in oesophagus and stomach. CONCLUSION: Our findings suggest that the PIP is caused by sliding of the high-pressure zone along pressure sensors rather than by the transition from the thoracic to the abdominal compartment.

Association between pain episodes and high amplitude propagated pressure waves in patients with irritable bowel syndrome.

OBJECTIVES: In the pathogenesis of irritable bowel syndrome (IBS), both increased visceral sensitivity and altered colonic motility seem to play a role. The aim of this study was to quantify the temporal relationship between pain episodes and the occurrence of high amplitude propagated pressure waves (HAPPWs). METHODS: A total of 11 IBS patients with the nonconstipation predominant pattern of IBS and 10 sex- and age-matched healthy volunteers were studied. On day 1, a solid state manometric catheter was positioned in the left colon and connected to a data logger. The subjects then went home. Thereafter they pressed a button on the data logger at the beginning and end of each pain episode. The 24-h manometric signal recorded on day 2 was divided into consecutive 5-min periods. These periods were evaluated for the occurrence of pain and HAPPWs. Fisher's exact test was applied to calculate the probability that HAPPWs and pain episodes were unrelated. The symptom association probability (SAP) was calculated as (1.0 - P) x 100%. A SAP of >95% was considered to indicate that the observed association did not occur by chance. RESULTS: In four of seven patients with pain on day 2, the SAP was >95%. HAPPWs that were related to pain originated at a more proximal level (p = 0.026) and occurred earlier (p = 0.007) than HAPPWs that were not related to pain. The duration of a pain period was correlated with the number of pain-related HAPPWs in that period (r = 0.906, p = 0.013). Two of the 10 healthy subjects experienced pain, and these pain episodes were not associated with HAPPWs. CONCLUSIONS: Using objective analysis techniques, an association between pain episodes and HAPPWs was found in nonconstipated IBS patients with pain. HAPPWs that are associated with pain are only slightly different from HAPPWs not associated with pain.

Elicitation of transient lower oesophageal sphincter relaxations in response to gastric distension and meal ingestion.

The aim of this study was to compare the effect of graded gastric barostat distension and meal-induced fundic relaxation on the elicitation of transient lower oesophageal sphincter relaxation (TLOSR). In 15 healthy subjects, stepwise fundic distension and oesophageal manometry were performed simultaneously. Next, the effect of meal ingestion on proximal stomach volume and lower oesophageal sphincter function was studied. During stepwise barostat distension of the proximal stomach, a significant linear correlation between intragastric pressure (r = 0.91; P < 0.01) and the TLOSR rate during inflation and subsequent deflation (r = 0.96; P < 0.01) was found. A similar relationship was found for volume. In addition, after meal ingestion, the TLOSR rate increased significantly from 1.40 +/- 3 to 5.4 +/- 1.5 h-1 (P < 0.01) and 5.2 +/- 1.7 h-1 (P < 0.01), respectively, during the first and second 30-min postprandially. However, at similar calculated intragastric volumes, barostat distension led to a significantly higher TLOSR rate than the meal. Similarly, distension-induced increase in gastric wall tension, estimated from the measured bag pressure and volume using Laplace's law, was associated with significantly higher TLOSR rates (P < 0.01). In conclusion, the rate of TLOSRs in healthy volunteers is directly related to the degree of proximal gastric distension and pressure-controlled barostat distension is a more potent trigger of TLOSRs than a meal. The latter finding suggests that tension receptor activation is an important stimulus for TLOSRs.