PubMed Health⌕ Search

Biomedical subjects

W J Pearce

Publications and source records attributed to W J Pearce.

80 records · Page 5Linked to original sources

Analytical diagnostic peritoneal lavage in the diagnosis of intra-abdominal injury.

Diagnostic peritoneal lavage (DPL) was modified to detect dynamic changes occurring in lavage fluid in dogs following liver, spleen, or intestinal injury. In 33 animals lavage fluid was serially sampled over 75 minutes and analyzed for RBC and other variables. The spun sediment was Gram stained. In control groups, either saline or autologous blood was instilled into the peritoneal cavity at a known rate. In these experiments, the composition of lavage fluid did not significantly change over time. Blood infused at a constant rate into the abdominal cavity produced corresponding, continuing increases in the RBC count. In experimental groups, the liver, spleen, or intestine were injured before lavage. Only initial RBC counts greater than 1 million/mm3 or rising RBC counts in serial lavage samples were associated with life-threatening hemorrhage. Gram stains of samples were positive for bacteria in 43% of fasted dogs and in 80% of fed dogs with intestinal perforation.

Albumins↗

Retroglenoid venoconstriction and its influence on canine intracranial venous pressures.

Using standard in vitro techniques, we found that the canine retroglenoid vein, a vessel that drains a significant fraction of canine cerebral venous effluent, demonstrated the following: an average wall thickness of approximately 240 microns; a norepinephrine (NE) content of approximately 3 micrograms/g tissue; a NE uptake capacity (uptake 1) of approximately 8 nmol/g tissue; an ED50 for NE of 1.9 X 10(-8) M; and a phentolamine-sensitive constriction during electric transmural stimulation that had a median effective frequency of approximately 3 Hz and a maximum response that was approximately 84% of the maximum response to exogenous NE. In a separate series of in vivo experiments conducted in six alpha-chloralose-anesthetized dogs, we found that electrical stimulation of the left superior cervical ganglion produced a phentolamine-sensitive, frequency-dependent increase in cerebral venous pressure (CVP) of up to 19 mm Hg when all cerebral venous effluent was diverted through the left retroglenoid vein. Taken together, our findings suggest that the canine retroglenoid vein undergoes a marked vasoconstriction during physiological frequencies of electric sympathetic nerve stimulation in vivo. Although our data further suggest that the retroglenoid is not a dominant influence on CVP in the intact dog, they do encourage a cautious interpretation of cerebral venous outflow data obtained with techniques in which cerebral effluent is drained primarily by extracranial veins.

Animals↗

The electroencephalogram, blood flow, and oxygen uptake in rabbit cerebrum.

In the present study, the relationships among electroencephalographic (EEG) amplitude shifts, cerebral blood flow (CBF), and cerebral oxygen uptake (CMRO2) have been characterized in halothane-anesthetized rabbits. CBF was measured by timed collection of venous effluent from the superior sagittal sinus. CMRO2 was calculated as the product of CBF and the arteriovenous difference in oxygen content. The depth of anesthesia in the first series of experiments was maintained at a constant level that was characterized by spontaneous EEG shifts from high- to low-voltage states (HV-LV shifts). These shifts were associated with transient decreases in mean arterial pressure (MAP), which averaged 23 +/- 2 mm Hg (n = 17). Ninety seconds after spontaneous HV-LV shifts, MAP had returned to its original value, CBF had increased by 26 +/- 7% (n = 8), and CMRO2 had increased 22 +/- 4% (n = 7). In a second series of experiments, HV-LV shifts were induced by a 90-s application of a standardized nociceptive stimulus (n = 13). Following these stimulation-induced HV-LV shifts, CBF increased 28 +/- 5% and CMRO2 increased 27 +/- 4%. Under scopolamine (0.35 mg/kg, i.v., n = 8), no change in CBF was observed following HV-LV shifts induced by 90-s of stimulation, although CMRO2 increased significantly by 14 +/- 3%. After 300 s of post-scopolamine stimulation, however, both CBF and CMRO2 had significantly increased by 12 +/- 3 and 15 +/- 3% (n = 8) of control, respectively. These results demonstrate that HV-LV shifts, whether spontaneous or stimulation-induced, are associated with significant increases in both CBF and CMRO2. Because the early (90-s) increases in CBF but not those in CMRO2 could be blocked by scopolamine, we suggest that the cerebral vasodilatation that occurs during the early phase of HV-LV shifts involves cholinergic mechanisms. Because scopolamine could not block the increase in CBF observed after 300 s of stimulation, we suggest that the final value of CBF obtained after an HV-LV shift is determined by a combination of both cholinergic and noncholinergic factors.

Animals↗

Specialization in cerebral and extracerebral neurovascular mechanisms.

The neuroeffector properties of four blood vessels with diverse characteristics are compared and contrasted. The variables include the density and distribution pattern of sympathetic innervation; size, direction, and nerve frequency-characteristics of the neurogenic response, nature of the sympathetic transmitter, receptor types, and receptor-response coupling; and the level and temperature sensitivity of myogenic tone. In many instances, these features can be related to the functional role of the vessels and their pharmacological characteristics. The underlying basis of this diversification, with one exception, which can be related to developmental origin, is entirely unknown.

Animals↗

Ca(2+) sensitivity of fetal coronary arteries exposed to long-term, high-altitude hypoxia.

OBJECTIVE: To determine the contribution of decreased calcium responsiveness of fetal coronary arteries to decreased contractile responses to potassium and the thromboxane A(2) analogue U46619 in these arteries after exposure to chronic hypoxemia. METHODS: Concentration-response curves to Ca(2+) in beta-escin-permeabilized left circumflex (LCx), left anterior descending (LAD), and right coronary artery (RCA) rings from high-altitude (HA) and control (CON) fetuses were measured. In a second set of beta-escin-permeabilized coronary artery rings, the effect of U46619 on Ca(2+) sensitivity was tested. RESULTS: Maximum Ca(2+)-activated force (T(max)) was decreased in HA LCx (CON 0.091+/-0.010 versus HA 0.057+/-0.006 g/cm(2); P<.05) and HA LAD (CON 0.065+/-0.012 versus HA 0.031+/-0.007 g/cm(2); P <.05). No significant difference was observed in the RCA. There was no change in the pD(2) (-log EC(50)) values between CON and HA coronary rings. The Ca(2+) sensitizing effect of U46619 on submaximal Ca(2+)-activated force was lower only in the HA LCx (CON 0.044+/-0.010 versus HA 0.023+/-0.006 g/cm(2) at 10(-5) mol/L; P<.05). CONCLUSION: These results indicate that maximum tension development in response to Ca(2+) was decreased in the HA LCx and LAD but not the RCA; however, Ca(2+) sensitivity of the contractile apparatus was unaltered in all of them. Decreased Ca(2+) responsiveness may partially explain the decreased contractile capability of fetal LCx and LAD during long-term, high-altitude intrauterine hypoxemia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Hemorrhage-induced cerebral vasoconstriction in dogs.

Cerebrovascular responses to a 20% volume hemorrhage were studied in chloralose-anesthetized dogs with the Doppler cerebral venous outflow method. Arterial PCO2, PO2, and pH were held constant by servocontrol of ventilation. The experimental results were divided into 2 groups as determined by the spontaneous responses of mean arterial pressure (MAP) to hemorrhage. In Group 1 (n = 11), steady state MAP decreased 25%, cerebral blood flow (CBF) decreased 15%, and cerebrovascular resistance (CVR) decreased 13% (autoregulatory vasodilatation). In group 2 (n = 23), MAP changed less than 10 mm Hg, CBF decreased 13%, and CVR increased 15%. The hemorrhage-induced cerebral vasoconstriction in Group 2 was characterized by the following: phenoxybenzamine (2 mg/kg i.v., n = 3) reduced post-hemorrhage CVR from 116% to 95% of prehemorrhage CVR (cCVR); phentolamine (2 mg/kg i.v., n = 5) reduced post-hemorrhage CVR from 114% to 91% of cCVR; and verified local anesthetization of both superior cervical ganglia (n = 5) reduced post-hemorrhage CVR from 116% to 94% of cCVR. Thus in Group 2, sympathetic vasoconstriction contributed approximately 5% of cCVR; following normotensive hemorrhage, it accounted for up to 20% of post-hemorrhage CVR. In combination with prevous studies, these data suggest that cerebrovascular responses to hemorrhage balance between autoregulatory vasodilatation and sympathetic vasoconstriction.

Animals↗