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Biomedical subjects

D L Jones

Publications and source records attributed to D L Jones.

At least 163 records · Page 9Linked to original sources
PubMed1988

Internal cardiac defibrillation: single and sequential pulses and a variety of lead orientations.

A sequential pulse system for internal cardiac defibrillation incorporating catheter and patch electrodes with two current pathways has been shown to reduce defibrillation threshold in comparison to the single pulse technique. The relative advantage of the sequential pulse over the single pulse technique with other lead systems is not known. We compared defibrillation thresholds using sequential and single pulses delivered to a variety of lead orientations with the same electrode surface areas, when possible. Defibrillation threshold totals determined in halothane-anesthetized open-chest pigs averaged: For the single pulse shock passed between (1) superior vena cava (SVC) and left ventricular apical patch (LVA), 27.2 +/- 9.1 joules (J) and (2) LV epicardial patch (LVE) to right ventricular epicardial (RVE) patch leads, 16.5 +/- 2.1 J; and for the sequential pulse shock with two pulses passed between: (1) the SVC to RV intracavitary apex (RVA) and a quadripolar catheter in the coronary sinus to the RVA, 11.6 +/- 1.0 J; (2) the SVC to LVA and the LVE to RVE, 9.6 +/- 1.3 J and (3) the SVC to RVA and the LVE to RVA, 8.9 +/- 0.4 J. Defibrillation thresholds for sequential pulse shocks were all significantly lower than either of the defibrillation thresholds for single pulse shocks (p less than 0.001). We conclude that the sequential pulse system provides a substantial reduction in defibrillation threshold over the single pulse regardless of the lead system when the surface area and pulse characteristics are controlled. Sequential pulse technique may be valuable in the design of an implantable automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat.

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-microL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3-5 min. Lesions of the median preoptic region produced by injecting 1.0 microgram of kainic acid in 0.25 microL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

Angiotensin II↗
PubMed1988

Hypothalamic alpha-adrenergic blockade modifies drinking and blood pressure responses to central angiotensin II in conscious rats.

These experiments investigated in the awake rat the involvement of noradrenergic projections to the rostral hypothalamus in the drinking and pressor responses elicited by intracerebroventricular (i.c.v.) injections of 25 ng of angiotensin II. Phentolamine mesylate in doses of 2.5-125 micrograms injected into the rostral hypothalamus produced a dose-dependent depression of both the drinking and pressor responses elicited by i.c.v. administration of angiotensin II. A paradoxical increase in heart rate was associated with a decrease in pressor responses with increasing doses of phentolamine. This response was due to tissue injections, since pretreatment by injecting 12.5 micrograms of phentolamine into the ventricle did not block either the cardiovascular or drinking responses to i.c.v. injections of angiotensin II. Yohimbine (0.33-3.3 micrograms), DL-propranolol (25 micrograms), and atenolol (25 micrograms) did not, but prazosin (0.7 microgram) did significantly alter the pressor responses. Although yohimbine also was without effect on drinking, prazosin reduced the drinking responses. These results suggest that alpha 1-adrenergic receptors in the rostral hypothalamus are involved in the control of both the drinking and pressor responses elicited by i.c.v. injections of angiotensin II. In the case of propranolol and atenolol, beta-adrenergic receptors altered only the drinking response in a nonspecific manner by eliciting competing behaviors. Whether they are involved in modifying the drinking response only remains to be demonstrated.

Adrenergic alpha-Antagonists↗
PubMed1988

Effect of paraventricular nucleus lesions on drinking and pressor responses to ANG II.

Experiments were done to investigate the contribution of cells of the paraventricular nucleus of the hypothalamus (PVH) to the drinking and pressor responses elicited by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake unrestrained rat. Microinjection of ANG II (5 eta g in 0.2 microliter) elicited drinking (7.1 +/- 0.7 ml in 15 min, n = 18) and pressor (19 +/- 1 mmHg, n = 17) responses. Bilateral lesions of the PVH by the administration of kainic acid (KA; 0.2 microgram in 0.2 microliter of phosphate buffer) resulted in the abolition of the drinking response (before, 7.8 +/- 1.8 ml in 15 min; after, 0 ml in 15 min, n = 6) and significant (P less than 0.05) attenuation of the pressor response (before, 15 +/- 1 mmHg; after, 5 +/- 2 mmHg, n = 5). Administration of 0.2 microliter of the phosphate buffer vehicle bilaterally into the PVH and KA into regions adjacent to the PVH had no significant effect on the drinking or pressor responses. KA injections into the PVH resulted in the loss of 70-80% of parvocellular cells in the posterodorsal component of the PVH compared with animals with KA injections into adjacent non-PVH tissue (n = 7) or vehicle injection into the PVH (n = 5). These results suggest that parvocellular cells of the PVH are an important component of the neural circuitry that mediates the drinking and pressor response to ANG II acting at the SFO.

Angiotensin II↗
PubMed1988

Prediction of defibrillation success from a single defibrillation threshold measurement with sequential pulses and two current pathways in humans.

The ultimate aim of defibrillation testing is to predict consistent defibrillation. This study tested the hypothesis that defibrillation success could be predicted from a single measurement of defibrillation threshold. We measured defibrillation threshold by using three patch electrodes and a standard protocol intraoperatively in 49 patients undergoing arrhythmia surgery. Each patient was then assigned to one of five energy subgroups (0.5, 1.0, 1.5, 2.0, or 2.5 times defibrillation threshold) for a single shock (followed by a rescue shock if necessary) for a subsequent ventricular fibrillation episode. A curve relating percent success to energy was then constructed for the group. Defibrillation threshold averaged 4.7 +/- 2.98 J for the group (mean +/- SD). There was a curvilinear relation between the energy of the defibrillation threshold ratio test shock and percent success: 33.3%, 58.3%, 81.8%, 91.7%, and 100% at mean defibrillation threshold ratios of 0.56 +/- 0.14, 1.02 +/- 0.07, 1.53 +/- 0.14, 1.88 +/- 0.09, and 2.60 +/- 0.14, respectively. We conclude that consistent defibrillation is predictable from a single measurement of defibrillation threshold. Furthermore, for an individual patient, a safety margin of 2.6 times defibrillation threshold should approximate 100% successful defibrillation for a single test shock.

Adult↗
PubMed1987

Isthmus and ligament interrelationships: a computerized analysis of the spatial relationships of the hinge structures in unionid mussels.

A study of the isthmus and ligament in unionid mussels was undertaken employing methods specifically designed to preserve the in vivo relationships of these interrelated structures. Serial sections of the hard and soft tissues were used for two-dimensional analysis. From these, a tridimensional computerized reconstruction was developed. Special dissections of the undisturbed isthmus were also utilized. By using such methodologies, a new description of the ligament has been developed employing such terminology as the foliated ligament and the posterior folding laminae. Similarly, for the isthmus, an anterior lyre, a pallial crest, a pallial peduncle, and a posterior lyre are described. Such entities are both morphologically and physiologically related to the shell and ligament.

Animals↗
PubMed1987

Mitogenicity of human fibroblasts in vivo for human breast cancer cells.

Stromal factors have been implicated in the regulation of mammary epithelial cell behaviour, but their influence on human breast cancer is unknown. Fibroblasts were grown in monolayer cell culture from explants of benign and malignant breast tissue and normal skin. MCF7 human breast cancer cells alone (2 X 10(6) cells) or in combination with live fibroblasts (MCF7 + F) were inoculated into the mammary fat pads of 6-8-week-old female nude mice. After 5 weeks tumours were excised, weighed and fixed for histological examination. Addition of live breast fibroblasts significantly increased the retrieval (127/135 versus 52/106, P less than 0.01, chi 2 test) and growth (tumour weight 174 +/- 11 versus 41 +/- 4 mg, mean +/- s.e.m., P less than 0.01, Mann-Whitney U test) of subsequent tumours. Histological examination did not reveal any morphological difference between the two tumour groups. Injection of fibroblasts alone did not produce tumours. Addition of skin fibroblasts was also stimulatory. Glutaraldehyde-killed fibroblasts increased tumour take but did not stimulate tumour growth. Mononuclear blood leucocytes were ineffective. The results demonstrate that, in this model, fibroblasts exert stimulatory influences on human breast cancer xenograft growth and development.

Adenocarcinoma↗
PubMed1987

Determination of dehydroepiandrosterone and dehydroepiandrosterone sulphate in blood and tissue. Studies of normal women and women with breast or endometrial cancer.

Radioimmunoassay methods for measuring dehydroepiandrosterone (DHA) and its sulphate (DHAS) in human plasma and tissues were developed and validated. Plasma levels were measured in men, pre- and postmenopausal women, and patients with endometrial or breast cancer. In the patients, tissue concentrations were also measured. Plasma DHA levels fluctuated synchronously with cortisol, but DHAS levels were less labile, and reached maximum levels during the day and were lowest at night. No obvious pattern was seen in relation to the menstrual cycle. Both DHA and DHAS levels fell with age, but DHA levels reached a plateau at about 60 years. No significant effect of weight on plasma levels was found. Plasma levels in the cancer patients were not significantly different from age-matched controls either when single samples were compared, or when mean 24 h levels were used. Endometrial tissue levels of DHA fell with age, unlike DHAS. In breast tumour tissue, DHA, but not DHAS concentrations were higher than in normal breast tissue. A good correlation between plasma and tissue DHAS levels was found, and DHA levels were also correlated in plasma and tissue. The correlations between plasma and tissue were not observed in tumour tissue, which may be due to altered tissue metabolism.

Adult↗
PubMed1987

Nerve sharing by an interpositional sural nerve graft between the great auricular and inferior alveolar nerve to restore lower lip sensation.

A case of bilateral nerve sharing via an autogenous sural nerve graft interposed between the ipsilateral great auricular nerve and the inferior alveolar nerve was used to restore sensation to the lower lip. To our knowledge this is the first report of successful nerve sharing between a sensory branch of the cervical plexus and the inferior alveolar nerve.

Adult↗
PubMed1987

A computerized analysis of the shape and stability of mandibular arch form.

To determine whether a particular ideal orthodontic arch form could be identified, the mandibular dental casts of 30 untreated normal cases, 30 Class I nonextraction cases, and 30 Class II nonextraction cases were examined. Following computerized digitizing and the use of a mathematic function called polynomial of the fourth degree, arch forms were generated for each sample and then compared to 17 commercially produced arch forms. Results showed that no particular arch form predominated in any of the three samples. A shape representing a combination of the "Par" and "Vari-Simplex" arch forms approximated to only 50% of the cases in the three samples. The remaining 50% of the cases displayed a wide variety of arch forms. Cases that had changes in arch form during nonextraction treatment frequently were not stable; almost 70% showed significant long-term posttreatment changes. Customizing arch forms appears to be necessary in many cases to obtain optimum long-term stability because of the great individual variability in arch form found in this study.

Adolescent↗
PubMed1987

Cryosurgical modification of the atrioventricular node: a closed heart approach in the dog.

Intraoperative modification of the atrioventricular (AV) node to prolong refractoriness could be an alternative to His bundle ablation in patients with refractory supraventricular arrhythmias. It was postulated that a cryosurgical lesion at the posterior interatrial septum in the closed heart could achieve this. An electrophysiologic study was performed in anesthetized dogs. The AV fat pad was mobilized to expose the posteroseptal region. A cryoprobe cooled to 0 to -10 degrees C was moved in the exposed region until reversible AV block indicated proximity of the AV node. The probe was then cooled to -70 degrees C for 30 seconds. Four weeks later, five dogs had a favorable result with a mean prolongation of Wenckebach cycle length of 45 +/- 7% (p less than 0.05). Two dogs had complete heart block. Decreased (one dog) or increased (one dog) duration of freezing resulted in no change and complete heart block, respectively. Histologic examination verified partial damage to the AV node with preservation of the His bundle. Thus, controlled cryoinjury to modify AV node function is feasible in the closed heart; preservation of AV conduction provides an advantage over His bundle ablation.

Animals↗
PubMed1987

Internal ventricular defibrillation with sequential pulse countershock in pigs: comparison with single pulses and effects of pulse separation.

We compared single to sequential pulse shocks with different pulse separations on internal cardiac defibrillation by using a catheter and plaque electrodes in open-chest halothane-anesthetized pigs. Ten seconds after fibrillation onset, defibrillation was attempted using trapezoidal pulses of 65% tilt, approximately 5 ms duration and fixed outputs from 1.0 to 50 joules (J). With single pulses, minimum defibrillation energy for the catheter alone was 2.4 +/- 0.3 J/kg (mean +/- standard error) and 2.1 +/- 0.2 J/kg for the catheter tip to plaque configuration. With sequential pulse shocks, the first pulse delivered via the catheter and the second pulse from the catheter tip to the plaque electrode, the energy necessary for defibrillation was dependent on the separation time between the two pulses (2.0 +/- 0.2, 1.5 +/- 0.2, 0.9 +/- 0.1, 1.3 +/- 0.3, 0.6 +/- 0.2, and 1.2 +/- 0.2 J/kg at 100, 10, 1, 0.5, 0.2, and 0.1 ms, respectively). Further, at the 0.2 ms separation, 100% of the animals could be defibrillated with less than 2.0 J/kg (35 J total). We conclude that sequential pulse defibrillation provides a significant improvement over single pulse defibrillation. The optimum separation between the sequential pulses in this study was 0.2 ms.

Animals↗
PubMed1987

Defibrillation threshold: a simple and quantitative estimate of the ability to defibrillate.

It has recently been shown that the probability of successful defibrillation as a function of energy has a sigmoidal dose-response relationship. Determination of a defibrillation "dose-response curve" is time consuming and requires multiple defibrillation attempts. On the other hand, determination of a defibrillation threshold is achieved rapidly and would be better suited to study the effect of interventions on the ability to defibrillate patients. We assessed the relationship of defibrillation threshold to the defibrillation "dose-response curve" in twelve open chest, halothane anesthetized pigs. Ventricular fibrillation was induced electrically, and defibrillation was attempted by passing sequential pulse shocks through an indwelling catheter and plaque electrodes. Defibrillation threshold was determined by decreasing the stored voltage of the initial shock until it failed to defibrillate the heart. Five different stored voltage levels distributed around defibrillation threshold were then randomly administered, six times for each level. A "dose-response curve" was obtained for each animal. Defibrillation threshold superimposed on the "dose-response curve" at 76 +/- 7.2 percent (mean +/- SEM) defibrillation success. Energy delivered at 1.5 times average defibrillation threshold was predicted to achieve 100 percent defibrillation success for a single shock in all animals. We conclude that defibrillation threshold provides a simple and quantitative estimate of the ability to defibrillate with a predictable relationship to the "dose-response curve."

Animals↗
PubMed1987

Cardioversion and defibrillation using a catheter electrode: myocardial damage assessed at autopsy.

A technique has been described for countershock in an intensive care setting using a catheter electrode in patients with recurrent ventricular tachyarrhythmias. During defibrillation or cardioversion an electrode in the superior vena cava acts as an anode and an electrode in the right ventricular apex is the cathode. This report describes the resultant changes in the hearts of four men who died with recent, large myocardial infarcts and who had received eight to 55 countershocks of 2.5-50 joules through the catheter. Mural thrombus and/or focal endothelial hemorrhage was found in three hearts at the anode site. Thrombus was seen at the cathode site in two hearts. Myocardial necrosis, secondary to the catheter, was present in only one heart which had a 2 mm rim of granulation tissue around the distal electrode. It is unlikely that this focal area of right ventricular damage would be clinically important. We conclude, therefore, that repeated countershocks delivered through the catheter system produce little myocardial damage.

Aged↗
PubMed1987

Adrenergic effects on internal cardiac defibrillation threshold.

Autonomic neural tone modulates arrhythmias and could affect the efficacy of an implantable defibrillator if defibrillation threshold is also altered by changes in neural activity. We determined the effects of alpha- and beta-adrenoceptor agonists and antagonists on the energy requirement for defibrillation using a sequential-pulse technique in anesthetized pigs. The doses for each drug were selected based on the results of dose-response curves. The mean defibrillation threshold was 10.2 +/- 0.65 J (mean +/- SE) in control and 10.0 +/- 0.84, 9.4 +/- 0.87 and 8.9 +/- 0.89 J during phenylephrine infusions of 0.7, 1.35, and 2.0-4.0 micrograms X kg-1 X min-1 [n = 8, P = not significant (NS)]. Phenylephrine at all infusion rates increased the ventricular fibrillation threshold, indicating that effects on the ventricular fibrillation threshold may occur independent of changes in defibrillation threshold. No significant change was observed in the defibrillation threshold before and after administration of isoproterenol (6.5 +/- 0.72 and 6.7 +/- 0.93 J, n = 8, P = NS). Similarly, no change in defibrillation thresholds was observed after 1.5-2.0 mg/kg phentolamine (8.5 +/- 0.85 and 7.9 +/- 0.93 J, n = 8, P = NS) or 3.0-6.0 mg/kg atenolol (10.0 +/- 1.7 and 10.3 +/- 2.6 J, n = 8, P = NS). However, when defibrillation threshold was determined using a single-pulse method, isoproterenol infusion produced a significant decrease (17.3 +/- 1.5 vs. 14.6 +/- 1.9 J, n = 7, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Sequential pulse defibrillation in man: comparison of thresholds in normal subjects and those with cardiac disease.

We compared the parameters describing the defibrillation threshold in patients with normal hearts and in patients with ischemic heart disease, using a special electrode system and sequential pulses of current. Twenty-eight patients consented to the study (mean age: 36.6 +/- 10.1 years; mean mass: 80.7 +/- 13.8 kg). Twenty-one patients underwent surgery for Wolff-Parkinson-White syndrome (relatively normal hearts). Six patients had a history of previous myocardial infarction and aneurysm or coronary artery disease; and one patient had been resuscitated from an episode of sudden death, without evidence of consequent myocardial damage. For 26 patients, defibrillation thresholds were determined intraoperatively by passing sequential pulses through a catheter electrode and epicardial mesh electrode. For 2 patients defibrillation thresholds were determined during electrophysiologic study, after ventricular fibrillation was induced by programmed stimulation, by passing sequential pulses through a catheter and skin-patch electrode. Parameters for sequential pulse defibrillation thresholds between the two groups did not differ appreciably. Total energy for patients with normal hearts averaged 9.9 +/- 6.3 J compared to 8.9 +/- 4.6 J for patients with cardiac disease. No patient with cardiac disease had defibrillation parameters that exceeded the range of the normal patients. These results suggest that the presence of cardiac disease may not significantly alter the parameters necessary for successful defibrillation when using sequential pulses for delivery of energy.

Adult↗