Search PubMed⌕ Search

Biomedical subjects

H R Hellstrom

Publications and source records attributed to H R Hellstrom.

At least 19 recordsLinked to original sources
PubMed1993

A case that biomedicine is unduly negative to radical hypotheses and to theorizing--evidence based on cardiology's reaction to the spasm of resistance vessel concept and on the nature of scientific research.

This communication will attempt to make a case that biomedicine is unduly negative to radical hypotheses and to theorizing. Evidence will be based on a proposed undue negativity by cardiology to a radical hypothesis I first described two and a half decades ago--the spasm of resistance vessel (S-RV) concept of ischemic heart disease (IHD). The theory is regarded as an alternate paradigm and deals with basic pathogenetic mechanisms of IHD, the most significant disorder of Western civilization. The concept, if valid, might help in reducing the impact of this disorder, and I believe that the evidence for the theory and the importance of IHD support a more open minded attitude toward the idea. Cardiology's negativity is attributed to the nature of research; the most important factor is considered to be the Kuhnian negativity of scientific communities to hypotheses which are destructive of conventional wisdom, and a second factor is the special nature of biomedical research. Biomedicine is regarded as special because a low level of specific information about complex biomedical processes has fostered an essentially total study-based approach. Such an approach is assumed to have resulted in biomedicine's use of induction as 'the' method of scientific inquiry, and prompted negativity towards the hypothetico-deductive method used to develop and test the theory. Also, the study-based nature of biomedicine appears to have fostered an intuitive reliance on only newly performed studies to test hypotheses, which led to ignoring evidence for the concept derived from known information about IHD. Biomedicine is also regarded as special because its infrequent use of paradigm-change has resulted in unfamiliarity with this method, and because the practical method of training in biomedical research has worsened the general unfamiliarity of scientists with theoretical aspects of science. Because of these factors, the S-RV concept has not yet been properly evaluated--a quarter of a century after it was first created.

Cardiology↗
PubMed1993

Evidence in support of the spasm of resistance vessel concept of ischemic heart disease: an update in 1993.

The goal of this communication is to provide more evidence for the ischemic heart disease (IHD) component of the spasm of resistance vessel (S-RV) concept of IHD and other ischemic diseases. The S-RV concept of IHD is considered to be an alternate paradigm which challenges the accepted understanding of this disorder. The theory asserts that primary S-RV directly induces symptoms in IHD, and this position is in opposition to the accepted view that symptoms are induced directly by primary occlusions of epicardial arteries by coronary artery disease, spasm, and thromboses. The theory, if valid, should be useful in reducing the impact of IHD, as it generally is accepted that the correct appreciation of basic pathophysiological mechanisms helps ensure the most appropriate prevention and treatment of disease.

Angina Pectoris↗
PubMed1990

The spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases.

This communication will discuss the spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases, and will focus on ischemic heart disease. The hypothesis is regarded as a separate model or paradigm, and is based on the principle that spasm of resistance vessels directly induces symptoms in these conditions. Resistance vessels help maintain vascular homeostasis through autoregulatory mechanisms, and spasm of resistance vessels is considered to represent 'inappropriate' activation of these mechanisms by disease states, which are equated with risk factors. For ischemic heart disease, the most important risk factor is stenotic coronary artery disease, and the concept asserts that severe ischemia secondary to coronary artery disease causes sufficient tissue injury to incite injury-spasm of resistance vessels. While it is universally accepted that occlusions of epicardial arteries by stenotic coronary artery disease, spasm, and thromboses directly induce clinical symptoms, the hypothesis suggests that these occlusions have other roles. The concept accepts all current treatments of ischemic heart disease, but as this disorder is viewed differently, a significantly different direction of research is proposed for improving its treatment and prevention.

Coronary Vasospasm↗
PubMed1990

Myocardial reperfusion injury: an assessment by the spasm of resistance vessel concept of ischemic heart disease.

Myocardial reperfusion injury will be discussed in context to the spasm of resistance vessel concept of ischemic heart disease. This hypothesis attributes symptoms in this disorder directly to primary spasm of resistance vessels, and is based in part on a study of no-reflow which provided evidence that no-reflow is due to ischemia-induced injury-spasm of resistance vessels. Studies of no-reflow and reperfusion injury are rather similar, and the concept asserts that ischemia-induced injury-spasm causing no-reflow is involved in reperfusion injury. It is recognized that oxygen free radicals cause both myocardial and vascular injury during reperfusion injury, and the concept suggests that vascular injury contributes significantly to reperfusion injury by inducing the sequence of injury-spasm, no-reflow, fresh ischemia, and fresh ischemic reperfusion injury. In keeping with this, the possible involvement of spasm and no-reflow in reperfusion injury occasionally is mentioned. However, it seems to be generally accepted that reperfusion injury is due essentially solely to direct myocardial injury by free radicals, and possible reasons will be explored for a relative disinterest in spasm and no-reflow in reperfusion injury.

Animals↗
PubMed1982

The injury-spasm (ischemia-induced hemostatic vasoconstrictive) and vascular autoregulatory hypothesis of ischemic disease. Resistance vessel-spasm hypothesis of ischemic disease.

THe injury-spasm concept assumes that severe myocardial ischemia secondary to stenotic coronary artery disease causes spasm of resistance vessels through ischemic tissue injury. In this communication the concept is developed further and is now extended to include other diseases. It is suggested that relative arterial insufficiency, as traditionally understood, is an invalid concept and that disorders usually attributed to it, including congestive heart failure and peripheral vascular disease, should be attributed to injury-spasm. Because a basic reaction to injury is to prevent bleeding, injury-spasm is identified as an exaggerated form of hemostatic vasoconstriction, and spasm is related to distorted vascular autoregulatory activities of resistance vessels. It is asserted that blood platelets probably are not involved int he initiation of ischemic attacks, and instead of a platelet thromboxane/vessel prostacyclin vasomotor balance of epicardial coronary arteries, the vasoconstrictive/vasodilative balance is centered in resistance vessels and is based on autoregulatory processes such as the hemostatic injury-spasm reaction and reactive hyperemia.

Animals↗
PubMed1979

Evidence in favor of the vasospastic cause of coronary artery thrombosis.

Evidence is presented which suggests that it is likely that vasospasm initiates coronary artery thrombosis. Spasm causes a violet constriction of the vessel and also produces stasis, and both factors are implicated in the thrombotic process. Spasm can occur in sclerotic segments, and intimal tears and plaque ruptures in arteriosclerotic plaques are attributed to spasm. The thrombus forms over the intimal disruption, abetted by the stasis of spasm. In arteries with mild or no intimal injury, continuing stasis over a period of time is considered as the major factor in thrombus formation. This ongoing stasis is attributed to an injury-spasm reaction to necrotic muscle, and probably is equivalent to the "no-reflow" phenomenon of infarction.

Constriction, Pathologic↗
PubMed1979

Eosinophilic pyeloureteritis: report of a case.

A case is reported of ureteral obstruction that was owing to eosinophilic pyeloureteritis, a previously unrecorded entity. The microscopic findings of extensive fibrosis and a relatively mild eosinophilic infiltrate were similar to those found in a series of eosinophilic cystitis, which was reported recently from this laboratory. Also, local injury appears to initiate some examples of eosinophilic cystitis and in the present case there was a striking history of injury 1 month before the symptoms of ureteral obstruction.

Adult↗
PubMed1979

Eosinophilic cystitis. A study of 16 cases.

The authors describe 16 examples of eosinophilic cystitis. Cases were predominately in older men, and usually were associated with other conditions of the bladder or prostate. In contrast, most of the 21 cases reported in the English language were in women and children who had a low incidence of associated bladder conditions, but often had allergic disorders and eosinophilia. It appears that either bladder injury or allergy predisposes to eosinophilic cystitis. The bladder-injury type probably occurs fairly commonly and can be misdiagnosed both clinically and pathologically. In most of the present series, the clinical diagnosis was carcinoma of the bladder, and some biopsy specimens superficially resembled specimens from cases of nonspecific chronic inflammation. There was muscle necrosis in most examples, and significant replacement fibrosis of muscle in all the latter sometimes masquerading as mucosal fibrosis. Giemsa stain for eosinophils and trichrome stain for muscle fibrosis are helpful diagnostic aids. Also, eosinophilic cystitis appears related to allergic cystitis and interstitial cystitis.

Aged↗
PubMed1979

Coronary artery vasospasm: the likely immediated cause of acute myocardial infarction.

Features of infarction can be divided into two types--the spasmodic and the mechanical. The former (pre-infarct angina and emotional factors in infarction) seem readily explainable by spasm, and are similar to the findings in angina which prompted Heberden to consider angina as spasmodic. The mechanical features of infarction (association with thrombosis and arteriosclerosis, and severe and unremitting chest pain) seem to be the antithesis of spasm and probably account for the reluctance to consider spasm seriously in infarction. The injury-vasospasm hypothesis of acute myocardial infarction explains both spasmodic and mechanical features. Spasm represents a dominance of vasoconstricting over vasodilating forces. Coronary sclerosis can result in both ischaemia (vasodilating) and ischaemic injury-spasm (vasoconstricting). The fight-flight component of the autonomic nervous system is considered to be vasodilating, and the conservation-withdrawal portion to be vasoconstricting. Once spasm occurs, a new balance of forces obtains which can lead either to vasodilatation and relief of symptoms or to infarction.

Acute Disease↗
PubMed1979

Cerebellar retraction: significance and sequelae.

Does cerebellar retraction during operations in the posterior fossa contribute to increased morbidity and mortality, and if so, what are the critical factors involved? In order to answer these questions, graded retractor pressures of 10, 20, and 30 mm Hg were applied for one hour to the cerebellar hemispheres of dogs in the sitting position. It was noted that the amount of mechanical pressure and the difference between systemic perfusion pressure and retractor pressure were important determinants of the outcome. The mechanism of damage from retractor pressure is discussed.

Animals↗